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PubMed2003

Synthesis and antifilarial evaluation of N1,Nn- xylofuranosylated diaminoalkanes.

A series of N(1),N(n)-xylofuranosylated diaminoalkanes (3-9 and 11-18) has been synthesized either by reductive amination of deoxy xylouloses (2a, 2b) with amines followed by one pot reduction with NaBH(4) or NaCNBH(3); or by 1,4-conjugate addition of amines to glycosyl olefinic esters (10a, 10b). The compounds were screened for their interference with filarial worms' glutathione metabolism, a potential target for chemotherapeutic attack. Interestingly, these compounds affected intracellular glutathione, gamma-glutamyl cysteine synthetase, glutathione reductase and glutathione-S-transferase(s) of bovine filarial worms to varying degrees. Some of the compounds though effected the motility and MTT reduction potential of filarial worms Brugia malayi, however, little microfilaricidal and macrofilaricidal were noted with compounds at 50mg/kg oral dose. Compounds 6, 16 and 17 were evaluated also for in vivo activity.

Alkanes↗

PubMed2004

Metabolism is required for the expression of ecstasy-induced cardiotoxicity in vitro.

Cardiovascular complications associated with 3,4-methylenedioxymethamphetamine (MDMA, ecstasy) abuse have increasingly been reported. The indirect effect of MDMA mediated by a sustained high level of circulating biogenic amines may contribute to the cardiotoxic effects, but other factors, like the direct toxic effects of MDMA and its metabolites in cardiac cells, remain to be investigated. Thus, the objective of the present in vitro study was to evaluate the potential cardiotoxic effects of MDMA and its major metabolites 3,4-methylenedioxyamphetamine (MDA), N-methyl-alpha-methyldopamine (N-Me-alpha-MeDA), and alpha-methyldopamine (alpha-MeDA) using freshly isolated adult rat cardiomyocytes. The cell suspensions were incubated with these compounds in the final concentrations of 0.1, 0.2, 0.4, 0.8, and 1.6 mM for 4 h. alpha-MeDA, N-Me-alpha-MeDA, and their respective aminochromes (oxidation products) were quantified in cell suspensions by HPLC-DAD. The toxic effects were evaluated at hourly intervals for 4 h by measuring the percentage of cells with normal morphology, glutathione (GSH), and glutathione disulfide (GSSG); intracellular Ca(2+), ATP, and ADP; and the cellular activities of glutathione peroxidase, glutathione reductase, and glutathione-S-transferase. No toxic effects were found after exposure of rat cardiomyocytes to MDMA or MDA at any of the tested concentrations for 4 h. In contrast, their catechol metabolites N-Me-alpha-MeDA and alpha-MeDA induced significant toxicity in rat cardiomyocytes. The toxic effects were characterized by a loss of normal cell morphology, which was preceded by a loss of GSH homeostasis due to conjugation of GSH with N-Me-alpha-MeDA and alpha-MeDA, sustained increase of intracellular Ca(2+) levels, ATP depletion, and decreases in the antioxidant enzyme activities. The oxidation of N-Me-alpha-MeDA and alpha-MeDA into the toxic compounds N-methyl-alpha-methyldopaminochrome and alpha-methyldopaminochrome, respectively, was also verified in cell suspensions incubated with these MDMA metabolites. The results obtained in this study provide evidence that the metabolism of MDMA into N-Me-alpha-MeDA and alpha-MeDA is required for the expression of MDMA-induced cardiotoxicity in vitro, being N-Me-alpha-MeDA the most toxic of the studied metabolites.

3,4-Methylenedioxyamphetamine↗

PubMed2001

Free radical oxidation and activity of enzymes catalyzing biotransformation of xenobiotics in the liver of rats with experimental acute pancreatitis.

The development of experimental acute pancreatitis in rats was accompanied by intensification of lipid peroxidation, activation of superoxide dismutase and glutathione reductase, inhibition of glutathione transferase, and deceleration of aniline N-hydroxylation by cytochrome P-450 in the liver. Antioxidants inhibited lipid peroxidation and antioxidant enzymes, but did not prevent inhibition of detoxifying enzymes.

