Effects of prolonged stanozolol treatment on antioxidant enzyme activities, oxidative stress markers, and heat shock protein HSP72 levels in rat liver

The abuse of anabolic-androgenic steroids (AAS) to enhance physical performance is widespread in sport communities despite their reported side effects. Since the biochemical bases for the hepatotoxic effects of these compounds are largely unknown, this investigation was aimed at testing whether prolonged (8 weeks) treatment with high doses (2 mg kg⁻¹ body weight; 5 d wk⁻¹) of stanozolol (ST), either alone or in conjunction with treadmill-exercise training, induced changes in oxidative stress biomarker levels and antioxidant defence systems in rat liver. After ST oral administration, the mean values of serum parameters related to hepatic function were within normal ranges. No changes in protein carbonyl content and in the reduced to oxidized glutathione (GSH/GSSG) ratio were detected in liver homogenates of ST-treated rats, whereas thiobarbituric acid-reactive substances (TBARS) levels resulted increased (P<0.05). Total superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities were higher (P<0.05) in the liver of treated rats but mitochondrial SOD and glutathione reductase (GR) activities, and the 72 kDa heat shock protein (HSP72) level were not modified. Chronic exercise alone did not change any of the above parameters except for a remarkable enhancement of HSP72 expression; in no case training modified the effects of ST treatment. The present data show that 8 wk ingestion of ST, either with or without concurrent exercise training, can induce oxidative stress in rat liver despite the up-regulation of enzymatic antioxidant activities.     

Combined effect of alcohol and cigarette smoke on lipid peroxidation and antioxidant status in rats

The effect of long-term administration of alcohol and cigarette smoke independently and both in combination on lipid peroxidation and antioxidant enzymes, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione-S-transferase (GST) was studied in liver, kidney, heart and lungs of albino rats. The levels of peroxidation products viz., malondialdehyde, hydroperoxides and conjugated dienes were increased in all the tissues of alcohol administered and smoke-exposed rats. Activities of SOD and CAT were decreased in alcohol-treated and alcohol and smoke combination groups, but increased in smoke-exposed group. Activities of GPx and GST have shown an increase, while concentration of reduced glutathione was found decreased in all the three groups.     

Relation between voluntary physical activity and oxidant/antioxidant status in rats

The relationship between voluntary distance running and antioxidant capacity was studied in rats after three weeks voluntary running. Hydroxyl radical level, reduced glutathione level, activities of glutathione reductase and superoxide dismutase were measured in plasma, liver, brain, soleus and gastrocnemius white muscle. Hydroxyl radical level of liver negatively correlated with the running distance (r=-0.616, P<0.001). The reduced glutathione levels of liver and brain increased depending on the running distance and the correlation was confirmed between them in liver (r=0.638, P<0.01) and brain (r=0.766, P<0.001). The hydroxyl radical level in liver positively correlated with the activities of glutathione reductase (r=0.464, P<0.05) and superoxide dismutase (r=0.549, P<0.05). A significant positive correlation was detected between the hydroxyl radical level and superoxide dismutase activity in brain (r=0.488, P<0.05). These results demonstrate that physical activity correlates well with glutathione level and anti-oxidant enzyme activities in liver, suggesting a close relation between physical activity and induction of antioxidant systems.     

Alteration of antioxidant status following sympathectomy: Differential effects of modified plasma levels of adrenaline and noradrenaline

