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PubMed1998

Topical application of alpha-tocopherol modulates the antioxidant network and diminishes ultraviolet-induced oxidative damage in murine skin.

The aim of this study was to investigate the effects of topical alpha-tocopherol application on epidermal and dermal antioxidants and its ability to prevent ultraviolet (UV)-induced oxidative damage. Hairless mice received topical applications of alpha-tocopherol 24 h before a single, acute UV irradiation (10 x minimal erythemal dose). The four major antioxidant enzymes (catalase, superoxide dismutase, glutathione reductase and glutathione peroxidase), hydrophilic and lipophilic antioxidants, and lipid hydroperoxides, markers of oxidative damage, were assayed in both epidermis and dermis of hairless mice. Topical alpha-tocopherol treatment increased dermal superoxide dismutase activity by 30% (P < 0.01) and protected epidermal glutathione peroxidase and superoxide dismutase from depletion after UV irradiation. Total and reduced glutathione levels in the epidermis increased by 50% after the topical treatment (P < 0.05), as did dermal ascorbate levels (by 40%: P < 0.01). The topical treatment increased alpha-tocopherol levels both in the epidermis (62-fold) and the dermis (22-fold: P < 0.001 in each layer). Furthermore, alpha-tocopherol treatment significantly reduced the formation of epidermal lipid hydroperoxides after UV irradiation (P < 0.05). These results demonstrate that topical administration of alpha-tocopherol protects cutaneous tissues against oxidative damage induced by UV irradiation in vivo, and suggest that the underlying mechanism of this effect involves the up-regulation of a network of enzymatic and non-enzymatic antioxidants.

Administration, Cutaneous↗

PubMedDate not supplied

Age-related differences in GSH-shuttle enzymes in NO2- or O3-exposed rat lungs.

The effect of age on changes in glutathione (GSH)-shuttle enzyme activities in rat lungs following a 72-hr exposure to NO2 (14 ppm) or O3 (approximately 0.9 ppm) was investigated. Exposed animals survived and were in the adaptive recovery phase at sacrifice. Glucose-6-phosphate dehydrogenase, glutathione reductase, and glutathione peroxidase levels were significantly elevated in young adult or older rats (maternal nursing or normal) and, to a lesser degree, in weanlings. Enzyme levels of neonates remained essentially unchanged and their lungs showed minimal morphological injury. At 50 ppm NO2, neonates also exhibited significant elevations in all three enzyme levels. The comparative unresponsiveness of neonates to short-term, low-level exposure to NO2 or O3, together with other observations, indicate that the relative importance of the GSH-shuttle in protecting lungs against injury requires further investigation.

Aging↗

PubMed2002

Acute phase immune response to exercise coexists with decreased neutrophil antioxidant enzyme defences.

Long-duration or damaging exercise initiates reactions that resemble the acute phase response to infection and induces neutrophil priming for oxidative activity. Our objective was to establish the status of the antioxidant defences and of the oxidative equilibrium in the neutrophils of sportsmen prior to and after intense physical exercise. Nine voluntary male professional cyclists participated in this study. The exercise was a cycling mountain stage (171 km) and the cyclists took a mean +/- SEM of 270 +/- 12 min to complete it. We determined the activities of catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), the levels and activity of superoxide dismutase (SOD), the concentrations of ascorbate, glutathione and glutathione disulphide (GSSG) and DNA levels in neutrophils. The cycling stage decreased enzyme activities expressed per DNA units: CAT (33%), SOD (38%), GPx (65%); increased ascorbate concentration in neutrophils and decreased the GSH/GSSG ratio and the enzyme activities expressed per DNA units. Neutrophils could contribute to plasma antioxidant defences against oxidative stress induced by exercise because they probably provide antioxidant enzymes and ascorbate.

Acute-Phase Reaction↗

PubMed2001

Lipid peroxidation and antioxidant enzyme activity in different organs of mice exposed to low level of mercury.

