Enhanced heme oxygenase activity increases the antioxidant defense capacity of guinea pig liver upon acute cobalt chloride loading: comparison with rat liver

Changes in the activity of so-called oxidative stress defensive enzymes, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and heme oxygenase, as well as changes in lipid peroxidation and reduced glutathione levels, were measured in guinea pig and rat liver after acute cobalt loading. Cobalt chloride administration produced a much higher degree of lipid peroxidation in guinea pig than in rat liver compared with the control animals. The intrahepatic reduced glutathione content in control guinea pig was higher than that in rat, but was equally decreased in both species after cobalt administration. The enzymatic scavengers of free radicals, superoxide dismutase, catalase and glutathione peroxidase, were significantly decreased in rat liver after acute cobalt loading, and as a compensatory reaction, the heme oxygenase activity was increased (seven-fold). In guinea pig liver, only superoxide dismutase activity was depleted in response to cobalt-induced oxidative stress, while catalase and glutathione peroxidase were highly activated and the heme oxygenase activity was dramatically increased (13-fold). It is assumed that enhanced heme oxygenase activity may have important antioxidant significance by increasing the liver oxidative-stress defense capacity.     

Hepatoprotective activity of <Emphasis Type="BoldItalic">Tribulus terrestris</Emphasis> extract against acetaminophen-induced toxicity in a freshwater fish (<Emphasis Type="BoldItalic">Oreochromis mossambicus</Emphasis>)

The potential protective role of Tribulus terrestris in acetaminophen-induced hepatotoxicity in Oreochromis mossambicus was investigated. The effect of oral exposure of acetaminophen (500 mg/kg) in O. mossambicus at 24-h duration was evaluated. The plant extract (250 mg/kg) showed a remarkable hepatoprotective activity against acetaminophen-induced hepatotoxicity. It was judged from the tissue-damaging level and antioxidant levels in liver, gill, muscle and kidney tissues. Further acetaminophen impact induced a significant rise in the tissue-damaging level, and the antioxidant level was discernible from the enzyme activity modulations such as glutamate oxaloacetic transaminase, glutamate pyruvic transaminase, alkaline phosphatase, acid phosphatase, glucose-6-phosphate dehydrogenase, lactate dehydrogenase, superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione S-transferase, lipid peroxidase and reduced glutathione. The levels of all these enzymes have significantly (p < 0.05) increased in acetaminophen-treated fish tissues. The elevated levels of these enzymes were significantly controlled by the treatment of T. terrestris extract (250 kg/mg). Histopathological changes of liver, gill and muscle samples were compared with respective controls. The results of the present study specify the hepatoprotective and antioxidant properties of T. terrestris against acetaminophen-induced toxicity in freshwater fish, O. mossambicus.     

Changes in apoplastic antioxidants induced by powdery mildew attack in oat genotypes with race non-specific resistance

Three oat (Avena sativa L.) lines which show differential responses to attack by the biotrophic fungal pathogen Blumeria graminis DC f. sp. avenae Marchal, which causes powdery mildew, were studied: Maldwyn shows the strongest resistance in adult plants; Selma shows greater susceptibility; while a Selma × Maldwyn hybrid, OM1387, has a similar degree of resistance to Maldwyn. Host responses to pathogen attack were complete 48 h after inoculation but largely accomplished within the first 24 h, the point when material was taken for enzyme and metabolic assays. In Maldwyn and OM1387 about 80% of attacked cells showed localized autofluorescent host-cell responses but this fell to less than 20% in Selma. A cytoplasmic marker enzyme, glucose 6-phosphate dehydrogenase, was used to determine contamination of the apoplastic extracts by cellular components. After correction for cytoplasmic contamination, up to 4% of the total foliar activities of superoxide dismutase, catalase, ascorbate peroxidase, glutathione reductase, dehydroascorbate reductase and monodehydroascorbate reductase activities were detected in the apoplast. The apoplast contained about 2% of the total foliar glutathione pool and dehydroascorbate, but not ascorbate, at values amounting to 10% of the total foliar ascorbate plus dehydroascorbate pool. Twenty-four hours after inoculation the foliar or apoplastic ascorbate pools were similar in inoculated and control leaves. Foliar catalase activity increased in both susceptible and resistant responses. Resistance correlated with increased total foliar glutathione, an increase in the ratio of reduced to oxidized glutathione and with decreased total activities of foliar ascorbate peroxidase, glutathione reductase, dehydroascorbate reductase and monodehydroascorbate reductase. Received: 17 April 1998 / Accepted: 28 August 1998     

