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PubMedDate not supplied

Oxidative stress in two populations of killifish (Fundulus heteroclitus) with differing contaminant exposure histories.

A population of killifish (Fundulus heteroclitus) inhabiting a creosote-polluted inlet of the Elizabeth River demonstrates tolerance to the acute toxic effects exerted by contaminated sediments on reference site killifish. Previous data have suggested that upregulated antioxidant defenses contribute to short-term tolerance in killifish exposed to Elizabeth River sediments. This study investigated population differences in antioxidant defenses from wild caught Elizabeth River and reference population killifish in different seasons, and after being held in the laboratory. Parameters measured in the killifish were total glutathione concentrations (GSH(T)), activities of glutathione reductase (GR), glutathione peroxidase (GPx), and lipid peroxidation (LPO), all in adult hepatic tissues. The Elizabeth River population exhibited greater GSH(T), higher GPx activities, and increased LPO as compared to the reference population. Sex specific population differences were also observed in GSH(T) and GPx. Both populations displayed decreased GSH(T) and increased GR from early to late summer, as well as after being held in the laboratory. This study indicates that there are many factors that may contribute to differences in levels of antioxidant defenses in addition to exposure to contaminants, including reproductive status and environmental conditions.

Analysis of Variance↗

PubMed2005

Aluminum-induced maternal and developmental toxicity and oxidative stress in rat brain: response to combined administration of Tiron and glutathione.

The current study was performed to assess the potential of 4,5-dihydroxy 1,3-benzene disulfonic acid di sodium salt (Tiron) and glutathione (GSH) either individually or in combination against aluminum (Al)-induced developmental toxicity in fetuses and sucklings of Wistar rats. Female rats were exposed to aluminum chloride at a dose of 345 mg/(kg day) oral from days 0 to 16 of gestation and 0 to 16 of post-partum (P.P.). Tiron and GSH were administered at a dose of 471 mg/(kg day) i.p. and 100 mg/(kg day) oral, respectively, on days 5, 7, 9, 11, 13, 15 and 17 of gestation and post-partum. Al caused reduction in number of corpora lutea, number of implantation sites, placental and fetal weight and stunted growth. Skeletal malformations were also observed in fetuses. Maternal toxicity was demonstrated by reduction in body weight gain. Induction of oxidative stress was also recorded in the brain of mother as well as in fetuses and sucklings after Al exposure. Significant decrease was recorded in reduced glutathione, glutathione reductase (GR), glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), acetyl cholinesterase (AChE) and increase was observed in TBARS and glutathione-S-transferase (GST) in brain of pregnant mothers, fetuses and sucklings. Most of the above parameters responded positively with individual therapy with Tiron, but more pronounced beneficial effects on the above-described parameters were observed when Tiron was administered in combination with GSH. Inductively coupled plasma-atomic emission spectroscopy (ICP-AES) studies also showed significantly high concentration of Al in suckling's brain and maternal blood, brain, placenta and fetal brain. Treatment with Tiron individually or in combination with glutathione, reduced the accumulation of the Al in almost all the organs studied. It is concluded that chelating agents reduced the Al-induced toxicity and Tiron was more effective in reducing blood Al concentration than glutathione when given individually.

1,2-Dihydroxybenzene-3,5-Disulfonic Acid Disodium ↗

PubMed2001

Effects of selected polychlorinated biphenyl (PCB) congeners on hepatic glutathione, glutathione-related enzymes, and selenium status: implications for oxidative stress.