The effects of mercuric chloride (Hg) on lipid peroxidation (LPO), glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD) and glutathione (GSH) levels in different organs of mice (CD-1) were evaluated. Mice were exposed (2 days/week) to 0.0 (control), 0.8 (low) and 8.0 (mid) and 80.0 (high) gHg/kg/day for 2 weeks. The high dose group was excluded from the study due to high mortality. LPO levels in kidney, testis and epididymus at low and mid doses; GR and GPx levels in testis at mid dose; SOD levels in brain and testis at both doses, liver and epididymus at mid dose; GSH levels in testis at both doses were significantly increased compared to their controls. However, the GR levels in kidney at both doses and in epididymus at mid dose; GPx levels in kidney and epididymus and SOD levels in kidney at both the doses; GSH levels in epididymus at mid dose were significantly decreased compared to their control. Body weight gain and food efficiency were significantly reduced (p<0.05) in mid dose. These results indicated that Hg treatment enhanced LPO in all tissues, but showed significant enhancement only in kidney, testis and epididymus suggesting that these organs were more susceptible to Hg toxicity. The increase in antioxidant enzyme levels in testis could be a mechanism protecting the cells against reactive oxygen species.

Animals↗

PubMed1981

Lead toxicity as related to glutathione metabolism.

The effect of lead poisoning on glutathione metabolism was studied in rat pups born of dams receiving a commercial laboratory diet supplemented with 0.5% lead acetate. Results showed that the body weight gain of the first 3 weeks of life and at the age of 6 weeks was significantly less in both male and female pups nourished by lead-fed dams than those raised by dams receiving the lab diet. Lead ingestion decreased hematocrit levels and hemoglobin values and increased the weights of liver, kidney, spleen and brain. Concentrations of plasma free histidine, glutamic acid and serine were decreased in lead-poisoned rats but glycine levels were markedly increased. After 4 weeks of lead feeding, both sexes had an increased glutathione concentration in erythrocytes, liver and kidney. Isotope studies further indicated that the incorporation of cystine-35S was significantly increased in glutathione but decreased in protein of liver and kidney of lead-fed rats. Similarly, lead ingestion significantly increased glycine-1-14C incorporation into renal glutathione. However, the activities of glutathione reductase and glutathione peroxidase were unaffected by lead poisoning. The data suggest a compensatory mechanism operates to overcome the toxicity of ingested lead by maintaining a high concentration of glutathione in the liver and kidney.

Amino Acids↗

PubMed1998

Chronic ethanol consumption affects glutathione status in rat liver.

There is no consensus yet on the role of oxidative stress in the nutritional outcome of chronic ethanol feeding and the status of cellular antioxidative defense systems against ethanol toxicity. In this study, chronic alcohol consumption in humans was reproduced in Sprague-Dawley rats to investigate the effect of ethanol ingestion on the regulation of oxidative stress in liver with a special focus on glutathione. Adult male rats were given 36% of total energy as alcohol in the Lieber-DeCarli liquid diet for 6 wk. The control group was pair-fed the diet containing isocaloric dextrin-maltose instead of ethanol. Chronic ethanol ingestion enhanced expression of cytochrome P450 II E1 in the liver, but did not significantly alter either the level of hepatic thiobarbituric acid reactive substances or the carbonyl group content of proteins. The hepatic concentrations of total and reduced glutathione and the activities of catalase, glutathione reductase and glutathione S-transferase were significantly higher in the ethanol group than in the control group. The activities of glutathione peroxidase and glucose-6-phosphate dehydrogenase were significantly lower in the ethanol group than in controls. Chronic ethanol consumption by well-nourished rats for 6 wk increased enzyme activities related to the recycling and utilization of glutathione in the liver. Such an enhancement in the activities of the hepatic antioxidative defense system may be one of the protective mechanisms of the body against oxidative tissue damage caused by ethanol-induced free radicals.

Alcohol Drinking↗

PubMed1981

Lipid peroxide formation and membrane damage in endotoxin-poisoned mice.