Changes in glutathione-related enzymes in tumor-bearing mice after cisplatin treatment

The effect of cisplatin on five glutathione-related enzymes was studied in liver, kidney, and Dalton lymphoma cells of tumor-bearing mice. In liver, the activities of glutathione S-transferase, glutathione peroxidase, catalase, and superoxide dismutase decreased approximately 30–40%, 60–67%, 35–50% and 70–80% respectively, while glutathione reductase increased about 36–45% after cisplatin treatment. In kidney, catalase activity decreased by 47–82% at all time points (24–96 h) of cisplatin treatment, while glutathione S-transferase activity decreased significantly (~24%) mainly at 72 h of treatment. An increase in glutathione reductase (~1.5–2.5 times), glutathione peroxidase (significant at 24 h, 47%), and superoxide dismutase (~15–60%) was noted in kidney after the treatment. In Dalton lymphoma cells, the activities of glutathione S-transferase, glutathione peroxidase, and catalase decreased very distinctly (~2–5, 2–5 and 5–11 times, respectively) at all time points, but glutathione reductase decreased significantly only at 72 h of cisplatin treatment. Interestingly, the superoxide dismutase activity in Dalton lymphoma cells increased initially at 24–48 h and then decreased (~60%) during later periods (72–96 h) of treatment. Cisplatin treatment caused a decrease in glutathione level in Dalton lymphoma cells (~14–20%) and kidney (~18–28%) but no change in liver. In view of the results, a definite correlation with the changes in glutathione concentrations and enzymatic activities in a tissue could not be firmly derived. It is suggested that the changes in various glutathione-related enzymes and glutathione levels in the tissues of the host during cisplatin-mediated chemotherapy could affect cellular antioxidant defense potential, which may play an important contributory role in cisplatin-mediated toxicity, particularly nephrotoxicity, and anticancer activity in the host. This revised version was published online in July 2006 with corrections to the Cover Date.     

Different effects of exercise tests on the antioxidant enzyme activities in lymphocytes and neutrophils

We have determined the effects of maximal and submaximal cycloergometer tests on the antioxidant enzyme defences of neutrophils and lymphocytes. We also compared the neutrophil and lymphocyte basal enzyme antioxidant activities. A total of 17 well-trained amateur athletes, runners, and cyclists participated in this study. Two tests were performed on an electromagnetic reduction cycloergometer: the maximal exercise test, and the submaximal prolonged exercise test. Blood samples were taken before and after the tests. Basal enzyme activity of superoxide dismutase was higher in lymphocytes but neutrophils presented higher activities of catalase and glutathione peroxidase. The maximal test increased the circulating number of lymphocytes and the activities of catalase and glutathione peroxidase. No changes were observed in lymphocyte number or in lymphocyte antioxidant enzyme activities after the submaximal test. The circulating number of neutrophils increased significantly after the submaximal test. Maximal and submaximal tests decreased the activities of neutrophil glutathione dependent antioxidant enzymes (glutathione peroxidase and glutathione reductase), but no changes were observed in catalase or superoxide dismutase activities after either test. Neither the maximal nor submaximal test produced increases in serum activities of lactate dehydrogenase and creatine kinase (CK).     

Lead and Cadmium Co-exposure Mediated Toxic Insults on Hepatic Steroid Metabolism and Antioxidant System of Adult Male Rats

The redox status and steroid metabolism of liver of adult male rat exposed to lead (Pb) and cadmium (Cd) either alone or in co-exposure (0.025 mg/kg body weight intraperitoneally/15 days) was studied. Pb and Cd significantly accumulated in the liver. The activity of steroid metabolizing enzymes 17-βhydroxysteroid oxidoreductase and uridine diphosphate–glucuronyltransferase were decreased in experimental animals. 17-β-Hydroxysteroid dehydrogenase was reduced to 33%, 38%, and 24% on treatment of Pb, Cd, and co-exposure (Pb + Cd). Furthermore, the activity of uridine diphosphate–glucuronosyltransferase was significantly reduced to 27% (Pb exposure), 36% (Cd exposure), and 25% (co-exposure of Pb + Cd). Cd exposure exhibited more toxic effect than Pb, while co-exposure demonstrated the least. The activities of antioxidant enzymes, superoxide dismutase, catalase, glutathione reductase, and glucose-6-phosphate dehydrogenase decreased and glutathione peroxidase increased in mitochondrial and post-mitochondrial fractions. The level of lipid peroxidation increased, and cellular glutathione concentration decreased. Hepatic DNA was decreased, whereas RNA content and the activity of alanine transaminase remained unchanged. Histological studies revealed that only Cd-exposed groups exhibited cytotoxic effect. These results suggest that when Pb and Cd are present together in similar concentrations, they exhibited relatively decreased toxic effect when compared to lead and cadmium in isolation with regard to decreased steroid metabolizing and antioxidant enzyme activities. This seems that the toxic effect of these metals is antagonized by co-exposure due to possible competition amongst Pb and Cd for hepatic accumulation.     

