Catalase Activity (catalase + activity)

Distribution by Scientific Domains

Selected Abstracts

Response of the freshwater alga Chlorella vulgaris to trichloroisocyanuric acid and ciprofloxacin,

Xiangping Nie
Abstract The effects of trichloroisocyanuric acid (TCCA) and ciprofloxacin (CPFX) on the freshwater alga Chlorella vulgaris were assessed by toxicity bioassays and by the values of biomarkers in phase I and phase II. The biomarkers included growth rate, concentration of chlorophyll a, activities of 7-ethoxyresorufin- O -dealkylases (EROD), glutathione S -transferase (GST), catalase (CAT), and total glutathione (GSH). Ciprofloxacin was a weaker growth inhibitor than TCCA but, at a concentration of greater than 12.5 mg/L, decreased the growth of C. vulgaris. Concentration of chlorophyll a showed a similar trend. The 96-h median effective concentration (EC50; i.e., 50% reduction in growth relative to the control) of CPFX was 20.6 mg/L. Trichloroisocyanuric acid was a strong growth inhibitor and, at concentrations of greater than 0.80 mg/L, caused 100% inhibition on 24-h exposure. The 96-h EC50 of TCCA was 0.313 mg/L. Ciprofloxacin and TCCA affected the phase I and phase II enzyme activities differently. On exposure to CPFX, both EROD and GSH decreased at low CPFX concentrations (<5.0 mg/L) and increased at high CPFX concentrations (>12.5 mg/L), and CAT and GST exhibited induction at low concentrations and inhibition at high concentrations. In TCCA exposure, GST activity was significantly stimulated, and GSH concentration was increased. Catalase activity increased only at TCCA concentrations of greater than 0.12 mg/L, and no change in EROD activity was observed. [source]

Response of Oryzacystatin I Transformed Tobacco Plants to Drought, Heat and Light Stress

K. Demirevska
Abstract Transformed tobacco plants expressing a rice cysteine proteinase inhibitor (OC-I) and non-transformed plants were grown in a controlled environment and subjected to various stresses. Two-month-old transformed and non-transformed plants were exposed for 5 days to drought conditions by withholding watering. High temperature (40 C) was applied additionally at day 6th for 5 h either individually or in combination with drought. All stress treatments were applied under low (150 ,mol m,2 s,1 PPFD) and high light intensity (HL) of 1000 ,mol m,2 s,1 PPFD to determine if OC-I expression might provide protection under combination of stresses usually existing in nature. Drought stress led to diminution in leaf relative water content, photosynthesis inhibition, decrease in chlorophyll content and accumulation of malondialdehyde and proline. Heat stress alone did not affect the plants significantly, but intensified the effect of drought stress. HL intensity further increased the proline content. OC-I transformed plants grown under low light intensity had significantly higher total superoxide dismutase and guaiacol peroxidase activities as well as their isoforms than non-transformed control plants under non-stress and stress conditions. Catalase activity was not highly affected by OC-I expression. Results indicate that OC-I expression in tobacco plants provides protection of the antioxidative enzymes superoxide dismutase and guaiacol peroxidise under both non-stress and stress conditions. [source]

Oxidative status in iron-deficiency anemia

Jong-Ha Yoo
Abstract Oxidative stress is an imbalance between free radicals and antioxidant molecules that can play an important role in the pathogenesis of iron-deficiency anemia (IDA). The aim of this study was to investigate oxidative status in patients with IDA and alteration of oxidative status after iron treatment. Thirty-three female patients with IDA and 25 healthy controls were included in this study. Oxidant and total antioxidant capacity were determined using free oxygen radicals test and free oxygen radicals defence (Form CR 3000, Callegari, Parma, Italy). Catalase activity was measured by spectrophotometer using a commercially available kit (Bioxytech Catalase-520, OxisResearch, Portland, OR). Oxidant activity in patients with IDA was significantly higher than controls (P<0.05), while total antioxidant and catalase activity were significantly lower (P<0.05). After treatment, oxidant, antioxidant, and catalase activity reached the levels of the control group, and no significant differences were observed among groups (P>0.05). In conclusion, our data indicate that blood reactive oxygen species was lower and total antioxidant and catalase activity were higher after rather than before treatment in patients with IDA. The results of our study support the higher oxidative stress hypothesis in IDA; however, due to the limited number of cases included, more studies may be required to confirm the results. J. Clin. Lab. Anal. 23:319,323, 2009. 2009 Wiley-Liss, Inc. [source]

Effect of a Photo-synthetic Inhibitor on Tryptamine Pathway-mediated Sekiguchi Lesion Formation in Lesion Mimic Mutant of Rice Infected with Magnaporthe grisea

A. Imaoka
Abstract A lesion-mimic mutant of rice (cv. Sekiguchi-asahi) showed enhanced resistance to Magnaporthe grisea infection, thereby inducing Sekiguchi lesion (sl) formation and tryptamine accumulation under light. Both Sekiguchi lesion formation and tryptamine accumulation in leaves infected with M. grisea were inhibited by pretreatment with the photosynthetic inhibitor, 3-(3, 4-Dichlorophenyl)-1,1-dimethylurea (DCMU), which suppressed the gene expression of tryptophan decarboxylase (TDC), monoamine oxidase activity, H2O2 generation and DNA fragmentation. Catalase activity was inhibited by M. grisea infection under light, but magnitude of the inhibition was reduced in leaves pretreated with DCMU. Furthermore, tryptophan accumulated in M. grisea- infected leaves under light but not in DCMU-pretreated ones. Interestingly, such DCMU inhibition was reduced in the presence of tryptophan. Our studies suggest that chloroplasts function as the inhibitor of anti-oxidant system such as catalase activity and the supplier of a precursor of tryptamine and tryptophan in the sl mutant infected with M. grisea. [source]