Lipid peroxide formation and plasma membrane damage in mouse liver following the administration of Salmonella endotoxin were examined. The liver lipoperoxide level was markedly elevated in animals given endotoxin compared with that in the controls, and returned to its normal range after 2 days. On the other hand, superoxide dismutase activity was decreased by 18--48 hr after endotoxin injection, thereafter tending to increase. Glutathione reductase and glutathione peroxidase activities declined in the liver 18 hr after the injection. The endotoxin resulted in much lower lipoperoxide formation in the livers of tolerant mice than in those of the poisoned mice. The lipoperoxide level in endotoxin-poisoned mice after the administration of alpha-tocopherol was lower than that in the controls, and alpha-tocopherol administration prevented completely the membrane protein damage that arose from endotoxin challenge. After glutathione administration the membranes of the poisoned mice also returned to almost the normal disk electrophoretic profile. These results suggest that lipid peroxide formation in the liver plasma membrane caused by free radicals might occur in a tissue ischemic state in endotoxicosis.

Adenosine Triphosphate↗

PubMed1989

Cytokines increase rat lung antioxidant enzymes during exposure to hyperoxia.

Pretreatment with the combination of tumor necrosis factor/cachectin (TNF/C) and interleukin 1 (IL-1) increased glucose-6-phosphate dehydrogenase (G6PDH), glutathione reductase (GR), glutathione peroxidase (GPX), catalase (CAT), and superoxide dismutase (SOD) activities in lungs of rats continuously exposed to hyperoxia for 72 h, a time when all untreated rats had already died. Pretreatment with TNF/C and IL-1 also increased, albeit slightly, lung G6PDH and GR activities of rats exposed to hyperoxia for 4 or 16 h. By comparison, no differences occurred in lung antioxidant enzyme activities of TNF/C and IL-1- or saline-pretreated rats exposed to hyperoxia for 36 or 52 h; the latter is a time just before untreated rats began to succumb during exposure to hyperoxia. The results raise the possibility that TNF/C and IL-1 treatment can increase lung antioxidant enzyme activities and that increased lung antioxidant enzymes may contribute to the increased survival of TNF/C and IL-1-pretreated rats in hyperoxia for greater than 72 h.

Animals↗

PubMed2000

Repeated acetaminophen dosing in rats: adaptation of hepatic antioxidant system.

Repeated dosing of acetaminophen (paracetamol) to rats is reported to decrease their sensitivity to its hepatotoxic effects, which are associated with oxidative stress and glutathione depletion. We determined if repeated acetaminophen dosing produced adaptive response of key antioxidant system enzymes. Male rats (Sprague-Dawley, 10 weeks) were given 800, 1200, or 1600 mg/kg/day acetaminophen by oral gavage for 4 days. Liver was assayed for oxidative stress and antioxidant markers: malondialdehyde (MDA), thiobarbituric acid reactive substance (TBARS), total antioxidant status (TAS), glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx), glucose-6-phosphate dehydrogenase (G6PD), catalase (CAT), and superoxide dismutase (SOD), and alanine transaminase (ALT) as a marker of hepatocellular injury. Acetaminophen at 1200/1600 mg/kg decreased GSH 26/47%, GPx 21/26%, CAT 35/28%, SOD 21/12%; and TAS 28/18% (correlated with CAT, r=0.91; SOD, r=0.66; GPx, r=0.45). Despite antioxidant deficiencies, and no TBARS change, MDA decreased 26%/33%/37% at 800/1200/1600 mg/kg, which correlated with increased GR (61%/62%/76%, r=0.77) and G6PD (130%/110%/190%, r=0.78). Both MDA (r=0.68) and G6PD (r=0.71) correlated with hepatic ALT, which decreased 27%/43%/48%, respectively. Resistance to acetaminophen hepatotoxicity produced by repeated exposure is partially attributable to upregulation of hepatic G6PD and GR activity as an adaptive and protective response to oxidative stress and glutathione depletion.

Acetaminophen↗

PubMed1983

Poor correlation between oxygen toxicity and activity of glutathione peroxidase.