Polychlorinated biphenyls (PCBs) induce drug metabolism that may lead to the bioactivation of PCBs themselves or alternatively may lead to oxidative events within the cell. The goal of the present study was to determine the influence of congeneric PCBs, selected as substrates for or inducers of drug metabolism, upon hepatic glutathione, glutathione-related enzymes, and selenium status. Male and female Sprague-Dawley rats received two i.p. injections per week of PCB 3 (4-chlorobiphenyl), PCB 28 (2,4,4'-trichlorobiphenyl), PCB 38 (3,4,5-trichlorobiphenyl), PCB 77 (3,3',4,4'-tetrachlorobiphenyl), PCB 153 (2,2',4,4',5,5'-hexachlorobiphenyl), or both PCBs 77 and 153 (100 micromol/kg/injection) and were killed at the end of 1, 2, or 3 weeks. Whole liver homogenates, hepatic cytosol, and microsomes were prepared. Both glutathione reductase and glutathione transferase activities were increased significantly in both male and female rats receiving PCB 77, an aryl hydrocarbon receptor agonist, as well as in those receiving both PCBs 77 and 153. No significant trend was observed in the levels of hepatic total glutathione. PCB 77 treatment decreased hepatic selenium-dependent glutathione peroxidase (SeGPX) activity in both male and female rats significantly. This decrease in activity following PCB 77 treatment was accompanied by a decrease in the cytosolic selenium-dependent glutathione peroxidase gene (GSPx1) transcript, as well as a decrease in hepatic total selenium levels. These data support the concept that exposure to the coplanar PCB 77 suppresses, via gene regulatory mechanisms, the cellular antioxidant enzyme SeGPX and that this decrease involves selenium. Lower halogenated PCBs that may be bioactivated to reactive oxygen species (ROS)-producing metabolites, and higher halogenated PCBs that are not Ah receptor agonists, were inactive.

Analysis of Variance↗

PubMed1997

Effects of N-nitrosodimethylamine on glutathione levels during development of chick-embryo.

Glutathione content in the liver, kidney and eye of chick embryo increased during development, having the maximum at day 17 after incubation of eggs. Activity of enzymes involved in glutathione metabolism changed during development. gamma-Glutamyltransferase activity increased gradually until day 17 in the liver and eye, but decreased thereafter, while the enzyme activity increased continuously in the kidney. Glutathione reductase and glutathione peroxidase activities did not change significantly during development. Administration of N-nitrosodimethylamine (NDMA) to the fertile eggs 2 days after incubation resulted in an increase of glutathione levels in the liver and kidney at a dose of 0.01 mmol NDMA/egg, but the effect was not significant for glutathione levels by increasing the dose of NDMA. Decrease in viability and increase in formation of thiobarbituric acid (TBA) reactive substance were observed in the liver and kidney by administration of NDMA at 0.1 mmol/egg. By administration of buthionine sulfoximine (BSO) alone, viability and glutathione levels were decreased and TBA reactive substance was increased in the liver. Fatal toxicity of NDMA was observed especially when BSO was administered together with NDMA. These results indicate that glutathione plays an important role in protecting chick embryos against toxic effects induced by administration of NDMA.

Animals↗

PubMed1997

Oxidative stress in cyclosporin and azathioprine treated renal transplant patients.

The major cause of death following transplantation is cardiovascular disease. Among the many processes involved in atherogenesis, oxidative stress and modification of low density lipoprotein has been assigned a major role. This in turn may be affected by the immunosuppressive regime used. We studied oxidative stress in 40 renal transplant patients receiving two different immunosuppressive regimens (20 on cyclosporin, 20 on azathioprine/prednisolone), and 19 normal controls. Changes in lipid peroxidation (assessed as thiobarbituric acid reacting substances, TBARS), antioxidant enzyme activities (glutathione reductase GSHPx, glutathione peroxidase GSHPx and superoxide dismutase SOD) vitamin E and antioxidant associated trace metals (selenium, copper, zinc) were studied. Alteration of erythrocyte membrane fluidity was examined using the fluorescent probe 1,6 diphenyl-1,3,5-hexatriene (DPH). Both transplant groups showed no difference in TBARS, lipid standardised vitamin E, copper or selenium compared to controls. Zinc was significantly increased in both the cyclosporin and azathioprine groups compared to controls (P < 0.05). SOD was reduced in both transplant groups compared to controls (P < 0.001). GSHPx was elevated in both groups compared to controls but only reached significance in the azathioprine treated group (P < 0.005). GSHRx was slightly elevated in both transplant groups but did not reach significance. Erythrocyte membrane anisotropy was decreased in the cyclosporin treated group (P < 0.05). There was no difference in the azathioprine group compared to controls. The present results suggest an adaptive response to increased oxidative stress in both transplant groups sufficient to minimise markers of oxidative stress (TBARS and anisotropy). The results also suggest no significant difference between the two immunosuppressive regimes with regard to oxidative stress.

Adult↗

PubMed2000

The protective effect of flavonol quercetin against ultraviolet a induced oxidative stress in rats.