Overexpression of bacterial catalase in tomato leaf chloroplasts enhances photo-oxidative stress tolerance

ABSTRACT The Escherichia coli gene katE, which is driven by the promoter of the Rubisco small subunit gene of tomato, rbcS3C, was introduced into a tomato (Lycopersicon esculentum Mill.) by Agrobacterium tumefaciens -mediated transformation. Catalase activity in progeny from transgenic plants was approximately three-fold higher than that in wild-type plants. Leaf discs from transgenic plants remained green at 24 h after treatment with 1 m paraquat under moderate light intensity, whereas leaf discs from wild-type plants showed severe bleaching after the same treatment. Moreover, ion leakage from transgenic leaf discs was significantly less than that from wild-type leaf discs at 24 h after treatment with 1 m paraquat and 10 mm H2O2, respectively, under moderate light intensity. To evaluate the efficiency of the E. coli catalase to protect the whole transgenic plant from the oxidative stress, transgenic and wild-type plants were sprayed with 100 m paraquat and exposed to high light illumination (800 mol m,2 s,1). After 24 h, the leaves of the transgenic plants were less damaged than the leaves of the wild-type plants. The catalase activity and the photosynthesis activity (indicated by the Fv/Fm ratio) were less affected by paraquat treatment in leaves of transgenic plants, whereas the activities of the chloroplastic ascorbate peroxidase isoenzymes and the ascorbate content decreased in both lines. In addition, the transgenic plants showed increased tolerance to the oxidative damage (decrease of the CO2 fixation and photosystem II activity and increase of the lipid peroxidation) caused by drought stress or chilling stress (4 C) under high light intensity (1000 mol m,2 s,1). These results indicate that the expression of the catalase in chloroplasts has a positive effect on the protection of the transgenic plants from the photo-oxidative stress invoked by paraquat treatment, drought stress and chilling stress. [source]

Oxidative stress, defense response, and early biomarkers for lead-contaminated soil in Vicia faba seedlings,

Cheng-Run Wang
Abstract Chemical analyses and biological measurements were investigated in leaves of Vicia faba seedlings exposed to extraneous lead (Pb) at 0 to 2,000 mg/kg of soil for a month. The results showed that superoxide radical (O,,2) production, increased along with total Pb in leaves and available Pb in soil, resulted in enhancement of malondialdehyde and carbonyl groups. Antioxidant enzymes, including corresponding isoenzymes and heat shock protein 70 (hsp 70), were also enhanced to some extent. Significant changes were detected in the patterns and intensities of guaiacol peroxidase isoenzymes, while superoxide dismutase, catalase, and ascorbate peroxidase isoenzymes only changed intensities. Superoxide dismutase activities increased with the increase of extraneous Pb at 0 to 500 mg/kg of soil and tended to decline thereafter, which might be responsible for the decrease of hydrogen peroxide and accumulation of O,,2. Guaiacol peroxidase and ascorbate peroxidase enzymes were upregulated to become major scavengers of excess hydrogen peroxide on the condition of decreased catalase activities. Levels of hsp 70 were well correlated with Pb contents in leaves (r = 0.777), O,,2 accumulation (r = 0.985, p < 0.01), and carbonyl groups (r = 0.920, p < 0.01) under extraneous Pb at 0 to 250 mg/kg of soil, suggesting that hsp 70 induced by O,,2 was possibly involved in disposal of denatured proteins. The results showed that O,,2, hsp 70, and guaiacol peroxidase isoenzymes had the most sensitive responses in the seedlings and these parameters could be potential early biomarkers of soil Pb contamination. [source]

Laminar xanthine oxidase, superoxide dismutase and catalase activities in the prodromal stage of black-walnut induced equine laminitis

Summary Reasons for study: Xanthine oxidase (XO)-dependent production of superoxide anion and hydrogen peroxide, a characteristic of ischaemia-reperfusion injury, may contribute to the development of equine laminitis. Objective: To determine the levels of XO and antioxidant enzymes (catalase, superoxide dismutase [SOD]) in the digital laminae of normal horses (CON) and horses in the developmental stage of laminitis using the black walnut extract (BWE) model. Methods: Healthy horses (n = 12) were administered BWE (BWE group, n = 6), or water (CON group, n = 6) through a nasogastric tube. At the onset of leucopenia in the BWE-treated animals, all horses were anaesthetised, digital laminae and other samples collected rapidly and flash frozen, and the animals subjected to euthanasia. Extracts of the frozen tissues were assayed for the 2 conformational forms of xanthine: oxygen oxidoreductase (XOR), namely, xanthine dehydrogenase (XDH) and xanthine oxidase (XO), as well as the antioxidant enzymes, SOD and catalase. Results: Extracts of liver, lungs and skin, but not digital laminae, from either CON or BWE-treated horses had endogenous SOD, whereas all had endogenous XO and catalase. The levels of XDH, XO and catalase were similar in extracts of laminae from CON and BWE-treated horses as was the ratio of XDH to XO in extracts. Conclusions and potential relevance: The absence of increased XO activity suggest against the involvement of this reactive oxygen intermediate-generating system in the development of laminar pathology in BWE-treated horses. Conversely, the absence of SOD from extracts of equine digital laminae, but not other tissues, suggests that the equine digital laminae are highly susceptible to damage by superoxide anion, produced, for example, by emigrant inflammatory leucocytes. [source]