Acute Disease↗

PubMed2004

Radioprotective mechanism of Podophyllum hexandrum during spermatogenesis.

RP-1, a herbal preparation of Podophyllum hexandrum has already been reported to provide protection against whole body lethal gamma irradiation (10 Gy). It has also been reported to render radioprotection to germ cells during spermatogenesis. Present study was undertaken to unravel the cellular and molecular mechanism of action of RP-1 on testicular system in strain 'A' mice. Various antioxidant parameters such as thiol content, glutathione peroxidase (GPx), glutathione reductase (GR), glutathione-S-transferase (GST) enzyme activity, lipid peroxidation (LPO) and total protein levels were investigated. Thiol content was seen to increase significantly (p < 0.05) in both RP-1 alone and RP-1 pretreated irradiated groups over the irradiated groups at 8, 16 and 24 h. Irradiation (10 Gy) significantly decreased GPx, GST and GR activity in comparison to untreated control but RP-1 treatment before irradiation significantly (p < 0.05) countered radiation-induced decrease in the activity of these enzymes. Radiation-induced LPO was also found to be reduced at all time intervals by RP-1 treatment before irradiation. As compared to irradiated group the protein content in testicular tissue was increased in RP-1 pretreated irradiated group at 4 and 16 h significantly (p < 0.05). Comets revealed by single-cell gel electrophoresis were significantly longer (p < 0.001) in irradiated mice than in unirradiated control. RP-1 treatment before irradiation, however, rendered significant increase (p < 0.05) in comet length over the corresponding control and irradiated group initially at 4 h but at later time points, this was reduced significantly (p < 0.01) as compared to the irradiated group. RP-1 treatment alone rendered shorter comets at 8, 16 and 24 h than irradiated groups (p < 0.001). This study implies that RP-1 offers radioprotection at biochemical and cytogenetic level by protecting antioxidant enzymes, reducing LPO and increasing thiol content.

Animals↗

PubMed2004

Remedial effect of DL-alpha-lipoic acid against adriamycin induced testicular lipid peroxidation.

Adriamycin (ADR), a cytotoxic antineoplastic drug is used in the treatment of various solid tumors. However, its efficacy continues to be challenged by significant toxicities including testicular toxicity. In the present study, the effect of lipoic acid, a "universal antioxidant" was investigated on ADR induced peroxidative damages in rat testis. Adult male albino rats of Wistar strain were administered ADR (1 mg/kg body weight, i.v.) once a week for 10 weeks. ADR injected rats showed a significant decline in the activities of enzymic antioxidants (catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase) and non-enzymic antioxidants (reduced glutathione, Vitamin A, Vitamin C and Vitamin E) with high malondialdehyde levels. The extent of testicular toxicity was evident from the decreased activities of testicular marker enzymes (sorbitol dehydrogenase and glucose-6-phosphate dehydrogenase). Treatment with lipoic acid (35 mg/kg body weight, i.p.) one day prior to ADR administration, maintained near normal activities of the enzymes and significantly reduced lipid peroxidation, thereby proving it to be an effective cytoprotectant.

Animals↗

PubMed1993

Do glutathione and related enzymes play a role in drug resistance in small cell lung cancer cell lines?

Small cell lung cancer (SCLC) is treated primarily with combination chemotherapy. Despite high initial response rates, most patients eventually die with drug resistant disease. In some tumours, resistance to multiple chemotherapeutic agents is attributed to overexpression of P-glycoprotein (P-gp). However, this does not appear to be a frequent occurrence in drug resistant SCLC. Increased levels of glutathione (GSH) and related enzymes may play a role in resistance to alkylating agents as well as natural product drugs. We measured levels of GSH, glutathione S-transferase (GST), glutathione reductase (GSH Red), glutathione peroxidase (GSH Px), and gamma-glutamyl transpeptidase (gamma-GT) in a panel of 20 SCLC cell lines. Most of these lines were established from patients treated at this centre. Each cell line had a characteristic and reproducible profile of GSH and related enzyme levels. Immunoblot analysis indicated that the predominant GST in the cell lines was the anionic pi isoenzyme. The relative sensitivity of each of these cell lines to 16 different chemotherapeutic agents was measured using a modified MTT assay. Spearman rank correlation analysis was used to determine the relationships between the relative chemosensitivity of these cell lines and the levels of GSH and related enzymes. The number of positive correlations was no greater than expected by chance alone. Furthermore, there was no correlation with the treatment history of the patients from whom the cell lines were derived. These data suggest that alterations in glutathione metabolism do not play a major role in resistance to chemotherapeutic agents in these human SCLC cell lines.

