Changes in activities of some ammonia-metabolizing enzymes in the rat liver and the brain after chronic ethanol administration

The changes in the activities of ammonia-metabolizing enzymes in liver and brain after ethanol intoxication has been investigated in rats. After administration of ethanol 30% (w/v) 6g kg-1 for 4 weeks we found an increase in liver glutamate dehydrogenase and glutaminase activity. In brain tissue the glutaminase activity was significantly higher and glutamate dehydrogenase was significantly lower. Glutamine synthetase activity in liver and brain was practically unchanged. The reasons for these changes in the activities of some ammonia-metabolizing enzymes in liver and brain after ethanol ingestion have been discussed.     

METABOLIC CONSEQUENCES OF ETHANOL OXIDATION IN BRAINS FROM MICE CHRONICALLY FED ETHANOL

Abstract— Effects of the acute and chronic administration of ethanol have been investigated in mouse brain on the redox-state, citric acid cycle function, levels of adenine nucleotides and other metabolites. Cerebral oxidation of ethanol, activity of alcohol dehydrogenase and the permeability of brain and liver mitochondrial preparations after chronic ethanol administration have been also investigated. Acute or chronic administration of ethanol resulted in a small but significant increase in the reduced components of certain dehydrogenase-linked substrate pairs in brain. Pyrazole, an inhibitor of alcohol dehydrogenase, prevented the ethanol-induced changes in brain. ¹⁴CO₂ production from several substrates was inhibited in brains from chronically ethanol-fed animals. Addition of pyrazole, however, prevented the ethanol-mediated inhibition of ¹⁴CO₂ production. Chronic administration of ethanol resulted in decreased levels of ATP and creatine phosphate in the brain, and increased contents of ADP and AMP. The cerebral activities of alcohol dehydrogenase and succinic dehydrogenase, oxidation of ethanol, mitochondrial oxidation of a-glycerophosphate, and levels of NADH remained unaffected by the chronic administration of ethanol. In contrast to liver, where chronic administration of ethanol increased the contribution of 'substrate shuttles'resulting in increased oxidation of ethanol; in brain, the contribution of these 'shuttles'remained unaffected.     

Influence of subacute treatment of some plant growth regulators on serum marker enzymes and erythrocyte and tissue antioxidant defense and lipid peroxidation in rats

This study aims to investigate the effects of the plant growth regulators (PGRs) (2,3,5-triiodobenzoic acid (TIBA), Naphthaleneacetic acid (NAA), and 2,4-dichlorofenoxyacetic acid (2,4-D)) on serum marker enzymes (aspartate aminotransferase (AST), alanin aminotransferase (ALT), creatine phosphokinase (CPK), and lactate dehydrogenase (LDH)), antioxidant defense systems (reduced glutathione (GSH), glutathione reductase (GR), superoxide dismutase (SOD), glutathione-S-transferase (GST), and catalase (CAT)), and lipid peroxidation content (malondialdehyde = MDA) in various tissues of rats. 50 and 100 ppm of PGRs as drinking water were administered orally to rats (Sprague-Dawley albino) ad libitum for 25 days continuously. The PGRs treatment caused different effects on the serum marker enzymes, antioxidant defense systems, and the MDA content in experimented rats compared to controls. Results showed that TIBA caused a significant decrease in serum AST activity with both the dosage whereas serum CPK was significantly increased with 100 ppm dosage of TIBA. Meanwhile, serum AST, CPK, and LDH activities were significantly increased with both dosage of NAA and 2,4-D. The lipid peroxidation end-product MDA significantly increased in the all tissues treated with both dosages of PGRs without any change in the brain and erythrocyte of rats treated with both the dosages of 2,4-D. The GSH depletion in the kidney and brain tissues of rats treated with both dosages of PGRs was found to be significant. Furthermore, the GSH depletion in the erythrocyte of rats treated with both dosages of PGRs except 50 ppm dosage of 2,4-D was significant too. Also, the GSH level in the liver was significantly depleted with 50 ppm of 2,4-D and NAA, whereas the GSH depletion in the same tissue did not significantly change with the treatment. The activity of antioxidant enzymes was also seriously affected by PGRs; SOD significantly decreased in the liver, heart, kidney, and brain of rats treated with both dosages of NAA, whereas the SOD activity in the erythrocytes, liver, and heart was either significantly decreased or not changed with two doses of 2,4-D and TIBA. Although the CAT activity significantly increased in the erythrocyte and brain of rats treated with both doses of PGRs, it was not changed in the liver, heart, and kidney. Meanwhile, the ancillary enzyme GR activity significantly increased in the brain, heart, and liver but decreased in the erythrocyte and kidney of rats treated with both doses of PGRs. The drug-metabolizing enzyme GST activity significantly increased in the heart and kidney but decreased in the brain and erythrocytes of rats treated with both dosages of PGRs. As a conclusion, the results indicate that PGRs might affect antioxidant potential enzymes, the activity of hepatic damage enzymes, and lipid peroxidation dose independently. Also, the rats resisted to oxidative stress via antioxidant mechanism but the antioxidant mechanism could not prevent the increases in lipid peroxidation in rat's tissues. These data, along with the determined changes, suggest that PGRs produced substantial systemic organ toxicity in the erythrocyte, liver, brain, heart, and kidney during the period of a 25-day subacute exposure.     