The influence of altered levels of endogenous catecholamines following adrenalectomy or 6-hydroxydopamine (6-OH) treatment (alone or in combination) on enzymatic (glutathione reductase, catalase, glutathione peroxidase and Cu,Zn superoxide dismutase) and non-enzymatic (glutathione) antioxidant components of heart, liver, kidney, lung and erythrocytes in male Wistar rats was investigated. Functional antioxidant status was assessed in terms of susceptibility to t-butylhydroperoxide-induced sulfhydryl group oxidation (an indirect measure of glutathione depletion) and lipid peroxidation, as measured by thiobarbituric acid-reactive substance (TBARS) formation. Reduced levels of adrenaline and noradrenaline resulted from adrenalectomy and 6-OH treatment, respectively, while a combination of these treatments led to a reduction in the levels of both catecholamines. Adrenalectomy was associated with alterations in glutathione reductase activity in the heart and liver (increased). 6-OH treatment alone produced an elevation in glutathione reductase activity only in the heart. In adrenalectomized animals, 6-OH treatment produced no further increases in glutathione reductase activities of heart or liver. In lung, however, the combination of adrenalectomy and 6-OH treatment caused an elevation in both glutathione peroxidase and glutathione reductase activities. Glutathione levels of liver alone were elevated following adrenalectomy, while those of erythrocytes and liver (but not other tissues investigated) were increased by the combination of adrenalectomy and 6-OH treatment. The kidney was relatively resistant to the effects of sympathectomy and showed no changes in any of the antioxidant components measured. Adrenalectomy alone or in combination with 6-OH produced an increase in susceptibility to peroxide-induced sulfhydryl group oxidation only in the heart. 6-OH treatment caused a reduction in peroxide-induced TBARS formation only in the kidney. Both adrenalectomy and the combination of adrenalectomy and 6-OH treatment were associated with reduced TBARS formation in the liver, lung and kidney, but not heart. Results from this study demonstrate that the effects of sympathectomy on antioxidant status vary among tissues. Differences between adrenalectomy and 6-OH treatment on antioxidant components are suggestive of differential actions of adrenaline and noradrenaline on tissue antioxidant status which may have important implications under conditions associated with elevations in levels of these catecholamines including chronic stress and myocardial infarction.     

Effect of dietary caffeine and zinc on the activity of antioxidant enzymes,zinc, and copper concentration of the heart and liver in fast-growing rats

The purpose of this study was to determine the relationship between concentrations of Zn and Cu and the activities of superoxide dismutase and glutathione peroxidase in the heart and liver of young rat pups whose dams were fed a diet supplemented with caffeine and/or Zn. Four groups of dams with their newborn pups were fed one of the following diets for 22 d: 20% protein basal diet; the basal diet supplemented with caffeine (2 mg/100 body wt); the basal diet supplemented with Zn (300 mg/kg diet); or the basal diet supplemented with caffeine plus Zn. The Cu levels in the livers of the pups were decreased by maternal intake of the caffeine and Zn diet. The maternal intake of the caffeine diet increased Mn-superoxide dismutase (MnSOD) activity and Cu, Zn-superoxide dismutase (CUZnSOD) in the heart of the pups. On the other hand, the activity of Cu,ZnSOD was significantly reduced in the liver of pups whose dams consumed a caffeine, Zn, or caffeine plus Zn diet. Cu, ZnSOD activity in the liver of the pups seems to be correlated with Cu levels in the tissue. Selenium-dependent glutathione peroxidase (GSH-Px) activities in the heart and liver showed no difference among the groups. The effect of dietary caffeine and/or Zn on the activity of antioxidant enzymes in the heart and liver were different in young rats. The activities of these enzymes in the heart were lower than in the liver of 22-d-old rats. Our experiments indicate that the heart has limited defenses against the toxic effects of peroxides when compared to the liver.     

Influence of treatment of diabetic rats with combinations of pycnogenol, beta-carotene, and alpha-lipoic acid on parameters of oxidative stress

Treatment with antioxidants may act more effectively to alter markers of free radical damage in combinations than singly. This study has determined whether treatment with combinations of pycnogenol, beta-carotene, and alpha-lipoic acid was more effective at reducing oxidative stress in diabetic rats than treatment with these antioxidants alone. It is not feasible, based on this study, to assume that there are interactive effects that make combinations of these antioxidants more effective than any one alone to combat oxidative stress. Female Sprague-Dawley rats, normal and streptozotocin-induced diabetic, were treated (10 mg/kg/day ip for 14 days) with pycnogenol, beta-carotene, pycnogenol + beta-carotene, or pycnogenol + beta-carotene + alpha-lipoic acid; controls were untreated. Concentrations of thiobarbituric acid reactive substances, glutathione and glutathione disulfide, and activities of glutathione reductase, glutathione peroxidase, superoxide dismutase, and catalase were measured in liver, kidney, and heart. Four types of effects were observed: (1) treatment with beta-carotene alone either reversed (cardiac glutathione disulfide) or elevated (cardiac glutathione, hepatic glutathione peroxidase activity) levels seen in diabetic animals; (2) beta-carotene alone produced no effect, but pycnogenol both alone and in combinations elevated (renal glutathione peroxidase and glutathione reductase activities, hepatic glutathione reductase activity and glutathione disulfide) or depressed (cardiac glutathione disulfide) levels seen in untreated diabetic animals; (3) all treatments with antioxidants, either alone or in combination, either normalized (lipid peroxidation in all tissues), elevated (hepatic GSH, cardiac glutathione peroxidase activity), or had no effect on (activities of hepatic catalase and superoxide dismutase in all tissues) levels seen in diabetic animals; (4) in only one case (cardiac glutathione reductase activity) levels in diabetic animals treated with combinations of antioxidants were normal, but elevated in animals treated with either antioxidant alone. Antioxidant effects seem to be dependent on the nature of the antioxidant used and not on combination effects.     