Pharmacological interventions in aging and age-associated disorders

Kenichi Kitani
In the present study, past attempts using different pharmaceuticals and chemicals which were reported to prolong lifespans of animals are critically reviewed. Despite a large number of trials in animals and humans, the validity of supplementation of antioxidant vitamins such as vitamins A, E and C for improving human health remains unresolved at present. A recent approach using antioxidant mimetics called the EUK series which, despite an initial enthusiastically reported success in prolonging the lifespan of nematodes, remains again unsettled because of the failure in reproducing the initial success by follow-up studies. ,-Phenyl- tert -butylnitrone and related nitrones were initially introduced as radical scavengers. Some of these (e.g. disodium 2,4-disulfophenyl-N- tert -butylnitrone) are at phase 3 clinical trials as an agent to treat cerebral stroke. This effect, however, appears at least in part to be related to signal transduction which makes these agents effective against cerebral stroke even when they are administered later than its onset. (,)Deprenyl is a monoamine oxidase-B inhibitor and has some neuroprotective and anti-apoptotic effects. The drug has also been shown to prolong the lifespans of at least four different animal species. The drug upregulates superoxide dismutase and catalase activities in selective brain regions of dopaminergic nature. These effects on antioxidant enzyme activities are suspected to be causally related to its effect on lifespans of animals. Future trials using these and other drugs are expected to open new doors for interventions in aging and age-associated disorders in humans. [source]

In vivo astaxanthin treatment partially prevents antioxidant alterations in dental pulp from alloxan-induced diabetic rats

M. F. Leite
Leite MF, de Lima A, Massuyama MM, Otton R.In vivo astaxanthin treatment partially prevents antioxidant alterations in dental pulp from alloxan-induced diabetic rats. International Endodontic Journal, 43, 959,967, 2010. Abstract Aim, To evaluate the effect of astaxanthin on antioxidant parameters of dental pulp from diabetic rats. The hypothesis tested was that supplementation of diabetic rats with astaxanthin might eliminate, or at least attenuate, the defect in their antioxidative status. Methodology, Wistar rats (n = 32) were divided into four groups: untreated control, treated control, untreated diabetic and treated diabetic rats. A prophylactic dose of astaxanthin (20 mg kg,1 body weight) was administered daily by gavage for 30 days. On day 23, diabetes was induced by injection of alloxan (60 mg kg,1 body weight). After 7 days of diabetes induction, the rats were killed, and pulp tissue from incisor teeth removed. Superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and reductase activities were determined. Data were compared by anova and the Newman,Keuls test (P < 0.05). Results, Diabetes caused a reduction in SOD, GPx and reductase activity in dental pulp tissue. Astaxanthin had no effect on SOD and catalase activities; however, it stimulated GPx in control and diabetic rats. Conclusions, Diabetes altered the antioxidant system in dental pulp tissue; astaxanthin partially improved the diabetic complications. [source]

Detoxification and antioxidant effects of curcumin in rats experimentally exposed to mercury

Rakhi Agarwal
Abstract Curcumin, a safe nutritional component and a highly promising natural antioxidant with a wide spectrum of biological functions, has been examined in several metal toxicity studies, but its role in protection against mercury toxicity has not been investigated. Therefore, the detoxification and antioxidant effects of curcumin were examined to determine its prophylactic/therapeutic role in rats experimentally exposed to mercury (in the from of mercuric chloride-HgCl2, 12,mol,kg,1 b.w. single intraperitoneal injection). Curcumin treatment (80,mg,kg,1 b.w. daily for 3 days, orally) was found to have a protective effect on mercury-induced oxidative stress parameters, namely, lipid peroxidation and glutathione levels and superoxide dismutase, glutathione peroxidase and catalase activities in the liver, kidney and brain. Curcumin treatment was also effective for reversing mercury-induced serum biochemical changes, which are the markers of liver and kidney injury. Mercury concentration in the tissues was also decreased by the pre/post-treatment with curcumin. However, histopathological alterations in the liver and kidney were not reversed by curcumin treatment. Mercury exposure resulted in the induction of metallothionein (MT) mRNA expressions in the liver and kidney. Metallothionein mRNA expression levels were found to decrease after the pre-treatment with curcumin, whereas post-treatment with curcumin further increased MT mRNA expression levels. Our findings suggest that curcumin pretreatment has a protective effect and that curcumin can be used as a therapeutic agent in mercury intoxication. The study indicates that curcumin, an effective antioxidant, may have a protective effect through its routine dietary intake against mercury exposure. [source]

The influence of curcumin and manganese complex of curcumin on cadmium-induced oxidative damage and trace elements status in tissues of mice

Vladislav Eybl
Abstract Curcumin (diferuoyl methane) from turmeric is a well-known biologically active compound. It has been shown to ameliorate oxidative stress and it is considered to be a potent cancer chemopreventive agent. In our previous study the antioxidative effects of curcumin in cadmium exposed animals were demonstrated. Also manganese exerts protective effects in experimental cadmium intoxication. The present study examined the ability of the manganese complex of curcumin (Mn-curcumin) and curcumin to protect against oxidative damage and changes in trace element status in cadmium-intoxicated male mice. Curcumin or Mn-curcumin were administered at equimolar doses (0.14 mmol/kg b.w.) for 3 days, by gastric gavages, dispersed in methylcellulose. One hour after the last dose of antioxidants, cadmium chloride (33 mol/kg) was administered subcutaneously. Both curcumin and Mn-curcumin prevented the increase of hepatic lipid peroxidation , expressed as MDA level, induced by cadmium intoxication and attenuated the Cd-induced decrease of hepatic GSH level. No change in hepatic glutathione peroxidase or catalase activities was found in Cd-exposed mice. A decreased GSH-Px activity was measured in curcumin and Mn-curcumin alone treated mice. Neither curcumin nor Mn-curcumin treatment influenced cadmium distribution in the tissues and did not correct the changes in the balance of essential elements caused by Cd-treatment. The treatment with Mn-curcumin increased the Fe and Mn content in the kidneys of both control and Cd-treated mice and Fe and Cu content in the brain of control mice. In conclusion, regarding the antioxidative action, introducing manganese into the curcumin molecule does not potentiate the studied effects of curcumin. Copyright 2005 John Wiley & Sons, Ltd. [source]