Effects of acetyl-L-carnitine on the formation of fatty acid ethyl esters in brain and peripheral organs after short-term ethanol administration in rat

Increasing evidence suggests that Fatty acid ethyl esters (FAEE) play a central role in ethanol induced organ damage. In the current study we measured FAEE formation in rats after short-term oral administration of ethanol, in the presence and absence of pre-treatment with acetyl-L-carnitine. Ethanol treatment caused a significant increase in the levels of FAEE, particularly in the brain and heart, but also in the kidney and liver. Increases in FAEE were associated with a significant increase in FAEE synthase activity, GSH transferase activity, and lipid hydroperoxide levels. Pre-treatment with acetyl-L-carnitine resulted in a significant reduction of FAEE accumulation, decrease in FAEE synthase and GSH transferase activities, and lipid hydroperoxide levels. Administration of acetyl-L-carnitine greatly reduced the metabolic abnormalities due to non-oxidative ethanol metabolism, through an increment in lipid metabolism/turnover and by the modulation of the activities of enzymes associated with FAEE synthesis. These results suggest a potentially important pharmacological role for acetyl-L-carnitine in the prevention of alcohol-induced cellular damage.     

Effect of lecithin with vitamin-B complex and tocopheryl acetate on long-term effect of ethanol induced immunomodulatory activities

The alcoholic liver disease usually causes overall immunological alterations which might be attributed to hepatic disease, to ethanol action, and/or to malnourishment. In the present study, efficacy of lecithin with vitamin-B complex to treat ethanol induced immunomodulatory activity was compared with the effect of lecithin alone and tocopheryl acetate (vitamin E). Ethanol (1.6 g/kg body wt/day for 12 weeks) exposure increased thiobarbituric acid reactive substance (TBARS) level, while decreased superoxide dismutase (SOD) activity and reduced glutathione (GSH) content in whole blood hemolysate of 8-10 week-old male BALB/c mice (weighing 20-30 g). The activities of transaminase (AST and ALT) enzymes, interleukin (IL)-10 and gamma interferon (IFN-gamma) elevated, while IL-2 and IL-4 reduced in mice serum due to ethanol exposure. These suggested that oxidative stress and immunomodulatory activities were interdependent and associated with ethanol induced liver damage. Lecithin treatment significantly reduced AST (32.44%), ALT (32.09%), IL-10 (25.63%) activities and TBARS content (12.76%) compared to ethanol treated group. However, lecithin with vitamin-B complex treatment, significantly reduced AST (62.83%); ALT (61.96%); IL-10 (35.88%); IFN-gamma (22.55%) activities and TBARS content (31.58%), while significantly elevated GSH content (36.49%) and SOD activity (61.21%). Tocopheryl acetate treatment significantly reduced AST (62.83%); ALT (61.54%); IL-10 (36.35%): IFN-gamma (23.28%) activities and TBARS content (35.84%). while significantly elevated GSH content (28.76%) and SOD activity (62.42%) compared to ethanol treated group. These findings persuasively argued that lecithin with vitamin-B complex was a new promising therapeutic approach in controlling ethanol induced immunomodulatory activities involving liver damage processes. Prevention of oxidative stress with correction of nutritional deficiency caused alteration in the ethanol-induced immunomodulatory activities and associated liver diseases.     