Chronic antioxidant enzyme mimetic treatment differentially modulates hyperthermia-induced liver HSP70 expression with aging.

One postulated mechanism for the reduction in stress tolerance with aging is a decline in the regulation of stress-responsive genes, such as inducible heat shock protein 72 (HSP70). Increased levels of oxidative stress are also associated with aging, but it is unclear what impact a prooxidant environment might have on HSP70 gene expression. This study utilized a superoxide dismutase/catalase mimetic (Eukarion-189) to evaluate the impact of a change in redox environment on age-related HSP70 responses to a physiologically relevant heat challenge. Results demonstrate that liver HSP70 mRNA and protein levels are reduced in old compared with young rats at selected time points over a 48-h recovery period following a heat-stress protocol. While chronic systemic administration of Eukarion-189 suppressed hyperthermia-induced liver HSP70 mRNA expression in both age groups, HSP70 protein accumulation was blunted in old rats but not in their young counterparts. These data suggest that a decline in HSP70 mRNA levels may be responsible for the reduction in HSP70 protein observed in old animals after heat stress. Furthermore, improvements in redox status were associated with reduced HSP70 mRNA levels in both young and old rats, but differential effects were manifested on protein expression, suggesting that HSP70 induction is differentially regulated with aging. These findings highlight the integrated mechanisms of stress protein regulation in eukaryotic organisms responding to environmental stress, which likely involve interactions between a wide range of cellular signals.     

Lactobacillus protected bone damage and maintained the antioxidant status of liver and kidney homogenates in female wistar rats

The aim of the study was to evaluate protective property of Lactobacillus casei and Lactobacillus acidophilus in minimizing oxidative stress associated with arthritis from liver and kidney. Subsequently, protective property of Lactobacillus against the bone damage was also taken into consideration. Arthritis was induced by injecting freund's complete adjuvant (100 μl) into sub plantar surface of hind paw. Oral administration of culture, vehicle, and drug started after induction of arthritis (i.e. on day 9th). Indomethacin was used as a standard drug. Radiographic analysis of the hind paw knee joint was also done at the end of the 21st day. Oxidative stress parameters were studied from liver and kidney homogenate. Histopathology of liver and kidney was also performed. Lactobacillus treatment significantly rescued the enzymatic level of catalase, superoxide dismutase, reduced glutathione, and glutathione peroxidase in both liver and kidney homogenates, whereas it has decreased the malonaldehyde accumulation. Oral administration of Lactobacillus also significantly decreased the serum ceruloplasmin level. Radiographic analysis also corroborated these findings. Lactobacillus treatment maintained the normal histopathology of liver and kidney. Results of this study clearly suggest that L. casei and L. acidophilus, alone or in combination, decreased the bone damaged and effectively restored antioxidant status of liver and kidney. Lactobacillus has a significant antiarthritic and antioxidant activity against freund's complete adjuvant induced arthritis in rats.     