Antineoplastic Agents↗

PubMedDate not supplied

Inhibitory effect of vitamin D3 on 3'methyl-4-dimethyl-amino-azobenzene-induced rat hepatocarcinogenesis: a study on antioxidant defense enzymes.

The anticarcinogenic effect of vitamin D3 (VD3) on 3,-methyl-4-dimethyl-amino-azobenzene (3,-Met-DAB)-induced hepatocarcinogenesis was investigated in male Sprague-Dawley rats. Anticancer efficacy of VD3 was estimated using different possible biomarkers, namely reduced glutathione (GSH) concentration, gamma-glutamyl transpeptidase (GGT) activity, glutathione S-transferase (GST) activity, glutathione reductase (GRd) activity, glutathione peroxidase (GPx) activity in hyperplastic nodules (HNs) and non-nodular surrounding parenchyma (NNSP) liver areas. VD3 was found to control the carcinogen-induced alterations in GSH level, GST, GGT, GRd and GPx activity both in HNs and NNSP liver areas during long-term exposure. A decrease in the number of HNs was also evident in the present investigation. VD3 was proved to be an effective antitumor drug during the initiation/promotion phases of hepatic carcinogenesis but the effect was found to be less prominent during initiation and promotion phases.

Animals↗

PubMed1993

Antioxidant enzyme activity in the muscles of calves depleted of vitamin E or selenium or both.

Feeding diets depleted of vitamin E and Se to cattle can induce a disease known as nutritional degenerative myopathy. It is believed that an increased peroxidative challenge in muscle is involved in the pathogenesis of this disease. A number of species can up-regulate the activity of some antioxidant enzymes, including glutathione reductase (EC 1.6.4.2), glutathione transferase (EC 2.5.1.18), glucose-6-phosphate dehydrogenase (EC 1.1.1.49), catalase (EC 1.11.1.6), and superoxide dismutase (EC 1.15.1.1), in an attempt to mitigate the effects of a peroxidative challenge. A 2 x 2 factorial study was set up to examine possible changes in the activities of these antioxidant enzymes in muscles of ruminant calves fed on diets low in either vitamin E or Se. Four groups of four calves each were fed on a basal diet of NaOH-treated barley which was supplemented with alpha-tocopherol or Se or both for a total of 50 weeks. Calves fed on diets depleted of vitamin E, but not those fed on diets low in Se, developed subclinical myopathy, as judged by increases in the activity of plasma creatinine kinase (EC 2.7.3.2), and had increased muscle concentrations of two indices of lipid peroxidation, namely thiobarbituric acid-reactive substances, with and without ascorbate activation. Feeding diets depleted of vitamin E and diets low in Se both increased muscle activities of glucose-6-phosphate dehydrogenase in heart, biceps and supraspinatus. This change may have occurred in an attempt to maintain intracellular pools of reduced glutathione. No other changes in antioxidant enzyme activity were observed.

Animals↗

PubMed2005

Effects of energy restriction and fish oil supplementation on renal guanidino levels and antioxidant defences in aged lupus-prone B/W mice.