Protective effect of L-carnitine on experimental lead toxicity in rats: a clinical,histopathological and immunohistochemical study

Abstract

Female Wistar-albino rats were given lead acetate (PbAc) for 60 days to investigate the protective effects of L-carnitine (CA) clinically and histopathologically on PbAc-induced tissue damage. Blood samples were obtained from the jugular vein for hemoglobin (HB), hematocrit (HCT), red blood cells (RBC), white blood cells (WBC), platelets (PLT), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and creatinine. PbAc treatment caused a significant decrease in HB, HCT and RBC, a significant increase in WBC, AST, ALT and creatinine compared to controls. Although administration of CA did not reverse HB and HCT values, it reversed both the decrease in RBC and the increase in WBC, AST, ALT and creatinine. After the experimental period, all rats were weighed, then decapitated for pathological examination. Control rat liver, kidney and brain showed normal histological architecture. Lead-induced nephropathic kidneys; degenerative changes, inflammation and portal edema of the liver; and brain neuropil vacuolation, neuronal vacuolation, satellitosis and neuronophagia were observed in experimental groups. All changes were reduced in the PbAc group treated with CA (PbAc + CA). PbAc caused copper/zinc superoxide dismutase (Cu/Zn-SOD) expression in both the hepatocytes and tubular epithelium of the kidney. PbAc + CA exposure caused moderate Cu/Zn-SOD immunoreactivity. While in the brain sections of the PbAc group the degenerative neurons were stained intensely with anti-ubiquitin antibody, PbAc + CA rats showed moderate staining in neurons with anti-ubiquitin antibody. These results show that CA as a food additive reduced the severity of tissue damage caused by PbAc.     

Potential role of antioxidants during ethanol-induced changes in the fatty acid composition and arachidonic acid metabolites in male Wistar rats

Biochemical assessment of liver damage during ethanol-induced stress was done by measuring the activities of serum enzymes, viz., aspartate transaminase (AST) and alkaline phosphatase (ALP), which were significantly elevated in rats fed ethanol. Ethanol administration for a period of 60 days modifies the fatty acid composition, and the analysis of fatty acids showed that there was a significant increase in the concentrations of palmitic acid (16:0), stearic acid (18:0), and oleic acid (18:1) in liver, kidney, and brain, whereas the concentrations of palmitoleic (16:1) and arachidonic acid (20:4) were significantly decreased. The breakdown products of arachidonic acids (20:4), prostaglandins, were elevated. The antioxidants curcumin and N-acetylcysteine (NAC) decreased the activities of serum AST and ALP. Curcumin and NAC decreased the concentrations of fatty acids, viz., palmitic, stearic, and oleic acid, whereas arachidonic acid and palmitoleic acid were elevated. The prostaglandin concentrations were also decreased after curcumin and N-acetylcysteine treatment. Thus the present investigation shows that curcumin and N-acetylcysteine prevent the fatty acid changes produced by ethanol and also reduce the inflammatory response of ethanol by reducing the level of prostaglandins. This revised version was published online in July 2006 with corrections to the Cover Date.     

A study of iodothyronine 5'-monodeiodinase activities in normal and pathological tissues in man and their comparison with activities in rat tissues

The present study was undertaken to investigate the peripheral iodothyronine 5'-monodeiodination in different human and rat tissues. We studied iodothyronine 5'-monodeiodinase type I (5'-DI) activity in liver, kidney, intestine, right cardiac atrium and skeletal muscle and we compared the results with those in rat tissues. Lodothyronine 5'- monodeiodinase type II (5'-DII) activity was studied in normal and ischemic human heart and in rat normal myocardium and brain. The 5'-DI activity (fmol/min x mg protein) in liver and kidney was significantly higher (p < 0.001, ANOVA) in normal rat tissue than in human. However, no significant differences were observed in 5'-DI activity between normal and tumoral human intestine or between intestinal tissue of man and rat. 5'-DI activity in normal human skeletal muscle was significantly higher than that in rat skeletal muscle (p < 0.05). The 5'-DI activity was lower in human ischemic myocardium when compared to normal myocardium either in humans (p < 0.05) or rat (p < 0.001). The Km of 5'-DI was significantly lower in rat than in human kidney and liver (p < 0.05). We conclude that 1) 5'-DI is distributed widely among extrathyroidal human and rat tissues and 5'-DII activity is detectable both in human and rat heart; 2) 5'-DI activity in liver and kidney is lower in man than in rat; 3) 5'-DI activity in the skeletal muscle is higher in man than in the rat; 4) 5'-DI activity is decreased in tumoral tissues of human liver and kidney and in ischemic myocardium, while no significant difference was found between human and rat cardiac 5'-DII activity.     