Influence of Methionine on Toxicity of Fluoride in the Liver of Rats

Oxidative stress is a common mechanism by which chemical toxicity can occur in the liver. The aim of the studies conducted has been to determine what influence the administration of methionine during intoxication with sodium fluoride may have upon the selected enzymes of the antioxidative system in rat liver. The experiment was carried out on Wistar FL rats (adult females) that, for 35 days, were administered distilled water, NaF, or NaF with methionine (doses: 10 mg NaF/kg bw/day, 10 mg Met/kg bw/day). The influence of administered NaF and Met was examined by analyzing the activity of the antioxidative enzymes: superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione transferase in the liver. The results suggest that fluoride reduces the efficiency of the enzymatic antioxidative system in the liver. Administration of methionine during intoxication with sodium fluoride does not have an advantageous influence upon the activity of superoxide dismutase, catalase, reductase, and glutathione transferase in the liver. The slight increase of the activity of glutathione peroxidase after administration of methionine may indicate its protective influence upon that enzyme.     

Lead-induced lipid peroxidation and antioxidant defense components of developing chick embryos.

Administration of lead (1.25 and 2.5 mumol/kg egg weight) to 14-day-old chick embryos enhanced the level of lipid peroxides (LPO) in tissues of liver, brain, and heart. Accumulation of LPO was maximum at 9 h after treatment with lead and returned to normal level by 72 h. Further, we have studied the levels of glutathione-S-transferase (GST), glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase. At 9 h posttreatment, the hepatic GR was reduced significantly with the induction of GST and considerable depletion of GSH. However, in brain and heart, both GR and GST activities were unaltered with significant reduction of GSH. Further, an increase of non-Se-dependent GPx and SOD activities were observed in liver, brain, and heart. Similarly, at 72 h, although the GPx activity was found decreased in liver and brain, the GST, catalase, and SOD activities were significantly increased in all the three tissues alike, suggesting tissue-specific changes of antioxidant defense components in response to lead treatment. Our results suggests that the elevated levels of GST, SOD, and catalase at 72 h were successful in bringing LPO levels back to normal.     

Influence of treatment of diabetic rats with combinations of pycnogenol, β‐carotene,and α‐lipoic acid on parameters of oxidative stress

Treatment with antioxidants may act more effectively to alter markers of free radical damage in combinations than singly. This study has determined whether treatment with combinations of pycnogenol, β‐carotene, and α‐lipoic acid was more effective at reducing oxidative stress in diabetic rats than treatment with these antioxidants alone. It is not feasible, based on this study, to assume that there are interactive effects that make combinations of these antioxidants more effective than any one alone to combat oxidative stress. Female Sprague‐Dawley rats, normal and streptozotocin‐induced diabetic, were treated (10 mg/kg/day ip for 14 days) with pycnogenol, β‐carotene, pycnogenol + β‐carotene, or pycnogenol + β‐carotene + α‐lipoic acid; controls were untreated. Concentrations of thiobarbituric acid reactive substances, glutathione and glutathione disulfide, and activities of glutathione reductase, glutathione peroxidase, superoxide dismutase, and catalase were measured in liver, kidney, and heart. Four types of effects were observed: (1) treatment with β‐carotene alone either reversed (cardiac glutathione disulfide) or elevated (cardiac glutathione, hepatic glutathione peroxidase activity) levels seen in diabetic animals; (2) β‐carotene alone produced no effect, but pycnogenol both alone and in combinations elevated (renal glutathione peroxidase and glutathione reductase activities, hepatic glutathione reductase activity and glutathione disulfide) or depressed (cardiac glutathione disulfide) levels seen in untreated diabetic animals; (3) all treatments with antioxidants, either alone or in combination, either normalized (lipid peroxidation in all tissues), elevated (hepatic GSH, cardiac glutathione peroxidase activity), or had no effect on (activities of hepatic catalase and superoxide dismutase in all tissues) levels seen in diabetic animals; (4) in only one case (cardiac glutathione reductase activity) levels in diabetic animals treated with combinations of antioxidants were normal, but elevated in animals treated with either antioxidant alone. Antioxidant effects seem to be dependent on the nature of the antioxidant used and not on combination effects. © 2005 Wiley Periodicals, Inc. J Biochem Mol Toxicol 18:345–352, 2004; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20046     

Effect of spirulina and Liv-52 on cadmium induced toxicity in albino rats

Oral administration of cadmium (6mg/kg body weight/day) as cadmium chloride (CdCl2) for 30 days resulted in a significant increase in thiobarbituric acid reactive substances (TBARS) level and a decrease in the levels of copper, zinc, iron, selenium, glutathione, superoxide dismutase, catalase, glutathione peroxidase when compared to normal control. Administration of either Liv-52 alone or in combination with spirulina produced a well pronounced protective effect in respect to these parameters in cadmium intoxicated rats. The protective effect of spirulina and Liv-52 in respect to biochemical changes were also confirmed by histopathological study in the liver and kidney sections.     