Ultraviolet A (UVA) light exposed cells can induce the production of reactive oxygen species (ROS) which can damage the cellular elements. Antioxidants can interfere with the production of ROS. In this study, malondialdehyde (MDA), reduced glutathione (GSH), glutathione reductase (GSSGR), glutathione peroxidase (GPx), catalase (CAT) and superoxide dismutase (SOD) levels were measured in the liver of rats exposed to UVA light in various doses. The effects of quercetin were determined as antioxidant on those parameters. Rats were divided into three groups as control, ultraviolet (UV), and ultraviolet+quercetin (UV+Q). UV and UV+Q group rats were irradiated 4 h per day with UVA light (1.25 mW/cm(2)) during periods of 0,3,6,9 days. Thus, on days 0,3,6 and 9, the rats have received 0,54,108,162 W/cm(2) light, respectively. Quercetin (50 mg/kg body wt.) was administered intraperitoneally before each irradiation period in the UV+Q group rats. MDA level in the UV group increased significantly on day-9 when compared to the control group (P<0.05). The MDA levels in the UV+Q group decreased significantly on day-6 and 9 in comparison with the UV group (P<0.05, P<0.001, respectively). GSH levels in all groups were not significantly different. GSSGR and GPx activities in the UV group were significantly lower on day-6 and 9 than in the control group (P<0.001). On all days these enzyme activities in the UV+Q group were significantly higher than in the UV group and higher than in the control group (P<0.001). SOD and CAT activities in the UV group decreased significantly on day-3, 6, and 9 in comparison with the control group (P<0.001). These enzyme activities also increased significantly in the UV+Q group on all days when compared to the UV group (P<0.001). This study demonstrated that the exposure of rats to UVA led to oxidative stress as reflected by increased MDA levels and reduced enzymic antioxidant levels, quercetin may be useful by reducing or preventing photobiologic damage.

Animals↗

PubMed2001

Antioxidant defense disruption by polycyclic aromatic hydrocarbons-coated onto Fe(2)O(3) particles in human lung cells (A549).

We addressed the hypothesis that in vitro short-term exposure to hematite (Fe(2)O(3)) and polycyclic aromatic hydrocarbons (PAHs) is more deleterious by virtue of their combinations being able to cause higher oxidative stress conditions in human lung cells (A549), than either chemical alone. Lipid peroxidation (malondialdehyde; MDA), antioxidant enzyme activities (superoxide dismutase; SOD, glutathione peroxidase; GPx, glutathione reductase; GR), glutathione status (reduced glutathione; GSH, oxidized glutathione; GSSG) and alpha-tocopherol (alpha-Toc) consumption were studied in cells exposed to Fe(2)O(3), benzo(a)pyrene (B(a)P) or pyrene, alone or in association. We found that increases in GSSG/GSH (P<0.01) and in alpha-Toc consumption (P<0.01) counteracted Fe(2)O(3)-induced lipid peroxidation. Exposure to B(a)P did not induce oxidative injury because of the involvement of non-enzymatic antioxidants in cell homeostasis. Pyrene did not induce free radicals (FR)-induced injury. Exposure to PAHs-coated onto Fe(2)O(3) particles damaged both the enzymatic (i.e. increases in SOD and GR activities; P<0.01) and the non-enzymatic (i.e. increases in GSSG/GSH; P<0.001, alpha-Toc consumption; P<0.01) antioxidant defenses, thereby allowing lipid peroxidation (i.e. MDA production; P<0.05). Exposure to PAHs-coated onto Fe(2)O(3) particles induced not only higher lipid peroxidation (i.e. MDA production; P<0.05) but also higher antioxidant alterations (i.e. SOD and GR activities; P<0.05, GSSH/GSH; P<0.01 or P<0.05) than either chemical alone. Several mechanisms could account for this result, enhanced uptake of Fe(2)O(3) and/or greater availability of PAHs. Hence, our results indicate that exposure to PAHs-coated onto Fe(2)O(3) particles is more deleterious in lungs than either chemical alone.

Antioxidants↗

PubMed2002

The effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin on the antioxidant system in mitochondrial and microsomal fractions of rat testis.