Characterization of Phaffia rhodozyma 3A 4,8 Generated by Low-dose ,-irradiation

S.H. Lee
ABSTRACT: Astaxanthin content, superoxide dismutase activity, catalase activity, and transmission electron microscopy (TEM) of astaxanthin-hyperproducing mutant 3A 4,8, previously isolated through repeated rounds of ,-irradiation below 10 kGy and visual screening, was examined and compared with wild strain 67,385 and parent strain 2A2N to characterize its mutant. Astaxanthin content of Phaffia rhodozyma was determined using high-performance liquid chromatography. After 10 d culture, 3A 4,8 produced 2.5 mg/g yeast, 78% higher astaxanthin content than parent strain. Mutant exhibited lower superoxide dismutase and higher catalase activities than parent strain. TEM study showed mutant had smaller-sized mitochondria than parent strain. These results indicate ,-irradiation is an effective means of mutagenesis for production of carotenoidhyperproducing mutants. [source]

Carbon Monoxide Alleviates Salt-Induced Oxidative Damage in Wheat Seedling Leaves

Ben-Kai Huang
Abstract Carbon monoxide (CO), a by-product released during the degradation of heme by heme oxygenases (EC in animals, is regarded as an important physiological messenger or bioactive molecule involved in many biological events that has been recently reported as playing a major role in mediating the cytoprotection against oxidant-induced lung injury. In the present study, we first determined the protective effect of exogenous CO against salt-induced oxidative damage in wheat seedling leaves. Wheat seedlings treated with 0.01 ,mol/L hematin as the CO donor demonstrated significant reversal of chlorophyll decay, dry weight, and water loss induced by 300 mmol/L NaCl stress. Interestingly, the increase in lipid peroxidation observed in salt-treated leaves was reversed by 0.01 nmol/L hematin treatment. Time-course analyses showed that application of 0.01 ,mol/L hematin enhanced guaiacol peroxidase, superoxide dismutase, ascorbate peroxidase and catalase activities in wheat seedling leaves subjected to salt stress. These effects are specific for CO because the CO scavenger hemoglobin (1.2 mg/L) blocked the actions of the CO donor hematin. However, higher concentration of the CO donor (1.0 ,mol/L) did not alleviate dry weight and water loss of salt-stressed wheat seedlings. These results suggest that exogenous application of low levels of a CO donor may be advantageous against salinity toxicity. (Managing editor: Ping He) [source]

Protective effect of Hachimi-jio-gan against renal failure in a subtotal nephrectomy rat model

Noriko Yamabe
The protective effect of Hachimi-jio-gan extract against chronic renal failure in a subtotal nephrectomy rat model was investigated. The level of serum urea nitrogen by nephrectomy was increased over 15 weeks, but the administration of Hachimi-jio-gan at 50 and 200 mg led to the decrease. In addition, the levels of creatinine (Cr), urinary methylguanidine (MG) and MG/Cr were increased, whereas Cr clearance dramatically decreased in nephrectomized rats. However, oral administration of Hachimi-jio-gan extract prevented the elevation of these uremic toxins in serum and urine, and the production of hydroxyl radical. Moreover, nephrectomy led to a significant decline in superoxide dismutase (SOD) and catalase activities, but increased glutathione peroxidase activity compared with normal levels, indicating an abnormal antioxidative system. The increased activity of both SOD and catalase by the oral administration of Hachimi-jio-gan suggested that these enzymes are associated with the protective role of Hachimi-jio-gan extract against oxidative stress by nephrectomy. Moreover, the decrease in serum albumin in nephrectomized control rats was increased and proteinuria was ameliorated by the administration of Hachimi-jio-gan with improved glomerular hyalinosis, interstitial fibrosis and inflammation, suggesting the beneficial effect of Hachimi-jio-gan to prevent glomerular sclerosis and progressive renal fibrosis. This study suggests that Hachimi-jio-gan plays a protective role in the progression of chronic renal failure through the decline in uremic toxins, elevation of antioxidative enzyme activity such as SOD and catalase, and amelioration of histopathological lesions in the kidney. [source]

Submicromolar hydrogen peroxide disrupts the ability of Fur protein to control free-iron levels in Escherichia coli

Shery Varghese
Summary In aerobic environments, mutants of Escherichia coli that lack peroxidase and catalase activities (Hpx,) accumulate submicromolar concentrations of intracellular H2O2. We observed that in defined medium these strains constitutively expressed members of the Fur regulon. Iron-import proteins, which Fur normally represses, were fully induced. H2O2 may antagonize Fur function by oxidizing the Fur:Fe2+ complex and inactivating its repressor function. This is a potential problem, as in iron-rich environments excessive iron uptake would endanger H2O2 -stressed cells by accelerating hydroxyl-radical production through the Fenton reaction. However, the OxyR H2O2 -response system restored Fur repression in iron-replete Luria,Bertani medium by upregulating the synthesis of Fur protein. Indeed, when the OxyR binding site upstream of fur was disrupted, Hpx, mutants failed to repress transporter synthesis, and they exhibited high levels of intracellular free iron. Mutagenesis and bacteriostasis resulted. These defects were eliminated by mutations or chelators that slowed iron import, confirming that dysregulation of iron uptake was the root problem. Thus, aerobic organisms must grapple with a conundrum: how to monitor iron levels in oxidizing environments that might perturb the valence of the analyte. The induction of Fur synthesis by the OxyR response comprises one evolutionary solution to that problem. [source]

Hypocholesterolaemic and antioxidant effects of Glycyrrhiza glabra (Linn) in rats