Combined effect of ascorbic acid and selenium supplementation on alcohol-induced oxidative stress in guinea pigs

Oxidative stress is a key step in the pathogenesis of ethanol associated liver injury. Ethanol administration induces an increase in lipid peroxidation either by enhancing the production of oxygen reactive species or by decreasing the level of endogenous antioxidants. In this present study, four groups of male guinea pigs (Cavia porcellus) were maintained for 45 days as follows: Control group (1 mg ascorbic acid (AA)/100 g body wt./day); Ethanol group (1 mg AA/100 g body wt./day+900 mg ethanol/100 g body wt./day); Selenium+AA group (25 mg AA+0.05 mg sodium selenite/100 g body wt./day); Ethanol+Se+AA group (25 mg AA+0.05 mg sodium selenite/100 g body wt.+900 mg ethanol/100 g body wt./day). Malondialehyde (MDA), hydroperoxides (HP) and conjugated dienes (CD) were significantly increased, while the activities of scavenging enzymes superoxide dismutase (SOD) and catalase were reduced in the alcohol administered groups. Co-administration of Se+AA along with alcohol increased the activities of scavenging enzymes and reduced the lipid peroxidation products level in hepatic tissues of guinea pigs. Activities of glutathione peroxidase (GPX) and glutathione reductase (GR) were enhanced in co-administered group. gamma-Glutamyl transpeptidase (GGT), a marker enzyme of alcohol induced toxicity, was also reduced, as was the glutathione content. This study suggests that the combined effect of Se+AA, provides protection against alcohol-induced oxidative stress as evidenced from the decreased levels of lipid peroxidation products and enhanced activities of scavenging enzymes.     

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 enzyme activity and lipid peroxidation in liver of female rats co-exposed to lead and cadmium: effects of vitamin E and Mn2+

The oxidative status of liver of female rats exposed to lead acetate and cadmium acetate either alone or in combination at a dose of 0.05 mg/kg body wt intraperitoneally for 15 days was studied. After the administration of lead alone, the activity of superoxide dismutase (SOD) decreased in liver, whereas no changes were observed in catalase (CAT) activity, and glutathione (GSH) and thiobarbituric acid (TBARS) levels. Cadmium exposure and combined exposure to lead and cadmium led to decrease in GSH content and increased TBARS levels. Moreover, animals exposed to either cadmium alone or in combination with lead showed a decrease in SOD activity and an increase in CAT activity. The in vitro experiments showed that vitamin E failed to restore the antioxidant enzyme activities in metal treated postmitochondrial supernatant fraction of liver. But Mn²⁺ ions protected the mitochondria from lipid peroxidation and could completely restore Mn-superoxide dismutase (Mn-SOD) activity following metal intoxication. The results of this study indicate that despite the ability of lead and cadmium to induce oxidative stress the effect in liver is not intensified by combined exposure to both lead and cadmium. The observed changes in various oxidative stress parameters in the liver of rats co-exposed to lead and cadmium may result from an independent effect of lead and /cadmium and also from their interaction such as changes in metal accumulation and content of essential elements like Cu, Zn and Fe. These results suggest that when lead and cadmium are present together in similar concentrations, cadmium mediates major effects due to its more reactive nature.     

Antioxidant enzyme activity and lipid peroxidation in liver of female rats co-exposed to lead and cadmium: Effects of vitamin E and Mn2+