The ability of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) to induce oxidative stress in hepatic and some extrahepatic tissues of animals has been reported. The precise nature and mechanism of action of TCDD on the male reproductive system is not clear. In the present study, we have investigated the induction of oxidative stress in the testis of rat after exposure to low doses of TCDD. TCDD (1, 10, and 100 ng/kg body weight per day) was administered orally to the rat for 45 days. After 24 h of the last treatment the rats were killed using anesthetic ether. The weights of the testis, epididymis, seminal vesicles and ventral prostate decreased while the body weight remained unchanged in the rats administered with TCDD. Mitochondrial and microsomal fractions of the testis were obtained by the method of differential centrifugation. The activity of antioxidant enzymes such as superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase decreased significantly in the animals treated with TCDD in a dose-dependent manner in the mitochondrial and microsomal fractions of rat testis. The levels of hydrogen peroxide generation (H(2)O(2)) and lipid peroxidation increased in mitochondrial, and microsomal fractions of the testis. The results suggested that the low doses of TCDD elicit depletion of antioxidant enzymes and concomitant increase in the levels of H(2)O(2) and lipid peroxidation differentially in mitochondrial and microsomal fractions of rat testis. In conclusion the adverse effect of TCDD on male reproduction could be due to induction of oxidative stress.

Animals↗

PubMed2002

Effect of methoxychlor on the antioxidant system in mitochondrial and microsome-rich fractions of rat testis.

Methoxychlor, an environmental contaminant, which is widely used as a pesticide in many countries, has been shown to induce reproductive abnormalities in male rats. The precise nature and mechanism of action of methoxychlor on the male reproductive system is not clear. In the present study, we have sought to investigate the induction of oxidative stress in the testis of rat after exposure to methoxychlor. Methoxychlor (1, 10, and 100 mg kg(-1) body weight per day) was administered orally to the rats for 45 days. After 24 h of the last treatment the animals were killed using anesthetic ether. The body weight of the animals administered with methoxychlor did not show any significant change. The weights of the testis, epididymis, seminal vesicles and ventral prostate decreased significantly in 100 mg dose but remained unchanged in 1 and 10 mg doses. Mitochondrial and microsome-rich fractions of the testis were obtained by the method of differential centrifugation. The activities of antioxidant enzymes such as superoxide dismutase, catalase, glutathione reductase and glutathione peroxidase decreased significantly in the animals treated with methoxychlor in a dose-dependent manner in the mitochondrial and microsome-rich fractions of rat testis. The levels of hydrogen peroxide generation (H(2)O(2)) and lipid peroxidation increased in mitochondrial and microsome-rich fractions of the testis of the rats treated with methoxychlor. The results suggested that the low to medium doses of methoxychlor elicit depletion of antioxidant enzymes and concomitant increase in the levels of H(2)O(2) and lipid peroxidation differentially in mitochondrial and microsome-rich fractions of rat testis. In conclusion, the adverse effect of methoxychlor on male reproduction could be due to the induction of oxidative stress in testis.

Animals↗

PubMed2003

Induction of oxidative stress by bisphenol A in the epididymal sperm of rats.

Bisphenol A has been shown to affect the reproduction of male rats and mice. However, the mechanism of action of bisphenol A on the epididymal sperm is not elucidated. The present study was undertaken to evaluate the effect of bisphenol A on the antioxidant system of rat epididymal sperm. Bisphenol A was administered orally to male rats at the dose levels of 0.2, 2 and 20 microg/Kg body weight per day for 45 days. After 24 h of the last treatment, rats were weighed and killed using anesthetic ether. The body weight of treated rats did not show significant change as compared with the corresponding control groups. In bisphenol A-treated rats there was a significant decrease in the weight of the testis and epididymis; the weight of ventral prostate increased significantly whereas there was no significant change in the weight of seminal vesicles as compared with the corresponding group of control animals. Sperm collected from the epididymis were used for sperm count and biochemical estimations. Administration of bisphenol A caused a reduction in the epididymal sperm motility and sperm count in a dose-dependent manner. The activities of superoxide dismutase, catalase, glutathione reductase and glutathione peroxidase were decreased while the levels of H(2)O(2) and lipid peroxidation increased significantly in the treated rats as compared with the corresponding group of control animals. The results suggested that graded doses of bisphenol A elicit depletion of antioxidant defence system and induce oxidative stress in epididymal sperm of rats. In conclusion, the adverse effect of bisphenol A on male reproduction may be due to induction of oxidative stress in sperm.