Energy restriction (ER) and dietary fish oil (FO) are known to reduce the severity of glomerulonephritis and increase the lifespan of lupus-prone (NZB x NZW) F1 (B/W) mice. In the present study, mice were fed either ad libitum or energy-restricted (a 40 % lower energy intake than the diet ad libitum), semi-purified diets containing 5 % maize oil or 5 % fish oil supplementation. To estimate the renal damage associated with oxidative stress, the total amounts of reactive oxygen species (ROS), cyclooxygenase-derived ROS and levels of guanidino compounds were measured. Additionally, we assessed the putative action of ER and FO on several key antioxidant enzymes measured in the kidney post-mitochondrial fraction. Results showed that the age-related increase in creatinine level was significantly reduced by ER and FO in old mice. In contrast, arginine and guanidino acetic acid levels showed a decrease with age but were increased by ER and FO. The GSH:GSSG ratio showed a significant decrease with age, whereas ER and FO feeding prevented the decrease. The age-related decrease in antioxidant scavenging superoxide dismutase, catalase and glutathione peroxidase activities were all reversed by ER and FO. The moderately decreased glutathione reductase and glutathione-S-transferase activities with age were significantly increased by ER and FO. Furthermore, the increased total ROS and cyclooxygenase-derived ROS levels were effectively reduced by ER and FO. In conclusion, our data strongly indicate that ER and FO maintain antioxidant status and GSH:GSSG ratio, thereby protecting against renal deterioration from oxidative insults during ageing.

Acetic Acid↗

PubMed1985

Effect of selenium deficiency on hydroperoxide-induced glutathione release from the isolated perfused rat heart.

Selenium deficiency has been implicated as a cause of the cardiomyopathy known as Keshan disease in China. Selenium is an essential constituent of glutathione peroxidase, an enzyme that destroys hydroperoxides by using the reducing equivalents of reduced glutathione (GSH). We studied glutathione-dependent hydroperoxide metabolism in isolated perfused rat hearts. Hearts from selenium-deficient rats contained 5% of the glutathione peroxidase activity found in control hearts. Glutathione reductase activity and glutathione content were not affected by selenium deficiency. Infusion of t-butylhydroperoxide into control hearts caused an increase in heart glutathione disulfide (GSSG) concentration proportional to the rate of hydroperoxide infusion up to 200 nmol/(g heart X min). GSSG was released into the perfusate in proportion to the hydroperoxide infusion rate up to 150 nmol/(g heart X min), but GSSG release did not increase further with higher infusion rates. Thus, GSSG release by the heart is saturable. It had a maximum rate of about 14 nmol GSH equivalents/(g heart X min) when stimulated by t-butylhydroperoxide infusion. This indicates that GSSG release by the heart is carrier-mediated and is not due to passive diffusion. Infusion of hydroperoxide into selenium-deficient hearts failed to cause increases in heart GSSG concentration and in GSSG release. This indicates that selenium-deficient heart cannot metabolize hydroperoxides through glutathione-dependent pathways. We suggest that selenium deficiency might predispose the heart to injury from oxidant stress.

Animals↗

PubMed1994

Dietary selenite modifies glutathione metabolism and 7,12-dimethylbenz(a)anthracene conjugation in rats.

The present studies determined the impact of dietary selenite on glutathione homeostasis in liver and mammary tissue and its relationship to biliary excretion of 7,12-dimethylbenz(a)anthracene (DMBA) conjugates. In Experiment 1, liver and mammary tissue concentration of reduced glutathione (GSH) and activities of gamma-glutamylcysteine synthetase (GCS), glutathione reductase (GR) and glutathione S-transferases (GST) were positively correlated with tissue selenium concentration in female rats fed semipurified diets supplemented with sodium selenite (0.05 to 4 mg Se/kg). The magnitude of the response was dependent upon total selenite intake and the tissue examined. Glutathione peroxidase activity did not correlate with tissue GSH concentration. Because both selenite and BHT have been reported to elevate liver GSH, Experiment 2 compared these agents (4 mg Se/kg and 6 g/kg BHT/kg, respectively) on the biliary excretion of DMBA metabolites. Five major biliary DMBA conjugates, three GSH and two beta-glucuronide, were identified. Dietary addition of selenite or BHT enhanced the excretion of these DMBA conjugates by over 100% during the 15-h collection period. These investigations suggest that dietary selenium can alter the concentration of GSH and the activities of three glutathione-dependent enzymes in mammary and liver, accounting for part of the expanded biliary excretion of DMBA conjugates. Enhanced biliary loss of DMBA conjugates likely relates to the reported depression in DMBA binding to mammary cell DNA and the inhibition of DMBA carcinogenesis caused by dietary selenite.