Diphenyl diselenide reverses cadmium-induced oxidative damage on mice tissues

The concept that selenium-containing molecules may be better antioxidants than classical antioxidants, has led to the design of synthetic organoselenium compounds. In the present investigation subchronic deleterious effects of cadmium-intoxication in mice and a possible protective effect of diphenyl diselenide (PhSe)2 (5 micromol/kg) were studied. Male adult Swiss albino mice (25-35 g) received CdCl2 (10 micromol/kg, subcutaneously), five times/week, for 4 weeks. A number of toxicological parameters in blood, liver, kidney, spleen and brain of mice were examined including delta-aminolevulinic acid dehydratase (delta-ALA-D) activity, lipid peroxidation and ascorbic acid content, the parameters that indicate tissue damage such as plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea, creatinine and lactate dehydrogenase (LDH) were also determined. The results demonstrated that cadmium caused inhibition of delta-ALA-D activity in liver (24%), kidney (33%) and spleen (73%) and (PhSe)2 therapy was effective in restoring enzyme activity in all tissues. A reduction in ascorbic acid content was observed in kidney (11%) and spleen (10.7%) of cadmium-treated mice and (PhSe)2 was only effective in improving this reduction in kidney. An increase of lipid peroxidation induced by cadmium was noted in liver (29%) and brain (28%) tissues and (PhSe)2 therapy was effective in restoring TBARS levels in both tissues. We also observed an increase on plasma LDH (1.99-times), AST (1.93-times) and ALT (4.24-times) activities. (PhSe)2 therapy was effective in restoring AST activity at control level. (PhSe)2 did not present toxic effects when plasma parameters were evaluated. The results suggest that the administration of an antioxidant (PhSe)2, during cadmium intoxication may provide beneficial effects by reducing oxidative stress in tissues.     

Studies on turnover rates of rat gamma-glutamyltranspeptidase after chronic ethanol administration in vivo

Chronic ethanol administration to rats was shown to result in a significant increase of hepatic and serum GGT activities, contrasting to the decreased levels observed in pancreas, intestine, brain, and kidney by the new alcock regimen method. The kinetics of rat GGT synthesis and degradation in vivo among the different sources after chronic ethanol administration has been studied by use of acivicin, which irreversibly inactivates GGT. The comparison of kinetics of GGT return after acivicin injection showed that the kidney and serum GGT exhibits biphasic half-lives in contrast to liver, pancreatic, intestinal, and brain GGT half-lives in chronic ethanol-administered rats. The present studies on kinetics of GGT synthesis (Ks) and degradation (Kd) in vivo would seem to indicate the existence of three types of systems. That is, Ks rather than Kd may be preferential in liver and serum whereas Kd is apparently increased in kidney and intestine without noticeable change in Ks. The reverse phenomenon is also observed for pancreas and brain. These findings suggest that the contributions of alterations in the rates of GGT synthesis and degradation to changing levels of GGT have been evaluated as a mechanism for enzyme adaptation in animal tissues as a change from the control diet to the ethanol diet.     

Ethanol and leucine oxidation--II. Leucine oxidation by rat tissue in vitro

The effect of ethanol upon leucine oxidation by rat tissues in vitro is reported. The activities of branched chain amino acid aminotransferase and 2-oxo acid dehydrogenase were decreased by chronic administration of ethanol (20% v/v solution as drinking water for 35 d) in muscle and kidney but were increased, although not significantly, in liver. Acute administration of ethanol (8 g kg-1 body-weight 0.73) did not affect enzyme activities. Tissue NAD+:NADH ratios, calculated from lactate:pyruvate ratios, were significantly decreased in the liver and kidney of rats receiving ethanol acutely. These data are consistent with the view that ethanol decreases leucine oxidation by decreasing availability of NAD+ when given acutely and by decreasing enzyme activity when administered chronically.     

Effects of L-Carnitine on the Formation of Fatty Acid Ethyl Esters in Brain and Peripheral Organs after Short-Term Ethanol Administration in Rat

A study was undertaken in rats to evaluate the effects of short-term oral ethanol administration on the levels of fatty acid ethyl esters (FAEE) in brain and peripheral organs in the presence and absence of pretreatment with L-carnitine. Administration of ethanol to rats for seven days resulted in fatty acid ethyl ester formation, particularly in the heart and brain, but also in the kidney and liver. FAEE generation was associated with a significant increase of GSH transferase activity. Treatment with L-carnitine significantly reduced both FAEE and GSH transferase activity, and these effects were associated with a significant decrease in alcohol blood concentrations. The present evidence supports the hypothesis that fatty acid ethyl esters could be mediators involved in the production of alcohol-dependent syndromes. Administration of L-carnitine through an increment in lipid metabolism and turnover, and by the modulation of cellular antioxidant enzymes, greatly reduces these metabolic abnormalities supporting its potential usefulness as a pharmacological tool in alcoholism management.I wish to dedicate this paper to the memory of Prof. Victor Rizza who tragically disappeared on the 2nd of September when this paper was in press     