Nishant P. Visavadiya
Abstract The hypocholesterolaemic and antioxidant effects of Glycyrrhiza glabra (GG) root powder were examined in hypercholesterolaemic male albino rats. A 4-week administration of GG root powder (5 and 10 gm% in diet) to hypercholesterolaemic rats resulted in significant reduction in plasma, hepatic total lipids, cholesterol, triglycerides and plasma low-density lipoprotein and VLDL-cholesterol accompanied by significant increases in HDL-cholesterol levels. Furthermore, significant increases in fecal cholesterol, neutral sterols and bile acid excretion along with an increase in hepatic HMG-CoA reductase activity and bile acid production were observed in these animals. The root powder administration to hypercholesterolaemic rats also decreased hepatic lipid peroxidation with a concomitant increase in superoxide dismutase (SOD) and catalase activities and total ascorbic acid content. Thus, the hypocholesterolaemic and antioxidant effects of GG root appeared to be mediated via (i) accelerated cholesterol, neutral sterol and bile acid elimination through fecal matter with an increased hepatic bile acid production and (ii) improving the activities of hepatic SOD, catalase and increasing the ascorbic acid content. The normo-cholesterolaemic animals when fed with GG root powder at 10 gm% level, registered a significant decline in plasma lipid profiles and an increase in HDL-cholesterol content. The antioxidant status of these animals also was improved upon treatment. [source]

Effect of some medicinal plants on plasma antioxidant system and lipid levels in rats

Eun-Mi Choi
Abstract Several inflammatory diseases are thought to be related to oxidative injury and free oxygen radicals have been proposed as important causative agents of heart disease and aging. To investigate the effects of daily intake of medicinal plants on antioxidant enzymes, lipid peroxidation and lipid profiles in rat, 28 rats were randomly divided into four groups and administered with three plant extracts (0.2 g/kg body weight): Piper cubeba (fruit), Physalis angulata (flower), Rosa hybrida (flower) and with saline as a control. After 3 weeks, superoxide dismutase (SOD), catalase, thiobarbituric acid reactive substance (TBARS), triglyceride (TG) and cholesterol levels in plasma were measured. The SOD activity of the Piper cubeba group and the catalase activity of the Piper cubeba and Rosa hybrida groups were significantly increased compared with the control group, while the SOD and catalase activities of the Physalis angulata group were not significantly changed (p < 0.05). TBARS, a marker of lipid peroxidation, was significantly lower in all experimental groups compeered with the control group. No significant changes occurred in the TG, total- and LDL-cholesterol of all groups, but the HDL-cholesterol of the Physalis angulata group was significantly increased. This study showed that the intake of medicinal plants in rats results in an increase in antioxidant enzyme activity and HDL-cholesterol, and a decrease in malondialdehyde, which may reduce the risk of inflammatory and heart disease. Copyright 2005 John Wiley & Sons, Ltd. [source]

Antioxidant enzyme activity and MDA level in the rat testis following chronic administration of ghrelin

ANDROLOGIA, Issue 6 2009
A. Kheradmand
Summary Ghrelin has recently been reported to exert beneficial effects on various oxidative stresses as a result of its antioxidant properties. Therefore, we designed this study to explore the probable antioxidative effects of this peptide in the testis. Twenty-eight male adult Wistar rats were divided into equal control and treatment groups. In the treatment group, 1 nmol of ghrelin was administered as subcutaneous injection for 10 consecutive days or vehicle (physiological saline) to the control rats. The control and treated rats were killed on days 6 and 10 after beginning of ghrelin injection (n = 7 from each group on each day). The testes were taken and measured for antioxidant enzyme activity and malondialdehyde (MDA) content. Glutathione peroxidase activity significantly increased on day 10 in the treated animals compared with the control group (P < 0.05). Although the mean activity of glutathione peroxidase was greater on day 6 in the ghrelin-treated group than in the control animals, it was not statistically significant. There were no significant differences in superoxide dismutase and catalase activities between the groups. However, MDA level decreased by ghrelin treatment on day 10 compared with the control rats (P < 0.05). The results of this study indicate for the first time novel evidences for antioxidant properties of ghrelin in the rat testis. [source]

Lycopene, a Carotenoid, Attenuates Cyclosporine-Induced Renal Dysfunction and Oxidative Stress in Rats

Ahmet Ate, ahin
Adult male Sprague-Dawley rats were randomly divided into four groups. The control group received physiological saline; animals in the lycopene group received only lycopene (10 mg/kg); animals in the cyclosporine A group received only cyclosporine A (15 mg/kg) and animals in cyclosporine plus lycopene group received cyclosporine and lycopene for 21 days. The effects of lycopene on cyclosporine A-induced nephrotoxicity were evaluated by plasma creatinine, urea, sodium and calcium concentrations; kidney tissue thiobarbituric acid reactive species, reduced glutathione (GSH), glutathione peroxidase (GSH-Px) and catalase activities and histopatological examinations. Administration of cyclosporine A to rats induced a marked renal failure, characterized with a significant increase in plasma creatinine and urea concentrations. Cyclosporine A also induced oxidative stress as indicated by increased kidney tissue concentrations of thiobarbituric acid reactive species and GSH, and reduced activities of GSH-Px and catalase. Moreover, the kidneys of cyclosporine A-treated rats showed tubular necrosis, degeneration, dilatation, thickened basement membranes, luminal cast formation and inter-tubular fibrosis. Lycopene markedly reduced elevated plasma creatinine, urea levels and counteracted the deleterious effects of cyclosporine A on oxidative stress markers. In addition, lycopene ameliorated cyclosporine A-induced pathological changes including tubular necrosis, degeneration, thickened basement membranes and inter-tubular fibrosis when compared to the alone cyclosporine A group. These data indicate that the natural antioxidant lycopene might have protective effect against cyclosporine-induced nephrotoxicity and oxidative stress in rat. [source]

Cyclosporine A-Induced Changes to Erythrocyte Redox Balance is Time Course-Dependent