9,10-Dimethyl-1,2-benzanthracene↗

PubMed2000

Sex differences in diquat-induced hepatic necrosis and DNA fragmentation in Fischer 344 rats.

Redox cycling metabolism of diquat catalyzes generation of reactive oxygen species, and diquat-induced acute hepatic necrosis in male Fischer 344 (F344) rats has been studied as a model of oxidant mechanisms of cell killing in vivo. At equal doses of diquat, female F344 rats sustained less hepatic damage than did male rats, as estimated by plasma alanine aminotransferase (ALT) activities after 6 h. Biliary efflux of glutathione disulfide (GSSG) was greater in male than in female rats at each dose of diquat, but even comparable rates of GSSG excretion were associated with less hepatic injury in female rats. Hepatic activities of superoxide dismutase (SOD) and glutathione peroxidase (GPX) were similar in the two genders, and activities of glutathione reductase (GR) and glutathione S-transferase-alpha (GST-alpha) activities were higher in the male rats. Previous studies in male rats have implicated formation of 2,4-dinitrophenylhydrazine (DNPH)-reactive "protein carbonyls" and related iron chelate-catalyzed redox reactions as mechanisms critical to diquat-induced acute cell death in vivo. However, diquat-treated female rats showed higher levels of DNPH-reactive proteins in livers and in bile than did males, both at identical doses of diquat and at doses that produced similar elevations in plasma ALT activities. In female rats, fragmentation of hepatic deoxyribonucleic acids (DNA) was increased by doses of diquat that did not increase plasma ALT activities, and increased fragmentation was observed prior to elevation of plasma ALT activities. In the present studies, hepatic necrosis was most closely associated with DNA fragmentation, although additional studies are needed to determine the mechanisms responsible for and the pathophysiological consequences of the fragmentation.

Alanine Transaminase↗

PubMed1984

Normal glutathione content and some related enzyme activities in the fetal erythrocytes.

Pure fetal blood was obtained by direct-vision fetoscopy from 66 fetuses at 17-24 weeks gestation. The concentration of GSH and the activities of the enzymes gamma-glutamylcysteine synthetase (GCS), glutathione synthetase (GS), glutathione reductase (GR) and glutathione peroxidase (GPx) were analysed by established techniques to find the normal ranges for this gestational age. The ranges were relatively narrow and could serve as reference values for the prenatal diagnosis of defects in the GSH metabolism of erythrocytes. The results were compared with those obtained from 38 normal adults and with published values on neonatal blood. In the case of GR a comparison was also made with maternal blood. In comparison with adults, fetal erythrocytes showed higher GSH concentration and GCS activity and lower GS and GPx activities. This pattern resembled that found in neonatal erythrocytes except for the GCS activity, which was higher in the fetal cells. Furthermore the differences between fetal and adult erythrocytes were more pronounced than those between neonatal and adult cells. The GR activity of fetal erythrocytes was also higher than that of either normal adult or maternal blood. This difference, however, was reduced to an insignificant level when the enzyme was activated in vitro by flavin adenine dinucleotide (FAD) because of a relatively low per cent activation of the GR in the fetal erythrocytes.

Enzyme Activation↗

PubMed1995

Protective effects of antioxidants against uraemia-induced lipid peroxidation and glutathione depletion in humans.