Administration, Oral↗

PubMed1999

Lead intoxication: antioxidant defenses and oxidative damage in rat brain.

Oxidative damage associated with the presence of lead (Pb) in the brain has been proposed as one possible mechanism involved in Pb toxicity. To investigate this hypothesis, we examined the long-term effects of Pb2+ on parameters of oxidative stress in the brain from rats chronically exposed to the metal (1 g Pb acetate/1 drinking water). After 8 weeks of treatment, Pb2(+)-intoxicated rats (blood Pb concentration > 100 microg/dl) showed lower body weight, and lower hematocrit and 5-aminolevulinic acid dehydratase activity as compared to controls. The content of brain 2-thiobarbituric acid-reactive substances (TBARS), an indicator of lipid oxidation, was significantly (P < 0.05) higher in the Pb2(+)-intoxicated animals than in controls. Higher activities of the antioxidant enzymes glutathione reductase and glutathione peroxidase, and a lower (44%) level of ubiquinol 10 were found in the brain of the Pb2(+)-treated rats, compared to controls. A negative correlation between brain ubiquinol 9 (r2 = 0.79), 10 (r2 = 0.84) and blood Pb concentration was observed. Brain alpha-tocopherol levels, superoxide dismutase activity and parameters of oxidative damage to proteins were similar between control and Pb2(+)-treated rats. The present results indicate that chronic Pb2+ intoxication induces an oxidative stress situation in rat brain.

Animals↗

PubMed2001

Benzo(a)pyrene-coated onto Fe(2)O(3) particles-induced lung tissue injury: role of free radicals.

Lipid peroxidation (as malondialdehyde; MDA), activities of some antioxidant enzymes (as superoxide dismutase; SOD, glutathione peroxidase; GPx, glutathione reductase; GR), glutathione status, and oxidative DNA damage (as 8-hydroxy-2'-deoxyguanosine; 8-OHdG) were investigated in the lungs of rats exposed to hematite (Fe(2)O(3); 3 mg), benzo(a)pyrene (B(a)P; 3 mg), or B(a)P (3 mg)-coated onto Fe(2)O(3) particles (3 mg). Approximately 2-fold increases in MDA production were seen in animals exposed to Fe(2)O(3), B(a)P, or B(a)P-coated onto Fe(2)O(3) particles (P<0.01). Decreases in SOD activities were observed in rats treated with Fe(2)O(3) (1.66-fold, P<0.01), B(a)P (1.66-fold, P<0.001) or B(a)P-coated onto Fe(2)O(3) particles (1.43-fold, P<0.01). GPx and GR activities could not be detected. No alteration of the glutathione status was observed. Significant increases in the 8-OHdG formation occurred in response to exposure to B(a)P (2.0-fold, P<0.01) or B(a)P-coated onto Fe(2)O(3) particles (23.7-fold, P<0.001). Our results demonstrate also that Fe(2)O(3) generates free radical (FR)-induced lung injury and is not an inert carrier. We established that exposure to B(a)P or B(a)P-coated onto Fe(2)O(3) particles resulted in lipid peroxidation and SOD inactivation, thereby leading to oxidative damages in DNA. The main findings of this work was that B(a)P-coated onto Fe(2)O(3) particles caused higher lung concentrations of 8-OHdG than B(a)P by itself. Hence, our data may explain why exposure to B(a)P-coated onto Fe(2)O(3) particles resulted in a decreased latency and an increased incidence of lung tumors in rodents compared to exposure to B(a)P.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2001

Changes in thiol content and expression of glutathione redox system genes in the hippocampus and cerebellum in Alzheimer's disease.

In this report, we compared total and protein-bound thiol levels in the hippocampus and cerebellum of six Alzheimer's disease (AD) patients and six age-matched control subjects. Total level of sulfhydryl (SH) groups, determined using the 5,5'-dithiobis(2-nitrobenzoic acid) method, was not significantly altered in the hippocampus and cerebellum of AD patients. The level of protein-bound SH groups, determined by labeling with 3-(N-maleimido-propionyl) biocytin, was decreased in the AD hippocampus compared with controls. Reverse transcription-polymerase chain reaction analysis of the expression of key glutathione redox system genes demonstrated the induction of glutathione reductase and glutathione peroxidase messages in the AD hippocampus. Levels of glutathione transferase mu and A4-4 messages were unchanged. This study suggests that protective antioxidant gene responses are insufficient to counteract the increased oxidative damage of proteins in a vulnerable region of the AD brain.