The oxidative status of liver of female rats exposed to lead acetate and cadmium acetate either alone or in combination at a dose of 0.05?mg/kg body wt intraperitoneally for 15 days was studied. After the administration of lead alone, the activity of superoxide dismutase (SOD) decreased in liver, whereas no changes were observed in catalase (CAT) activity, and glutathione (GSH) and thiobarbituric acid (TBARS) levels. Cadmium exposure and combined exposure to lead and cadmium led to decrease in GSH content and increased TBARS levels. Moreover, animals exposed to either cadmium alone or in combination with lead showed a decrease in SOD activity and an increase in CAT activity. The in vitro experiments showed that vitamin E failed to restore the antioxidant enzyme activities in metal treated postmitochondrial supernatant fraction of liver. But Mn²⁺ ions protected the mitochondria from lipid peroxidation and could completely restore Mn-superoxide dismutase (Mn-SOD) activity following metal intoxication. The results of this study indicate that despite the ability of lead and cadmium to induce oxidative stress the effect in liver is not intensified by combined exposure to both lead and cadmium. The observed changes in various oxidative stress parameters in the liver of rats co-exposed to lead and cadmium may result from an independent effect of lead and /cadmium and also from their interaction such as changes in metal accumulation and content of essential elements like Cu, Zn and Fe. These results suggest that when lead and cadmium are present together in similar concentrations, cadmium mediates major effects due to its more reactive nature.     

Effect of lead acetate on superoxide anion generation and its scavengers in mice given endotoxin

The administration of endotoxin to mice rendered hypersensitive by lead acetate resulted in profound lipid peroxide formation in the liver 6 hr postintoxication. Endotoxin plus lead acetate administration depressed glutathione peroxidase and superoxide dismutase activities in mouse liver, whereas superoxide anion generation significantly increased in the livers of endotoxin plus lead acetate-treated mice compared with that in mice treated with endotoxin alone. Serum acid phosphatase and lactate dehydrogenase isozyme exhibited much more leakage in endotoxin plus lead acetate-injected mice than in sera of mice given endotoxin alone. Nonprotein SH level in the liver was reduced markedly in endotoxin-lead treated mice compared with those receiving endotoxin alone. The plasma vitamin E level was found to decline by 6 hr postintoxication in both endotoxin-lead and endotoxin alone-treated mice, and the transient elevation of the plasma level at 18 hr may be considered to indicate mobilization from other tissues into the blood.     

Hepato-protective potential of carotenoid meso-zeaxanthin against paracetamol, CCl4 and ethanol induced toxicity

Hepato-protective potential of carotenoid meso-zeaxanthin [(3R, 3'S)-beta, beta-carotene-3, 3'-diol] was studied using in vivo rat models. Paracetamol (3 g/kg body wt, orally), 20% ethanol (7.5 g/kg body wt, orally) and CCl4 (2.5 ml /kg, ip) were used as hepato toxins. Levels of marker enzymes of hepatic injury such as serum glutamate oxaloacetate transaminase, serum glutamate pyruvate transaminase and alkaline phosphatase, and serum bilirubin, which were drastically elevated by these hepato toxins were significantly decreased by meso-zeaxanthin pretreatment in a dose-dependent manner. Oxidative stress markers, tissue lipid peroxidation, conjugated dienes and tissue hydroperoxides, were high in the paracetamol treated control group animals, which were lowered by meso-zeaxanthin administration. Level of glutathione and antioxidant enzymes, superoxide dismutase, catalase and glutathione peroxidase, in liver tissue was increased by meso-zeaxanthin pretreatment compared to control group during alcohol and CCl4 induced hepatotoxicity. Hydroxyproline, an indicator of fibrosis in liver tissue, decreased remarkably by meso-zeaxanthin administration despite its notable elevation in ethanol treated rats. Histopathological analysis of liver tissue showed the hepatoprotective potential of meso-zeaxanthin.     

HSP70 induction in the brain following ethanol administration in the rat: regulation by glutathione redox state

Changes in glutathione (GSH) and glutathione disulfide (GSSG) levels and/or redox status have been suggested to mediate the induction of heat shock proteins (HSPs) that follows exposure to oxidizing agents such as ethanol. Here we report the effects of ethanol administration to rats at intracellular levels of GSH, GSSG, HSP70, and protein carbonyls in brain and liver. Following 7 days of ethanol administration, there was a significant decrease in GSH, a significant induction of HSP70, and a significant increase in protein carbonyls in all brain regions studied and in liver. In cortex, striatum, and hippocampus there was a significant correlation between (a) the decrease in GSH, (b) the increase in GSSG, and (c) the decrease in GSH/GSSG ratio and HSP70 levels induced in response to ethanol. These data support the hypothesis that a redox mechanism may be involved in the heat-shock signal pathway responsible for HSP70 induction in the brain.