To test the postulate that increased activity of the glutathione peroxidase system is required for the increased tolerance to oxygen toxicity that develops after several days of prior exposure to 85% oxygen we searched for a combination of increased tolerance but normal activity of the glutathione system. We exposed rats to 85% oxygen for 7 days and then placed them in air. After 0, 10, 20, and 30 days we estimated the potential role of an antioxidant system by measuring activities of glucose-6-phosphate dehydrogenase (G6PD), glutathione reductase (GR), glutathione peroxidase (GP), and the nonprotein sulfhydryl content (NPSH) of lung tissue. After 7 days in 85% oxygen (0 days in air) activities of G6PD, GR, and GP, were elevated above control values by 189%, 32%, and 126%, respectively, and NPSH was 146% higher. Twenty days later these activities and NPSH were not significantly different from those of control animals never exposed to 85% oxygen. We also tested these rats without increased enzyme activities for oxygen "tolerance" by exposing them, after 20 days of recovery in air, to 100% oxygen for 3 days and found that some were "tolerant" as judged by a mortality rate of only 42% compared with 100% in a group not previously exposed to oxygen. To determine if this degree of tolerance could be related to accelerated increases of enzyme activities during the exposures we measured the enzyme activities and NPSH of lungs at 12, 24, 36, 48 and 60 hr after the start of exposure to 100% oxygen in two groups: one preexposed to 85% oxygen 20 days earlier and the other not previously exposed to oxygen.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2003

Studies on the effect of monosodium glutamate [MSG] administration on some antioxidant enzymes in the arterial tissue of adult male mice.

The subcutaneous administration of monosodium glutamate to normal adult male mice at dose levels of 4 and 8 mg/g body weight caused a significant increase in lipid peroxidation level in the arterial tissue. The levels of total sulfhydryl and protein-bound sulfhydryl groups were found to be significantly increased, whereas non-protein-bound sulfhydryl, representing the glutathione level, was significantly decreased. It was also observed that the administration of monosodium glutamate at a dose level of 4 mg/g body weight and above induced oxidative stress by significantly lowering the activities of antioxidant enzymes like superoxide dismutases, catalase, and glutathione metabolizing enzymes like glutathione reductase and glutathione peroxidase in the arterial tissue.

Analysis of Variance↗

PubMed1976

Erythrocyte glutathione metabolism in cobalt-deficient goats.

Cobalt deficiency was produced in goats by feeding them rhode grass hay. The deficient animals excreted increased amounts of methyl malonic acid in their urine, indicating a lack of vitamin B12. Erythrocyte reduced glutathione levels increased with the onset of anemia. There was a concomitant increase in the levels of erythrocyte glutathione reductase (GSSG NADPH Reductase) and glutathione peroxidase (GSH:H2O2 peroxidase)during deficiency. These results are compared with similar observations reported for vitamin B12 deficiency in humans.

Anemia, Macrocytic↗

PubMed1999

[Indices of lipid peroxidation and antioxidants in workers of ecologically unfavorable productions].

Studied was the antioxidants-lipid peroxidation balance in erythrocytes of workers from the shop of plasticizers cleared with ozone, known as a strong oxidizer. Dynamics of the dependence of accumulation of lipid peroxidation products including diene conjugates, coupled ketotriene, and Schiff bases on length of service was shown. Alterations in the activity of enzymatic antioxidants (catalase, superoxidismutase, glutathione reductase, and glutathione peroxidase) against adaptation to ecologically ill productions were assessed.

Adult↗

PubMed2001

Effect of lindane on antioxidant enzymes in epididymis and epididymal sperm of adult rats.

AIM: To find out the changes induced by lindane on the antioxidant enzymes in epididymis and epididymal sperm of adult rats. METHODS: Adult male rats were orally administered lindane at a dose of 5.0 mg/kg body weight per day for 30 days. At the end of the treatment, the rats were sacrificed. The epididymis was removed and weighed and sperm were collected for sperm count, motility and biochemical studies. A 1% homogenate of epididymis was prepared and used for biochemical estimations. RESULTS: In lindane-treated rats, there were significant reductions in the epididymal weight, epididymal sperm count and motility compared with the controls. Significant decreases in the superoxide dismutase (SOD), catalase, glutathione reductase and glutathione peroxidase activities and significant increases in the H2O2 generation and lipid peroxidation were also observed in the epididymis and epididymal sperm of lindane-treated rats. CONCLUSION: Lindane decreases the levels of antioxidant enzymes in the epididymis and epididymal sperm of adult rats thereby inducing oxidative stress.

Age Factors↗

PubMed2003

Effect of Zn7-metallothionein on oxidative stress in liver of rats with severe thermal injury.