Aged↗

PubMed2000

Polycyclic aromatic hydrocarbon coated onto Fe(2)O(3) particles: assessment of cellular membrane damage and antioxidant system disruption in human epithelial lung cells (L132) in culture.

The aim of this study was to investigate the oxidative effects of Fe(2)O(3), benzo(a)pyrene (B(a)P) and pyrene, alone or in association (B(a)P or pyrene coated onto Fe(2)O(3) particles), in normal human embryonic lung epithelial cells (L132) in culture. We evaluated: (i) membrane integrity, through fatty acid release (stearic acid, oleic acid, linoleic and linolenic acids, homolinolenic acid, arachidonic acid) and malondialdehyde (MDA) production; and (ii) antioxidant status, through enzymatic and non-enzymatic antioxidant defenses (superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione status, beta-carotene). Fe(2)O(3) did not induce any change in L132 cells. In pyrene-treated cells, SOD induction (P<0. 05), glutathione oxidation (P<0.05) and beta-carotene consumption (P<0.001) may counteract free radicals (FR)-induced damage. However, in B(a)P-incubated cells, SOD inactivation (P<0.05), GR increases (P<0.05), glutathione oxidation (P<0.05) and beta-carotene decreases (P<0.001) showed high disruption of antioxidants, thereby allowing FR-induced damage (i.e. arachidonic acid release, P<0.01; MDA production, P<0.01). Our main finding was that both associations caused higher FR-induced damage (i.e. MDA production, P<0.001; SOD inactivation, P<0.01) than either chemical alone. Several mechanisms could account for this result: enhanced uptake of Fe(2)O(3) particles and/or greater availability of polycyclic aromatic hydrocarbons (PAHs). We hypothesized also that Fe(2)O(3) and polycyclic aromatic hydrocarbons are more deleterious by virtue of their associations being able to produce higher oxidative effects than either chemical alone.

Antioxidants↗

PubMedDate not supplied

The effect of methoxychlor on the epididymal antioxidant system of adult rats.

Methoxychlor is widely used as a pesticide in many countries and has been shown to induce reproductive abnormalities in male rats, causing reduced fertility. The mechanism of action of methoxychlor on the male reproductive system is not clear. In the present study we investigated whether administration of methoxychlor induces oxidative stress in the epididymis and epididymal sperm of adult rats. Methoxychlor (50, 100, or 200 mg/kg body weight/day) was administered orally for 1, 4, or 7 days. The animals were killed using anesthetic ether 24 h after of the last treatment. Epididymal sperm were collected by cutting the epididymis into small pieces in Ham's F-12 medium at 35 degrees C. The body weight and weights of the testis, liver, and kidney did not show any significant changes in the methoxychlor-treated rats. The weight of the epididymis, seminal vesicles, and ventral prostate as well as epididymal sperm counts decreased after 50, 100, or 200 mg/kg/day for 7 days but remained unchanged after shorter courses of treatment. Epididymal sperm motility was decreased in a dose-dependent manner in the animals treated with methoxychlor for 4 or 7 days. The activities of the antioxidant enzymes superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase were decreased while the levels of hydrogen peroxide and lipid peroxidation were increased in the epididymal sperm as well as in the caput, corpus, and cauda epididymis after 4 or 7 days of treatment. The activities of superoxide dismutase decreased while the levels of lipid peroxidation increased in the liver but not in the kidney in all groups. Co-administration of the antioxidant vitamin E (20 mg/kg body weight/ day) to the 200 mg/kg/d methoxychlor-treated rats for 7 days prevented significant changes in the antioxidant systems in the epididymis and epididymal sperm and prevented alterations in sperm counts and motility. The results indicated that methoxychlor induces oxidative stress in the epididymis and epididymal sperm by decreasing antioxidant enzymes, possibly by inducing reactive oxygen species. In conclusion the adverse effect of methoxychlor on the male reproduction could be due to induction of oxidative stress.

Animals↗

PubMed1997

Abnormalities of retinal metabolism in diabetes or experimental galactosemia. IV. Antioxidant defense system.