Parameters of Metabolic Syndrome and Its Relationship with Zincemia and Activities of Superoxide Dismutase and Glutathione Peroxidase in Obese Women

Alterations in antioxidant defense in obese people with metabolic syndrome can contribute to oxidative stress. This study assessed the relationship between the parameters of metabolic syndrome and the zincemia, activity of superoxide dismutase, and glutathione peroxidase enzymes in obese women. Seventy-three premenopausal women, aged between 20 and 50 years, were divided into two groups: case group, composed of obese (n = 37), and control group, composed of no obese (n = 36). Analyses of zinc intake, parameters of metabolic syndrome, plasma, and erythrocyte zinc, and activities of superoxide dismutase and glutathione peroxidase were carried out. The mean values of body mass index of obese women and control group were 34.5 ± 3.4 and 21.7 ± 1.9 kg/m², respectively (p < 0.05). In the study, body mass index, waist circumference, and zinc intake were higher in obese women than control group (p < 0.05). The plasma zinc and activity of superoxide dismutase did not show significant differences between obese and controls (p > 0.05). The values of erythrocyte zinc was 36.4 ± 15.0 μg/gHb and 45.4 ± 14.3 μg/gHb and of glutathione peroxidase was 46.4 ± 19.4 U/gHb and 36.7 ± 13.6 U/gHb in obese women and controls, respectively (p < 0.05). The study shows that there are alterations in biochemical parameters of zinc in obese women, with low zinc concentrations in erythrocytes. Regression analysis demonstrates that the erythrocyte zinc and activity of superoxide dismutase enzyme is influenced by components of the metabolic syndrome, and the plasmatic glucose, body mass index, and waist circumference have a negative correlation with this enzyme.     

Impact of chromium on lipoperoxidative processes and subsequent operation of the glutathione cycle in rat renal system.

Oral administration of K2Cr2O7 to male albino rats at an acute dose of 1500 mg/kg body wt/day for 3 days brought about sharp decrease in the activities of glucose-6-phosphate dehydrogenase and glutathione reductase of kidney epithelial cells. The scavenging system of kidney epithelium is also affected as evident by the highly significant fall in the activities of glutathione peroxidase, superoxide dismutase and catalase which ultimately leads to the increase in lipid peroxidation value in kidney cortical homogenate. However, glutathione-s-transferase activity in cytosol and glutathione and total thiol content in cortical homogenate were not altered. Chronic oral administration of K2Cr2O7 (300 mg/kg body wt/day) for 30 days to rats lead to elevation in the activities of glutathione peroxidase, glutathione reductase, glutathione-s-transferase, superoxide dismutase and catalase with no change in glucose-6-phosphate dehydrogenase activity in epithelial cells. This might lead to the increase in glutathione and total thiol status and decrease in lipid peroxidation value in whole homogenate system.     

Butyrate increases catalase activity and protects rat pulmonary artery smooth muscle cells against hyperoxia

A protective effect of butyrate against hyperoxia was found with adult rat pulmonary artery smooth muscle cells. Butyrate (5mM) when added just prior to the hyperoxic exposure (95%) markedly decreased lactate dehydrogenase release from cells during 68 hours of exposure (22% release with butyrate versus 98% without). The uptake and reduction of a tetrazolium compound as another index of cell viability also showed similar improvement with butyrate. Butyrate was associated with a striking increase of catalase to three times the control in the air exposed group while GSH content and the activities of superoxide dismutase and glutathione peroxidase were not significantly changed. In the groups exposed to hyperoxia alone, both enzyme activities were decreased compared to the air exposed controls. When butyrate was present with hyperoxia, the superoxide dismutase was maintained closer to the air exposed control values and the catalase activity remained nearly twice as high as the air exposed control cells. These results suggest that butyrate protects rat pulmonary artery smooth muscle cells from hyperoxia by increasing catalase activity which may help to preserve superoxide dismutase activity. This may be a good model to determine the biological significance of catalase and its interrelationships with other antioxidant systems within the cell.     