The effects of uraemias and antioxidant therapy for 40 days with vitamin A, vitamin C and vitamin E on blood and erythrocyte sulfhydryl (glutathione, GSH) content and on erythrocyte glutathione-S transferase (GST), glutathione reductase (GSR) and glutathione peroxidase activities were studied in six uraemic patients maintained on haemodialysis. In addition, the effect of antioxidant therapy on erythrocyte lipid peroxidation was determined, and erythrocyte haemoglobin content was measured. Uraemic patients in dialysis exhibited significant decreases in blood and erythrocyte GSH content as well as significant decreases in the activities of GST, GSR and GSH-peroxidase relative to control subjects. Furthermore, the uraemic patients had elevated erythrocyte malondialdehyde levels. Blood and erythrocyte GSH content from uraemic patients was significantly elevated after 20 days of antioxidant treatment and remained elevated thereafter throughout the remaining 20 days of the study (130% and 173%, respectively). Antioxidant therapy also produced significant increases in GSR and GSH-peroxidase activities after 20 days of treatment which remained relatively constant thereafter. No significant change in GST activity was observed. Erythrocyte malondialdehyde levels, as an index of oxidative tissue damage, exhibited a significant decrease (70%) in the patients after 40 days of antioxidant therapy. A gradual increase in erythrocyte haemoglobin content was observed following treatment of the uraemic subjects (45% at day 40). The results suggest that antioxidant therapy may protect against oxidative stress associated with uraemia.

Antioxidants↗

PubMed2004

Pentoxifylline does not prevent hypoxia/reoxygenation-induced necrotizing enterocolitis. An experimental study.

Hypoxia/reoxygenation (H/R)-induced intestinal injury plays a significant role in the development of necrotizing enterocolitis (NEC). We experimentally explored the effect of pentoxifylline (PTX) on an NEC model. Twenty-one newborn rabbits were divided into three groups: group 1 (control), group 2 (H/R) and group 3 (H/R + PTX). Five minutes of reoxygenation following 5 min of hypoxia was performed three times a day during 3 days. Before each H/R procedure in the H/R + PTX group, the rabbits were treated with PTX 25 mg/kg intraperitoneally. Animals were sacrificed on the third day and ileum samples were taken for histopathological examination and biochemical enzyme studies [superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione S-transferase (GST)]. There was a significant difference in the grade and number of the intestinal lesions between controls and the H/R and H/R + PTX groups (p < 0.001), but no significant difference was found between the H/R and the H/R + PTX groups (p > 0.05). Intestinal SOD, GR and GST activities in the H/R and H/R + PTX groups were significantly higher than in the control group (p < 0.05); however, there was no significant difference between the H/R and H/R + PTX groups (p > 0.05). Significantly reduced GPx activity was found in the H/R and H/R + PTX groups compared with the controls (p < 0.05). No significant difference in GPx activity existed between the H/R group and the H/R + PTX group (p > 0.05). Ischemia/reperfusion injury was responsible for mediating hypoxia-induced intestinal necrosis in NEC and PTX pretreatment did not have a protective effect on NEC.

Animals↗

PubMed1998

alpha-Tocopherol (vitamin-E) ameliorates ferric nitrilotriacetate (Fe-NTA)-dependent renal proliferative response and toxicity: diminution of oxidative stress.

Ferric nitrilotriacetate (Fe-NTA) is a potent nephrotoxic agent. In this communication, we show the modulatory effect of DL-alpha-tocopherol (Vitamin-E) on ferric nitrilotriacetate (Fe-NTA)-induced renal oxidative stress, toxicity and hyperproliferative response in rats. Fe-NTA-treatment enhances the susceptibility of renal microsomal membrane for iron-ascorbate-induced lipid peroxidation and hydrogen peroxide generation which are accompanied by a decrease in the activities of renal antioxidant enzymes, catalase, glutathione peroxidase, glutathione reductase and glutathione-S-transferase and depletion in the level of renal glutathione. Parallel to these changes, a sharp increase in blood urea nitrogen and serum creatinine has been observed. In addition, Fe-NTA-treatment also enhances renal ornithine decarboxylase activity (ODC) and increases [3H]thymidine incorporation in renal DNA. Prophylactic treatment of animals with Vit.E daily for 1 week prior to the administration of Fe-NTA resulted in the diminution of Fe-NTA-mediated damage. Enhanced susceptibility of renal microsomal membrane for lipid peroxidation induced by iron-ascorbate and hydrogen peroxide generation were significantly reduced (P < 0.05). In addition, the depleted level of glutathione and inhibited activities of antioxidant enzymes recovered to significant levels (P < 0.05). Similarly, the enhanced blood urea nitrogen and serum creatinine levels which are indicative of renal injury showed a reduction of about 50% at a higher dose of Vit.E. The pretreatment of rats with Vit.E reduced the Fe-NTA-mediated induction in ODC activity and enhancement in [3H]thymidine incorporation in DNA. The protective effect of Vit.E was dose dependent. In summary, our data suggest that Vit.E is an effective chemopreventive agent in kidney and may suppress Fe-NTA-induced renal toxicity.