Effect of subchronic administration of ethanol and methylmercury in combination on the tissue distribution of mercury in rats

The effect of oral administration for 14 weeks of 8 g.kg-1.day-1 ethanol and 0.5 mg.kg-1.day-1 methylmercuric chloride in combination to rats fed isocaloric diets has been investigated. Ethanol, in contrast to published studies, failed to influence the tissue distribution of methylmercury and its inorganic mercury metabolite in brain and kidney, and did not inhibit the increase in kidney weight induced by methylmercury. Ethanol and methylmercury, in combination and individually, reduced the renal but not the hepatic activity of gamma-glutamyltransferase, but did not affect the renal and biliary concentration of reduced glutathione. Further study is required to determine the circumstances under which ethanol can influence the tissue distribution of methylmercury and its inorganic mercury metabolite.     

Biochemical effects of Nigella sativa L seeds in diabetic rats

Oral administration of ethanol extract of N. sativa seeds (300 mg/kg body weight/day) to streptozotocin induced diabetic rats for 30 days significantly reduced the elevated levels of blood glucose, lipids, plasma insulin and improved altered levels of lipid peroxidation products (TBARS and hydroperoxides) and antioxidant enzymes like catalase, superoxide dismutase, reduced glutathione and glutathione peroxidase in liver and kidney. The results confirm the antidiabetic activity of N. sativa seeds extract and suggest that because of its antioxidant effects its administration may be useful in controlling the diabetic complications in experimental diabetic rats.     

Effect of clofibrate treatment on glutathione content and the activity of the enzymes related to peroxide metabolism in rat liver and heart

Clofibrate treatment was shown to increase the content of reduced glutathione in rat liver and kidney, but did not alter the glutathione level in heart, brain, spleen and small intestine. Clofibrate did not affect the activity of superoxide dismutase, glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase in rat liver and heart. The drug decreased the activity of glutathione-S-transferase in the cytosolic fraction of liver homogenate. Glutathione-S-transferase activity in small intestine was also reduced. The administration of clofibrate decreased the content of polypeptides with mol. wt of 22,000 and 24,000 (possible monomers of glutathione-S-transferase) in the cytosolic fraction of liver cells.     

Metabolization of Porphyrinogenic Agents in Brain: Involvement of the Phase I Drug Metabolizing System. A Comparative Study in Liver and Kidney

(1) We evaluated the involvement of brain mitochondrial and microsomal cytochrome P-450 in the metabolization of known porphyrinogenic agents, with the aim of improving the knowledge on the mechanism leading to porphyric neuropathy. We also compared the response in brain, liver and kidney. To this end, we determined mitochondrial and microsomal cytochrome P-450 levels and the activity of NADPH cytochrome P-450 reductase. (2) Animals were treated with known porphyrinogenic drugs such as volatile anaesthetics, allylisopropylacetamide, veronal, griseofulvin and ethanol or were starved during 24 h. Cytochrome P-450 levels and NADPH cytochrome P-450 reductase activity were measured in mitochondrial and microsomal fractions from the different tissues. (3) Some of the porphyrinogenic agents studied altered mitochondrial cytochrome P-450 brain but not microsomal cytochrome P-450. Oral griseofulvin induced an increase in mitochondrial cytochrome P-450 levels, while chronic Isoflurane produced a reduction on its levels, without alterations on microsomal cytochrome P-450. Allylisopropylacetamide diminished both mitochondrial and microsomal cytochrome P-450 brain levels; a similar pattern was detected in liver. Mitochondria cytochorme P-450 liver levels were only diminished after chronic Isoflurane administration. In kidney only mitochondrial cytochrome P-450 levels were modified by veronal; while in microsomes, only acute anaesthesia with Enflurane diminished cytochrome P-450 content. (4) Taking into account that δ-aminolevulinic acid would be responsible for porphyric neuropathy, we investigated the effect of acute and chronic δ-aminolevulinic acid administration. Acute δ-aminolevulinic acid administration reduced brain and liver cytochrome P-450 levels in both fractions; chronic δ-aminolevulinic acid administration diminished only liver mitochondrial cytochrome P-450. (5) Brain NADPH cytochrome P-450 reductase activity in animals receiving allylisopropylacetamide, dietary griseofulvin and δ-aminolevulinic acid showed a similar profile as that for total cytochrome P-450 levels. The same response was observed for the hepatic enzyme. (6) Results here reported revealed differential tissue responses against the xenobiotics assayed and give evidence on the participation of extrahepatic tissues in porphyrinogenic drug metabolization. These studies have demonstrated the presence of the integral Phase I drug metabolizing system in the brain, thus, total cytochrome P-450 and associated monooxygenases in brain microsomes and mitochondria would be taken into account when considering the xenobiotic metabolizing capability of this organ. Dedicated to the memory of Dr. Susana Afonso     