Louise A. Lexis
These experiments investigated the time-course of cyclosporine A-induced changes to redox balance in plasma and erythrocytes. Rats were randomly assigned to either a control or cyclosporine A-treated group. Treatment animals received 25 mg/kg of cyclosporine A via intraperitoneal injection for either 7 days or a single dose. Control rats were injected with the same volume of the vehicle. Three hours after the final injections, plasma was analysed for total antioxidant status, ,-tocopherol, malondialdehyde, and creatinine. Erythrocytes were analysed for reduced glutathione (GSH), ,-tocopherol, methaemoglobin, malondialdehyde, and the activities of superoxide dismutase, catalase, GSH peroxidase, and glucose-6-phosphate dehydrogenase (G6PD). Cyclosporine A administration for 7 days resulted in a significant increase (P<0.05) in plasma malondialdehyde, methaemoglobin, and superoxide dismutase and catalase activities. There was a significant decrease (P<0.05) in erythrocyte GSH concentration and G6PD activity in cyclosporine A animals. There were no significant differences (P>0.05) between groups following a single dose of cyclosporine A in any of the measures. In summary, cyclosporine A alters erythrocyte redox balance after 7 days administration, but not after a single dose. [source]

The protective and healing effects of a natural antioxidant formulation based on ubiquinol and Aloe vera against dextran sulfate-induced ulcerative colitis in rats

BIOFACTORS, Issue 1-4 2003
Ludmila Korkina
Abstract Oxygen/nitrogen reactive species (ROS/RNS) are currently implicated in the pathogenesis of ulcerative colitis, drawing attention on the potential prophylactic and healing properties of antioxidants, scavengers, chelators. We evaluated the possible protective/curative effects of a natural antioxidant preparation based on Aloe vera and ubiquinol, against intestinal inflammation, lesions, and pathological alterations of the intestinal electrophysiological activity and motility, in a rat model of DSS-induced colitis. 5% dextrane sulfate (DDS) (3 days), followed by 1% DSS (4 days) was administered in drinking water. The antioxidant formulation (25 mg/kg) was delivered with a pre-treatment protocol, or simultaneously or post-colitis induction. Spontaneous and acetylcholine-stimulated electrical activity were impaired in the small intestine and in distal colon, upon exposure to DSS only. Severe inflammation occurred, with increased myeloperoxidase activity, and significant alterations of the oxidant/antioxidant status in colonic tissue and peritoneal cells. Lipoperoxidation, superoxide production, glutathione peroxidase and glutathione-S-transferase activities, and reduced glutathione content increased, whilst superoxide dismutase and catalase activities were sharply suppressed in colon tissue. ROS/RNS formation in peritoneal cells was strongly inhibited. Inflammation, electrical/mechanical impairment in the gut, and a great majority of oxidative stress parameters were improved substantially by pre-treatment with the antioxidant preparation, but not by simultaneous administration or post-treatment. [source]

Effects of a selective Rho-kinase inhibitor Y-27632 on oxidative stress parameters in acute dichlorvos poisoning in rats

N. Gunay
Abstract This study examined the effects of Y-27632, a selective Rho-kinase inhibitor, on organophosphate-induced acute toxicity in rats. Rats were randomly divided into four groups as control (corn oil), dichlorvos (30,mg,kg,1 i.p.), 1 and 10,mg,kg,1 Y-27632,+,dichlorvos groups. Cholinergic signs (fatigue, tremor, cyanosis, hyper-secretion, fasciculations) were observed in all the rats in the dichlorvos group and the mortality rate was 50%. No cholinergic findings and deaths were observed in the control and Y-27632 groups. Plasma cholinesterase activities were suppressed with dichlorvos and these reductions were attenuated with Y-27632 pretreatment. There was a marked increase in plasma malondialdehyde level in the dichlorvos group, but Y-27632 pretreatment abolished this elevation. Dichlorvos markedly depressed cardiac paraoxonase activity, but these changes were not markedly modified with Y-27632. Total antioxidant capacities, total oxidant status, oxidative stress index, total free sulfhydryl groups and catalase activities in plasma and cardiac tissues were not markedly different between the groups. No significant changes were observed with cardiac myeloperoxidase activities or plasma arylesterase and ceruloplasmin activities. In conclusion, our results suggest that Rho-kinase pathway is involved in organophosphate intoxication, and a decrease in cardiac paraoxonase activities may play a role in the pathogenesis of acute organophosphate poisoning in rats. Copyright 2008 John Wiley & Sons, Ltd. [source]

Relationship between anti-oxidant activities and doxorubicin-induced lipid peroxidation in P388 tumour cells and heart and liver in mice

Qi-Yuan Liu
Summary 1.,The present study found that, compared with mouse heart and liver, P388 ascitic tumour had significantly lower superoxide dismutase (SOD) activity and that compared with the mouse liver, the heart had significantly lower SOD and catalase activities, as well as a lower glutathione content. 2.,At 7.5 mg/kg, doxorubicin (DOX), a superoxide radical inducer, induced significant lipid peroxidation only in the tumour, whereas 15.0 mg/kg DOX induced lipid peroxidation in both the tumour and heart, but not in the liver. 3.,Overall, the results of the present study suggest that the differential anti-oxidant activities in P388 ascitic tumour, heart and liver in mice may explain their differential responses and, hence, susceptibility to DOX-induced lipid peroxidation. [source]

Changes in antioxidant defense status in response to cisplatin and 5-FU in esophageal carcinoma