AIM: Using the model of burned animal with delayed resuscitation to study antagonistic effect of Zn7-metallothionein (Zn7-MT) on oxidative stress in the liver of rats suffered from severe thermal injury on skin. METHODS: To compare the changes in antioxidant concentrations and antioxidative enzyme activities in the liver or plasma of burned rats with or without Zn7-MT in resuscitation fluid by biochemical assay. RESULTS: After injury, glutathione concentration was progressively decreased with time. At 24 h after injury, activities of glutathione reductase and glutathione peroxidase in the liver of burned rats were increased and then decreased at 48 h postburn. Alpha-tocopherol in plasma was reduced at 24 h and malondialdehyde in the liver was increased significantly postburn. MT and MT-1 mRNA expression in burned rats were activated. Taken together, oxidative stress in the liver of burned rats occurred. Exogenous Zn7-MT attenuated the changes in antioxidant concentrations and antioxidative enzyme activities in the liver or plasma of burned rats. The effect of Zn7-MT was in a concentration-dependent manner and the concentration of 10 micromol/L was the most effective. Exogenous Zn7-MT also inhibited MT-1 mRNA overexpression and increased MT protein concentration. CONCLUSION: Zn7-MT effectively antagonized oxidative stress in the liver of rats with severe thermal injury.

Animals↗

PubMed1992

[The glutathione enzymatic redox system in the blood of patients with lymphoproliferative diseases].

The study deals with an evaluation of activity of cellular antioxidative system enzymes such as glutathione reductase and glutathione: H2O2 peroxidase in blood plasma, leukocytes and lymphocytes of healthy subjects and patients with lymphoproliferative diseases such as Hodgkin's disease, acute leukemia ana lymphosarcoma. A decrease in enzymatic activity in blood and glutathione redox-system dysbalance was identified in the patients group.

Acute Disease↗

PubMed2004

[Determination of antioxidants in plasma and erythrocyte in patients with epilepsy].

OBJECTIVE: To explore the changes of antioxidants in plasma and erythrocyte in epileptic patients. METHODS: The levels of erythrocyte enzymes glutathione reductase (GR), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), catalase and erythrocyte membrane lipid peroxidation (MDA), the percentage hemolysis, and plasma ceruloplasmin, vitamin A, vitamin C, vitamin E were measured in 39 controls, 32 epileptic patients and 26 follow-up patients. RESULTS: The levels of MDA, the percentage hemolysis, GSH-Px, CAT and plasma CER in the epileptic patients were significantly higher than those of the controls. While the levels of vitamin A, vitamin C, vitamin E, SOD and GR in the epileptic patients were markedly lower than those of controls. In the follow-up patients, the levels of GR, SOD, vitamin C and vitamin E were significantly higher than those of the epileptic patients. CONCLUSION: Free radicals and antioxidants play important roles in the etiology of epilepsy.

Adult↗

PubMed2005

[Protective effects of extract of Ginkgo biloba against ethanol-induced oxidative injury in rat testes].

OBJECTIVE: This study was designed to investigate whether EGB protect against ethanol-induced oxidative injury in rat testes. METHODS: The rats were pretreated with EGB (4.8,9.6 mg/100g bw per day) before 30% ethanol administration (2.37g/kg bw by gastric incubation). Ninety days later, the rats were killed in order to measure the activities of Superoxide Dismutase (SOD), Glutathione Reductase (GST), Glutathione Peroxidase (GSH-Px), Catalase (CAT) and the contents of Glutathione (GSH), Reactive Oxygen Species (ROS), Malondialdehyde (MDA)in rat testes. The microsomal fractions were obtained by the method of differential centrifugation, and HO-1 (Heme Oxygenase-1) activity in testicular microsomal was measured. To examine the expression of HO-1 mRNA by reverse transcription polymerase chain reaction (RT-PCR). RESULTS: Compared with ethanol group, ROS, and MDA contents significantly decreased in EGB group testes, respectively (P < 0.05). GST, GSH-Px, CAT, SOD activities, and GSH content in EGB group testes elevated markedly (P <0.05). EGB could enhance HO-1 mRNA expression remarkably. CONCLUSION: It is suggested that EGB as a preventive antioxidant can protect against ethanol-induced testicular injury, which may be associated with HO-1 activity enhancement, free radicals elimination, lipid per-oxidation reaction inhibition.

Animals↗