Procyanidins protect Fao cells against hydrogen peroxide-induced oxidative stress

In this paper, we evaluate the extent to which flavonoids in red wine (catechin, epicatechin, quercetin and procyanidins) protect against hydrogen peroxide-induced oxidative stress in Fao cells. When cells were exposed to H(2)O(2), malondialdehyde (MDA) levels, oxidized glutathione (GSSG) levels and lactate dehydrogenase (LDH) release increased, indicating membrane damage and oxidative stress. All the flavonoids studied, and in particular epicatechin and quercetin, protected the plasma membrane. Only procyanidins lowered MDA levels and LDH leakage, maintained a higher reduced/oxidized glutathione ratio, and increased catalase/superoxide dismutase and glutathione peroxidase/superoxide dismutase ratios, and glutathione reductase and glutathione transferase activities. These results show that the procyanidin mixture has a greater antioxidant effect than the individual flavonoids studied, probably due to its oligomer content and/or the additive/synergistic effect of its compounds. This suggests that the mixture of flavonoids found in wine has a greater effect than individual phenols, which may explain many of the healthy effects attributed to wine.     

Correlation between superoxide dismutase,glutathione peroxidase and catalase in isolated rat hepatocytes during fetal development

Superoxide dismutase, glutathione peroxidase and catalase activities were determined in isolated fetal rat hepatocytes of various ages and compared with the values of neonatal and adult cells. The developmental pattern of superoxide dismutase and glutathione peroxidase were very similar with a low constant activity in the fetal cells and a postnatal burst. On the contrary catalase begins to increase already since the 18th day of the fetal life. The results suggest a functional correlation of superoxide dismutase and glutathione peroxidase in the antioxidative enzyme defense of liver cells.     

Antioxidant enzymatic systems in neuronal and glial cell-enriched fractions of rat brain during aging

The activities of Cu,Zn superoxide dismutase, glutathione peroxidase, catalase and glutathione reductase in neuronal and glial cell-enriched fractions obtained from the cerebral cortex of rat brain during aging (15, 30, 90, 350, 750 days of age) were assayed. Our results showed that glutathione peroxidase, catalase and glutathione reductase activities varied little during the examined periods. Only the Cu,Zn superoxide dismutase activity decreased notably from 15th to 750th day of age in both neuronal and glial cells, moreover the activities of all enzymes studied were always detected at lower levels in neuronal cells with respect to glial cells. In agreement with diminished SOD activity, the lipid peroxidation showed an elevated increase with aging; this fact is more evident in neuronal than in glial cells. In conclusion our data show that Cu,Zn superoxide dismutase is the most affected antioxidant enzymatic system of brain aging and it could be responsible for the increased lipid peroxidation in both cell types examined.A preliminary report of these results was presented at the 19th Meeting F.E.B.S. Rome July 2–7, 1989.     

Expression of antioxidant enzymes in rat kidney during ischemia-reperfusion injury

The effect of ischemia-reperfusion on activity, protein and m-RNA levels of catalase, copper-zinc and manganese containing superoxide dismutases and glutathione peroxidase, the enzymes that are involved in free radical detoxification was studied in rat kidney. Ischemia alone did not alter either the activities or protein levels of superoxide dismutase and glutathione peroxidase. However, catalase activity was found to be inhibited to 82% of control. The inhibition of catalase was due to the inactivation of the enzyme as there was no significant change in enzyme protein level. Reperfusion following ischemia, however, led to a significant decrease in both the activities as well as the protein levels of all the antioxidant enzymes. The observed overall decrease in total superoxide dismutase activity was the net effect of a decrease in copper-zinc superoxide dismutase while manganese superoxide dismutase activity was found to be increased following reperfusion. This observed increased manganese superoxide dismutase activity was the result of its increased protein level. The mRNA levels for catalase, superoxide dismutases, and glutathione peroxidase were observed to be increased (100–145% of controls) following ischemia; reperfusion of ischemic kidneys, however, resulted in a significant decrease in the levels of mRNAs coding for all the enzymes except manganese superoxide dismutase which remained high. These results suggest that in tissue, the down regulation of the antioxidant enzyme system could be responsible for the pathophysiology of ischemia-reperfusion injury.     