T. Kaur
SUMMARY., The ability of reactive oxygen species to induce cellular damage and to cause cell death opens the possibility of exploiting this property in the treatment of esophageal cancer through a free radical mediated mechanism. The present study was carried out with the aim of evaluating the changes in the antioxidant defense status in esophageal cancer patients treated without and with neoadjuvant therapy (NAT). Forty surgically resected tissue specimens from tumors, tissue adjoining the tumors and paired macroscopically normal mucosa were obtained from esophageal cancer patients treated with or without chemo-radiotherapy. An evaluation of antioxidant defense system in the normal, adjoining and tumor esophageal tissues in response to NAT revealed decreased catalase activity in tumor and adjoining tissues as compared to their respective normal tissue levels. Similarly, decreased superoxide dismutase activity was observed in tumor tissue in response to NAT. In both the treatment groups (with and without NAT), no significant change was observed in the enzyme activity of glutathione reductase in the normal, adjoining and tumor tissues. Enhanced glutathione peroxidase activity was found in tumor tissue, as compared to the adjoining and paired normal tissue of patients after NAT. Estimation of reduced glutathione (GSH) levels showed a significant decline in GSH levels in esophageal tumors after NAT. Depletion of GSH, an endogenous antioxidant, would elevate drug sensitivity and might predispose neoplastic cells to apoptosis in response to NAT. The antioxidant enzymes in the esophageal carcinoma thus may play an important role in influencing the final outcome upon NAT course. [source]

Adaptative response of antioxidant enzymes in different areas of rat brain after repeated d -amphetamine administration

Flix Carvalho
d-Amphetamine has been shown to be a potential brain neurotoxic agent, particularly to dopaminergic neurones. Reactive oxygen species indirectly generated by this drug have been indicated as an important factor in the appearance of neuronal damage but little is known about the adaptations of brain antioxidant systems to its chronic administration. In this study, the activities of several antioxidant enzymes in different areas of rat brain were measured after repeated administration of d-amphetamine sulphate (sc, 20 mg/kg/day, for 14 days), namely glutathione-S-transferase (GST), glutathione peroxidase (GPx), glutathione reductase (GRed), catalase, and superoxide dismutase (SOD). When compared to a pair-fed control group, d-amphetamine treatment enhanced the activity of GST in hypothalamus to 167%, GPx in striatum to 127%, in nucleus accumbens to 192%, and in medial prefrontal cortex to 139%, GRed in hypothalamus to 139%, as well as catalase in medial prefrontal cortex to 153%. However, the same comparison revealed a decrease in the activity of GRed in medial pre-frontal cortex by 35%. Food restriction itself reduced GRed activity by 49% and enhanced catalase activity to 271% in nucleus accumbens. The modifications observed for the measured antioxidant enzymes reveal that oxidative stress probably plays a role in the deleterious effects of this drug in CNS and that, in general, the brain areas studied underwent adaptations which provided protection against the continuous administration of the drug. [source]

Outer sphere mutagenesis of Lactobacillus plantarum manganese catalase disrupts the cluster core

FEBS JOURNAL, Issue 6 2003
Mechanistic implications
X-ray crystallography of the nonheme manganese catalase from Lactobacillus plantarum (LPC) [Barynin, V.V., Whittaker, M.M., Antonyuk, S.V., Lamzin, V.S., Harrison, P.M., Artymiuk, P.J. & Whittaker, J.W. (2001) Structure9, 725,738] has revealed the structure of the dimanganese redox cluster together with its protein environment. The oxidized [Mn(III)Mn(III)] cluster is bridged by two solvent molecules (oxo and hydroxo, respectively) together with a 1,3 bridging glutamate carboxylate and is embedded in a web of hydrogen bonds involving an outer sphere tyrosine residue (Tyr42). A novel homologous expression system has been developed for production of active recombinant LPC and Tyr42 has been replaced by phenylalanine using site-directed mutagenesis. Spectroscopic and structural studies indicate that disruption of the hydrogen-bonded web significantly perturbs the active site in Y42F LPC, breaking one of the solvent bridges and generating an ,open' form of the dimanganese cluster. Two of the metal ligands adopt alternate conformations in the crystal structure, both conformers having a broken solvent bridge in the dimanganese core. The oxidized Y42F LPC exhibits strong optical absorption characteristic of high spin Mn(III) in low symmetry and lower coordination number. MCD and EPR measurements provide complementary information defining a ferromagnetically coupled electronic ground state for a cluster containing a single solvent bridge, in contrast to the diamagnetic ground state found for the native cluster containing a pair of solvent bridges. Y42F LPC has less than 5% of the catalase activity and much higher Km for H2O2 (,1.4 m) at neutral pH than WT LPC, although the activity is slightly restored at high pH where the cluster is converted to a diamagnetic form. These studies provide new insight into the contribution of the outer sphere tyrosine to the stability of the dimanganese cluster and the role of the solvent bridges in catalysis by dimanganese catalases. [source]

The catalytic role of the distal site asparagine-histidine couple in catalase-peroxidases

FEBS JOURNAL, Issue 5 2003
Christa Jakopitsch
Catalase-peroxidases (KatGs) are unique in exhibiting an overwhelming catalase activity and a peroxidase activity of broad specificity. Similar to other peroxidases the distal histidine in KatGs forms a hydrogen bond with an adjacent conserved asparagine. To investigate the catalytic role(s) of this potential hydrogen bond in the bifunctional activity of KatGs, Asn153 in Synechocystis KatG was replaced with either Ala (Asn153,Ala) or Asp (Asn153,Asp). Both variants exhibit an overall peroxidase activity similar with wild-type KatG. Cyanide binding is monophasic, however, the second-order binding rates are reduced to 5.4% (Asn153,Ala) and 9.5% (Asn153,Asp) of the value of native KatG [(4.8 0.4) 105 m,1s,1 at pH 7 and 15 C]. The turnover number of catalase activity of Asn153,Ala is 6% and that of Asn153,Asp is 16.5% of wild-type activity. Stopped-flow analysis of the reaction of the ferric forms with H2O2 suggest that exchange of Asn did not shift significantly the ratio of rates of H2O2 -mediated compound I formation and reduction. Both rates seem to be reduced most probably because (a) the lower basicity of His123 hampers its function as acid-base catalyst and (b) Asn153 is part of an extended KatG-typical H-bond network, the integrity of which seems to be essential to provide optimal conditions for binding and oxidation of the second H2O2 molecule necessary in the catalase reaction. [source]