Activities of enzymes that protect the retina from reactive oxygen species were investigated in experimentally diabetic rats and experimentally galactosemic rats, two animal models known to develop vascular lesions consistent with diabetic retinopathy. Diabetes or experimental galactosemia of 2 months duration significantly decreased the activities of glutathione reductase and glutathione peroxidase in the retina while having no effect on the glutathione synthesizing enzymes glutathione synthetase and gamma-glutamyl cysteine synthetase. Activities of two other important antioxidant defense enzymes-superoxide dismutase (SOD) and catalase-also were decreased (by more than 25%) in retinas of diabetic rats and galactosemic rats. Administration of supplemental antioxidants, vitamins C and E, for the 2 months prevented the diabetes-induced impairment of antioxidant defense system in the retina. In experimentally galactosemic rats, the supplemental antioxidants were not as effective: SOD activity was normalized, but the enzymes of the glutathione redox cycle were only partly restored, and the subnormal catalase activity was unaffected. Diabetes or experimental galactosemia results in significant impairment of the antioxidant defense system in the retina, and exogenous antioxidant supplementation can help alleviate the subnormal activities of antioxidant defense enzymes.

Animals↗

PubMed1999

Low-dose gamma-ray irradiation reduces oxidative damage induced by CCl4 in mouse liver.

We examined the effects of irradiation (50 cGy of gamma-ray) reducing the oxidative damage in carbon tetrachloride (CCl4)-hepatopathy mice. We made pathological examinations and analyzed transaminase activity (glutamic oxaloacetic transaminase and glutamic pyruvic transaminase), lipid peroxide level and the activities of endogenous antioxidants in the mouse. The irradiation was found to accelerate the recovery. Based on pathological examination as well as changes in each transaminase activity and lipid peroxide levels, it was shown that hepatopathy improved 3 d after the irradiation. The activities of glutathione reductase and glutathione peroxidase rapidly elevated after irradiation, and the total glutathione content gradually increased in the irradiation group. Both activities of gamma-glutamylcysteine synthetase and catalase were higher than normal at all times after the irradiation and gradually increased. In addition, the gamma-glutamylcysteine synthetase activity changed in a similar fashion to the total glutathione content. However, superoxide dismutase activity in both groups decreased and that of the irradiation group was significantly lower than that of the sham-irradiation group. These findings suggest that low-dose radiation relieved functional disorder at least in the liver of mice with active oxygen diseases.

Alanine Transaminase↗

PubMed1998

Postnatal expression of glucose-6-phosphate dehydrogenase in different brain areas.

The activity of glucose-6-phosphate dehydrogenase (G6PD) was studied in five brain areas of rats aged 5 to 90 days. The areas studied were: the olfactory bulb (OB), cortex, hippocampus, striatum and septum. The G6PD activity increased more than 2-fold from 5 to 90 days in the OB, while it was almost constant in the other areas. At every stage of development, the G6PD activity was significantly higher in the OB than in the other areas. The G6PD pattern was compared with 6-phosphogluconate dehydrogenase (6PGD), glutathione reductase (GR); glutathione peroxidase (GPX), catalase (CAT) and superoxide dismutase (SOD) in order to find synergistic interactions among activities of these enzymes during development. Over the considered period, the activity of 6PGD increased significantly in the OB, while no significant difference in activity was detected in the other areas. GR increased significantly and progressively at each developmental stage in all areas. GPX showed a progressive increase in the OB, while in other areas a significant increase was detected at 90 days only. CAT and SOD showed a different and independent pattern which differed from the G6PD pattern. CAT showed the highest level of activity at 5 days then progressively decreased or was constant until 90 days; SOD had the highest value at 5 days, than it decreased at 10 days and increased from 10 to 90 days. In all areas, G6PD activity showed three electrophoretic bands, whose relative activity changed with development. At histochemical level, we found a marked G6PD activity in the periglomerular zone of the OB, which increased with age, while other areas showed a homogeneous staining. The present results demonstrate that G6PD activity increases in the OB during the developmental stages and there is a coordinated simultaneous activation of 6PGD, GPX and GR. It is likely that this enzyme induction increases the antioxidant defense of periglomerular cells that are subject to a rapid renewal and thus much more exposed to oxidant stress.

Aging↗