Stimulation of hepatic and renal diamine oxidase activity after acute ethanol administration

The effect of a single administration of ethanol (2 g/kg body weight) on hepatic and renal diamine oxidase activity was studied in fasted rats. Diamine oxidase activity significantly increased in liver and kidney 6 h after ethanol intubation. Pyrazole (an inhibitor of alcohol dehydrogenase), cycloheximide or actinomycin D (inhibitors of macromolecular syntheses), as well as prior adrenalectomy, prevented the ethanol-induced stimulation of diamine oxidase in the liver, but not in the kidney. The results demonstrated that the enhancement of diamine oxidase activity in the liver was due to an enzyme induction mediated by alcohol metabolism as well as by adrenals. In contrast, the stimulation of diamine oxidase activity in the kidney did not depend on synthesis of new enzyme molecules and was not mediated by ethanol metabolism or adrenal hormones.     

Effect of caffeine on ornithine metabolism in rat brain, liver and kidney

Prolonged treatment with caffeine promotes in rats an increase of liver ornithine carbamyltransferase activity (14-day treatment). In contrast, arginase activity is already reduced in brain and kidney after 10 days, and in the liver much later (17 days). Ornithine transaminase activity was increased in both liver and kidney, while in the brain it was reduced (17 days). Ornithine decarboxylase activity showed only minor modifications in kidney, while it was unchanged in brain. Of the polyamines, only spermidine was significantly modified, being increased in brain, decreased in liver and kidney. Although these results do not explain the mechanism of the modification of brain arginine and ornithine concentration promoted by caffeine, they point to further marked effects, i.e. on OAT activity and on spermidine concentration, which could have a relevant metabolic role.     

Circadian rhythms in the activities of brain and liver aldehyde dehydrogenase isozymes in mice

Circadian variations in the activities of aldehyde dehydrogenase (ALDH) isozymes in the subcellular fractions of the brain and liver were investigated in male and female mice of C57BL/6J strain. The rhythms in high Km-ALDH activities of brain and liver mitochondrial fractions which existed in ordinary light-dark cycle were not observed in animals maintained in the continuous darkness for two weeks. The rhythms in high Km-ALDH activities of hepatic soluble and microsomal fractions existed in both ordinary cycle and total darkness but the rhythmic phases were different. In the low Km-ALDH activity of hepatic mitochondrial fraction, the circadian rhythm was similar in two lighting conditions. There was sex difference in the existence of the circadian rhythm. It seems that the ALDH activity of mice is influenced by light-dark cycle and sex hormones.     

The influence of chromium chloride consumption on lipid peroxidation and activity of the antioxidant defense in rat tissues

The effect of food supplementation with chromium (CrCl₃ · 6H₂O) on intensity of peroxide processes and activity of antioxidant enzymes has been investigated in some rat tissues. Food supplementation with 200 μg/kg CrCl₃ · 6H₂O for 30 days resulted in the increase of tissue chromium. The tissue chromium content of chromium-treated rats decreased in the following order: spleen, heart, kidney, lung, brain, liver, skeletal muscles. All organs and tissues (except skeletal muscles) of chromium-treated rats were characterized by decreased content of lipid peroxidation (LPO) products: hydroperoxides and thiobarbituric acid reactive substances (TBARS). The maximal reduction in LPO products was observed in spleen, kidney, liver, and lung. Treatment with chromium also caused an increase in the activity of glutathione peroxidase, glutathione reductase, and calatase in all tissues and organs studied. In the brain and kidney an increase in the content of reduced glutathione was observed. Superoxide dismutase activity was higher in myocardium and skeletal muscles, basically equal in lung and liver, while in other organs (brain, kidney, spleen) of experimental animals it was lower than in control animals. Results of this study suggest that chromium exhibits tissue/organ-specific regulatory effects on enzymes of the antioxidant defense