Buffalo (<Emphasis Type="Italic">Bubalus bubalis</Emphasis>) Epiphyseal Proteins Counteract Arsenic-Induced Oxidative Stress in Brain,Heart, and Liver of Female Rats

Arsenic (As) toxicity through induction of oxidative stress is a well-known mechanism of organ toxicity. To address this problem, buffalo epiphyseal proteins (BEP, at 100 μg/kg BW, i.p. for 28 days) were administered intraperitoneally to female Wistar rats exposed to As (100 ppm sodium arsenite via drinking water for 28 days). Arsenic exposure resulted in marked elevation in lipid peroxidation in brain, cardiac, and hepatic tissues, whereas significant (p < 0.05) adverse change in catalase, superoxide dismutase, glutathione reductase, glutathione peroxidase, and reduced glutathione level were observed in cardiac, hepatic, and brain tissues of As-administered animals. BEP significantly (p < 0.05) counteracted all the adverse changes in antioxidant defense system brought about by As administration. Based on these results, we consider BEP as a potent antioxidant to be used for protection from arsenic-induced oxidative stress related damage of vital organs.     

Radioprotective effect of <Emphasis Type="SmallCaps">dl</Emphasis>-α-lipoic acid on mice skin fibroblasts

During the course of cancer radiation treatment, normal skin invariably suffers from the cytotoxic effects of γ-radiation and reactive oxygen species (ROS), which are generated from the interaction between radiation and the water molecules in cells. The present study was designed to investigate the radioprotective role of α-lipoic acid (LA), an antioxidant on murine skin fibroblasts exposed to a single dose of 2, 4, 6, or 8Gy γ-radiation. Irradiation of fibroblasts significantly increased ROS, nitric oxide, and lipid peroxidation (P < 0.001); all of these factors substantially decreased with 100 μM LA treatment. Hydroxyl radical (OH^⋅) production from 8Gy irradiated fibroblasts was measured directly by electron spin resonance using spin-trapping techniques. LA was found to inhibit OH^⋅ production at 100-μM concentrations. Dose-dependent depletion of antioxidants, such as catalase and glutathione reductase, was observed in irradiated fibroblasts (P < 0.001), along with increased superoxide dismutase (P < 0.001). LA treatment restored antioxidant levels. Concentration of the pro-inflammatory cytokine IL-1β was significantly reduced in irradiated fibroblasts when treated with LA. MTT and lactate dehydrogenase assays demonstrated that LA treatment reduced cell injury and protected cells against irradiation-induced cytotoxicity. Thus, we conclude that results are encouraging and need further experiments to demonstrate a possible benefit in cancer patients and the reduction of harmful effects of radiation therapy.     

Chemopreventive effect of <Emphasis Type="BoldItalic">Padina boergesenii</Emphasis> extracts on ferric nitrilotriacetate (Fe-NTA)-induced oxidative damage in Wistar rats

The present study was designed to investigate the prophylactic effect of extracts of the brown alga Padina boergesenii against potent nephrotoxic agent ferric nitrilotriacetate (Fe-NTA), in blood circulation of rats. Administration of Fe-NTA for seven consecutive days significantly enhanced lipid peroxidation accompanied with reduction in glutathione content. Together with this, the level of antioxidant enzymes, glutathione peroxidase, superoxide dismutase, and catalase was significantly (P < 0.05) diminished. Pretreatment of rats with P. boergesenii (150 mg kg⁻¹ body weight) reversed Fe-NTA-induced oxidative damage in lipid peroxidation and glutathione content significantly (P < 0.05). Further, the activity of antioxidant enzymes was also restored significantly. In order to assess the role of polyphenolic components in the relevant activity, phenolic contents of the extract was found to be 1.78 ± 0.02% in the methanol extract and 1.30 ± 0.30% in the diethyl ether extract. Hence, the present results confirm that the brown alga P. boergesenii preclude its role in Fe-NTA-induced oxidative damage and hyperproliferative response in circulation.     