Possible involvement of GABAergic modulation in the protective effect of gabapentin against immobilization stress-induced behavior alterations and oxidative damage in mice

Anil Kumar
Abstract Introduction Acute stress may be experienced in response to an immediate physical, emotional or psychological stimulus. Stress has been known to affect several brain activities and promote long-term changes in multiple neural systems. In the present study, we investigated the possible involvement of GABAergic modulation in the protective effect of gabapentin in acute immobilization-induced behavioral alterations and oxidative damage in mice. Materials and methods Mice were immobilized for periods of 6 h. Animals were divided into different groups, consisting of six in each. Various GABAergic modulators were administered either alone or in their combinations, 30 min before subjecting the animals for immobilization stress. Various behavioral tests (mirror chamber, actophotometer) followed by oxidative parameters (malondialdehyde level, glutathione, catalase, nitrite and protein) were assessed in animals. Results Six hours acute immobilization stress caused significant locomotor impairment, anxiety-like behavior in mice. Biochemical analyses also revealed an increase malondialdehyde, nitrite level and depletion of glutathione and catalase activity in 6 h stressed brains. Pretreatment with gabapentin (50 and 100 mg/kg, i.p.) significantly improved ambulatory movements, anti-anxiety effect (decreased time latency to enter in mirror chamber, increased number of entries and duration in mirror chamber) and antioxidative activity in stressed mice (P < 0.05). Further, picrotoxin (1.0 mg/kg) blocked and muscimol (0.05 mg/kg) potentiated the protective action of gabapentin (50 mg/kg). Results of both behavior as well as biochemical alterations in combination studies were significant as compared to their effect per se (P < 0.05). Conclusion Results of present study suggest GABAergic modulation might be involved in the protective effect of gabapentin against immobilization-induced behavior alteration and oxidative damage in mice. [source]

Oral administration of diphenyl diselenide potentiates hepatotoxicity induced by carbon tetrachloride in rats

Cristina W. Nogueira
Abstract Carbon tetrachloride (CCl4) is a model for studying free radical-induced liver injury and screening hepato-protective drugs. Numerous studies have reported the involvement of oxidative stress in CCl4 -induced liver damage and the hepato-protective effects mediated by different antioxidants. The present study examined the effects of diphenyl diselenide, (PhSe)2, on hepatotoxicity induced by CCl4 in rats. To this end, male Wistar rats received (PhSe)2 by oral route at the dosage of 31.2 mg/kg for one or two days. After the second day of treatment, rats received CCl4 orally in a single dose. The liver and kidney were utilized for determination of histopathology, biochemical [aspartate (ALT) and alanine (AST) aminotransferases, alkaline phosphatase (ALP), total bilirrubin (TB) and gamaglutamyl transferase (GGT)] and toxicological parameters [thiobarbituric reactive species (TBARS) levels, catalase activity, ascorbic acid, nonprotein thiols (NPSH) and aminolevulinate dehydratase (, -ALA-D) activity]. Repeated administration of (PhSe)2 caused a marked potentiation of hepatotoxicity induced by CCl4 exposure, as manifested by an increase in biochemical parameters (AST, ALT, ALP, GGT and BT) and severe alteration in histopathology. This study also demonstrated a potentiation of TBARS levels and a consequent depletion of important antioxidant defenses including catalase and ascorbic acid. Pre-treatment with a single dose of (PhSe)2 prevented the effect of strychnine, a substrate for CYPs, abolishing lethality in mice. This result indicates that (PhSe)2 prevented animal death, suggesting an activator action of (PhSe)2 in CYPs. This study clearly indicates that (PhSe)2 potentiated acute hepatic damage induced by CCl4. Copyright 2008 John Wiley & Sons, Ltd. [source]

Subchronic toxicity of chloral hydrate on rats: a drinking water study

R. Poon
Abstract The subchronic toxicity of chloral hydrate, a disinfection byproduct, was studied in rats following 13 weeks of drinking water exposure. Male (262 10 g) and female (190 8 g) Sprague-Dawley rats, ten animals per group, were administered chloral hydrate via drinking water at 0.2, 2, 20 and 200 ppm. Control animals received distilled water only. Gross and microscopic examinations, serum chemistry, hematology, biochemical analysis, neurogenic amine analysis and serum trichloroacetic acid (TCA) analysis were performed at the end of the treatment period. Bronchoalveolar fluids were collected at necropsy and urine specimens were collected at weeks 2, 6 and 12 for biochemical analysis. No treatment-related changes in food and water intakes or body weight gains were observed. There were no significant changes in the weights of major organs. Except for a mild degree of vacuolation within the myelin sheath of the optic nerves in the highest dose males, there were no notable histological changes in the tissues examined. Statistically significant treatment-related effects were biochemical in nature, with the most pronounced being increased liver catalase activity in male rats starting at 2 ppm. Liver aldehyde dehydrogenase (ALDH) was significantly depressed, whereas liver aniline hydroxylase activity was significantly elevated in both males and females receiving the highest dose. A dose-related increase in serum TCA was detected in both males and females starting at 2 ppm. An in vitro study of liver ALDH confirmed that chloral hydrate was a potent inhibitor, with an IC50 of 8 M, whereas TCA was weakly inhibitory and trichloroethanol was without effect. Analysis of brain biogenic amines was conducted on a limited number (n = 5) of male rats in the control and high dose groups, and no significant treatment-related changes were detected. Taking into account the effect on the myelin sheath of male rats and the effects on liver ALDH and aniline hydroxylase of both males and females at the highest dose level, the no-observed-effect level (NOEL) was determined to be 20 ppm or 1.89 mg kg,1 day,1 in males and 2.53 mg kg,1 day,1 in females. This NOEL is ca. 1000-fold higher than the highest concentration of chloral hydrate reported in the municipal water supply. Copyright 2002 Crown in the right of Canada. Published by John Wiley & Sons, Ltd. [source]