Animals↗

PubMed2001

Differential stress responses of antioxidative systems to drought in pendunculate oak (Quercus robur) and maritime pine (Pinus pinaster) grown under high CO(2) concentrations.

Maritime pine (Pinus pinaster), a drought-avoiding species, contained 2--4-fold lower activities of superoxide dismutase, ascorbate peroxidase, catalase, dehydroascorbate reductase, and glutathione reductase than pendunculate oak (Quercus robur), a drought-tolerant species. The levels of ascorbate, monodehydroascorbate radical reductase activity, and glutathione in pine needles were similar to those in oak leaves. In both species the development of drought stress, characterized by decreasing predawn water potentials, caused gradual reductions in antioxidant protection, increased lipid peroxidation, increased oxidation of ascorbate and glutathione and in pine also significant loss in soluble proteins and carotenoids. These results support the idea that increased drought-tolerance in oak as compared with pine is related to increased biochemical protection at the tissue level. To test the hypothesis that elevated CO(2) ameliorated drought-induced injury, young oak and pine trees acclimated to high CO(2) were subjected to drought stress. Analysis of plots of enzymatic activities and metabolites against predawn water potentials revealed that the drought stress-induced decreases in antioxidant protection and increases in lipid peroxidation were dampened at high CO(2). In pine, protein and pigment degradation were also slowed down. At high CO(2), superoxide dismutase activities increased transiently in drought-stressed trees, but collapsed in pine faster than in oak. These observations suggest that the alleviation of drought-induced injury under elevated CO(2) is related to a higher stability of antioxidative enzymes and an increased responsiveness of SOD to stressful conditions. This ameliorating mechanism existed independently from the effects of elevated CO(2) on plant water relations and is limited within a species-specific metabolic window.

Antioxidants↗

PubMed2002

Lead stimulates the glutathione system in selective regions of rat brain.

Lead (Pb) is a highly neurotoxic agent that causes functional and structural abnormalities in the brain. Glutathione (GSH) is a main molecule involved in the protection mechanisms against Pb itself and against reactive oxygen species generated by the metal. This study was carried out to investigate the effect of Pb on the glutathione system in several regions of adult rat brain. In the model of Pb toxicity, adult Wistar rats were exposed to 25 mg of lead acetate/kg b.w. for 3 days. Glutathione and the related enzymes i.e. gamma-glutamylcysteine synthetase (gamma-GCS), glutathione reductase (GR) and glutathione S-transferases (GSTs) were examined in the hippocampus, cerebellum and forebrain. In the cytosolic fraction the concentration of total GSH and the activity of GR increased only in the cerebellum of Pb-exposed rats. Higher increases of both parameters were observed in mitochondrial fraction obtained from the cerebellum and hippocampus. The activity of cytosolic enzyme--gamma-GCS was enhanced only in the forebrain. Regarding cytosolic GSTs, changes in the activity together with enhanced relative density of enyme protein were found in the cerebellum and hippocampus. Generally, activation of the glutathione system observed shortly after Pb treatment suggests the protective response of the brain to toxic insult. Regional differences in the pattern of these changes may coincide with different susceptibility to Pb. Present results suggest also that mitochondrial mechanisms might account for lead toxicity.

Animals↗