Effect of Selenium Supplementation on Lipid Peroxidation,Antioxidant Enzymes,and Lactate Levels in Rats Immediately After Acute Swimming Exercise

The present study aims to evaluate the effect of selenium supplementation on lipid peroxidation and lactate levels in rats subjected to acute swimming exercise. Thirty-two adult male rats of Sprague–Dawley type were divided into four groups. Group 1, control; group 2, selenium-supplemented; group 3, swimming control; group 4, selenium-supplemented swimming group. The animals in groups 2 and 4 were supplemented with (i.p.) 6 mg/kg/day sodium selenite for 4 weeks. The blood samples taken from the animals by decapitation method were analyzed in terms of erythrocyte-reduced glutathione (GSH), serum glutathione peroxidase (GPx) and superoxide dismutase (SOD), and plasma malondialdehyde (MDA) and lactate using the colorimetric method, and serum selenium values using an atomic emission device. In the study, the highest MDA and lactate values were found in group 3, while the highest GSH, GPx and SOD values were obtained in group 4 (p < 0,001). Group 2 had the highest and group 3 had the lowest selenium levels (p < 0,001). Results of the study indicate that the increase in free radical production and lactate levels due to acute swimming exercise in rats might be offset by selenium supplementation. Selenium supplementation may be important in that it supports the antioxidant system in physical activity.     

Stable overexpression of DJ‐1 protects H9c2 cells against oxidative stress under a hypoxia condition

It has been well accepted that increased reactive oxygen species (ROS) and the subsequent oxidative stress is one of the major causes of ischemia/reperfusion (I/R) injury. DJ‐1 protein, as a multifunctional intracellular protein, plays an important role in regulating cell survival and antioxidant stress. Here, we wondered whether DJ‐1 overexpression attenuates simulated ischemia/reperfusion (sI/R)‐induced oxidative stress. A rat cDNA encoding DJ‐1 was inserted into a mammalian expression vector. After introduction of this construct into H9c2 myocytes, stable clones were obtained. Western blot analysis of the derived clones showed a 2.6‐fold increase in DJ‐1 protein expressing. Subsequently, the DJ‐1 gene‐transfected and control H9c2 cells were subjected to sI/R, and then cell viability, lactate dehydrogenase, malondialdehyde, intracellular ROS and antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) were measured appropriately. The results showed that stable overexpression of DJ‐1 efficiently attenuated sI/R‐induced viability loss and lactate dehydrogenase leakage. Additionally, stable overexpression of DJ‐1 inhibited sI/R‐induced the elevation of ROS and MDA contents followed by the increase of antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) activities and expression. Our data indicate that overexpression of DJ‐1 attenuates ROS generation, enhances the cellular antioxidant capacity and prevents sI/R‐induced oxidative stress, revealing a novel mechanism of cardioprotection. Importantly, DJ‐1 overexpression may be an important part of a protective strategy against ischemia/reperfusion injury. Copyright © 2012 John Wiley & Sons, Ltd.     

Protective Effect of Naringenin Against Lead-Induced Oxidative Stress in Rats

Oxidative stress is thought to be involved in lead-induced toxicity. The aim of this study was to investigate the possible protective role of naringenin on lead-induced oxidative stress in the liver and kidney of rats. In the present investigation, lead acetate (500 mg Pb/L) was administered orally for 8 weeks to induce hepatotoxicity and nephrotoxicity. The levels of hepatic and renal markers such as alanine aminotransferase, aspartate aminotransferase, urea, uric acid, and creatinine were significantly (P < 0.05) increased following lead acetate administration. Lead-induced oxidative stress in liver and kidney tissue was indicated by a significant (P < 0.05) increase in the level of maleic dialdehyde and decreased levels of reduced glutathione, superoxide dismutase, catalase, and glutathione peroxidase. Naringenin markedly attenuated lead-induced biochemical alterations in serum, liver, and kidney tissues (P < 0.05). The present study suggests that naringenin shows antioxidant activity and plays a protective role against lead-induced oxidative damage in the liver and kidney of rats.     

Antioxidant enzymatic systems in pigment tissue of amphibia

Superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase activities in pigmented and unpigmented liver tissues of frog and albino rat, respectively, were studied. Our results show that pigmented tissue is lacking in manganese superoxide dismutase activity and that the main enzymatic activity utilized in the cytosol by pigmented cells to reduce the hydrogen peroxide to water is represented by catalase; on the contrary, for the same reaction, the cells of albino rat liver primarily utilize the glutathione peroxidase activity. Both a low glutathione peroxidase activity and a low glutathione reductase activity were found in pigmented tissue of frog liver when compared with unpigmented tissue of rat liver. In light of our results, we also report a hypothetical interrelationship between melanin and reduced glutathione: We believe that in pigmented cells the melanin could act as a reducing physiological agent replacing the glutathione in the reduction of hydrogen peroxide. This reducing action of melanin could cause a diminished need for GSH and therefore could provoke the low glutathione peroxidase and reductase activities in pigmented tissue.