Effect of acute ethanol intoxication on the content of reduced glutathione of the liver in relation to its lipoperoxidative capacity in the rat

Videla, Luis A.; Fernández, Virgínia; Ugarte, G; Valenzuela, Alfonso; Villanueva, Andrea

doi:10.1016/0014-5793(80)80749-6

Cited by 123 publications

(34 citation statements)

References 31 publications

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“…al. (1989) (17). The changes in absorbance were recorded at 340 nm and enzyme activity was calculated as nmol CDNB conjugate formed/min/mg protein using a molar extinction coefficient of 9.6 x 103 M -1 cm -1.…”

Section: Post Mitochondrial Supernatant (Pms) and Microsomes Preparationmentioning

confidence: 99%

An opium alkaloid-papaverine ameliorates ethanol-induced hepatotoxicity: Diminution of oxidative stress

Chandra

Aneja

Rewal³

et al. 2000

Indian J Clin Biochem

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In this communication, we show the modulatory potential of papaverine, an opium alkaloid and a well known vasodilator agent on the ethanol-induced hepatic oxidative stress in male Wistar rats. Ethanol treatment (50% v/v) enhanced lipid peroxidation significantly accompanied by a decline in the activities of glutathione peroxidase (G-Px), glutathione reductase (GR) and depletion in levels of hepatic glutathione (GSH). Ethanol administration increased hepatic glutathione-s-transferases (GST).Enhanced lipid peroxidation induced by ethanol was significantly reduced when papverine was coadministered (P<0.05). In addition, the depleted levels of glutathione and inhibited activities of G-Px and GR recovered significantly (P<0.05) levelling off to control values on co-exposure. Papaverine (200 mglkg bw) effectively antagonised the ethanol-induced lipid peroxidation and impaired glutathione levels and glutathione dependent enzyme systems. Our results suggest that papaverine is an effective chemopreventive agent in the liver and may suppress the ethanol-induced hepatotoxicity.

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Section: Post Mitochondrial Supernatant (Pms) and Microsomes Preparationmentioning

confidence: 99%

An opium alkaloid-papaverine ameliorates ethanol-induced hepatotoxicity: Diminution of oxidative stress

Chandra

Aneja

Rewal³

et al. 2000

Indian J Clin Biochem

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“…The latter in its reduced form is the single most important protective and regulatory antioxidant. Since lipid peroxidation markedly lowers its level, glutathione together with MDA are used as indicators of oxidative stress in the liver [4] . Melatonin is a serotonin-derived neurohormone formed primarily in the brain by the pineal gland of all mammals, including man [5] .…”

Section: Introductionmentioning

confidence: 99%

Melatonin attenuates high fat diet-induced fatty liver disease in rats

Hatzis¹,

Ziakas²,

Kavantzas³

et al. 2013

WJH

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the statistical analysis and contributed to the interpretation of the data; Kavantzas N did histopathological examinations of the tissue biopsies; Triantafyllou A performed the biochemical tests and the malondialdehyde and glutathione assays; Sigalas P was responsible for the welfare of the animals and the collection and storage of tissues and sera; Andreadou I performed the biochemical tests and the malondialdehyde and glutathione assays; Ioannidis K was responsible for the welfare of the animals and the collection and storage of tissues and sera; Chatzis S was a contributor in writing and revising the manuscript; Filis K was responsible for the welfare of the animals and the collection and storage of tissues and sera; Papalampros A performed invasive procedures on the animals; Sigala F contributed to the conception of the study, performed the invasive procedures, and oversaw the welfare of the animals as well as the collection and storage of tissues and sera. Abstract AIM: To investigate melatonin's preventive action in oxidative stress in a rat model with high fat diet-induced non-alcoholic fatty liver disease (NAFLD). METHODS:NAFLD was induced by high fat diet (HFD) in adult, male, Wistar rats, weighing 180-230 g. After acclimatization for one week, they were randomly assigned to 6 experimental groups that comprised animals on regular diet plus 5 or 10 mg/kg melatonin, for 4 or 8 wk; animals on HFD, with or without 5 or 10 mg/kg melatonin, for 4 or 8 wk; and animals on HFD for 8 or 12 wk, with melatonin 10 mg/kg for the last 4 wk. Liver damage was assessed biochemically by the serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and histologically. Lipid peroxidation and oxidative stress were assessed by malondialdehyde and glutathione levels in liver tissue. Lipidemic indices and portal vein pressure were also measured. RESULTS:Compared to rats not receiving melatonin, rats on 5 or 10 mg/kg of melatonin had lower mean liver weight (-5.0 g and -4.9 g) (P < 0.001) and lower liver weight to body weight ratio (-1.0%) (P < 0.001), for the two doses, respectively. All rats fed HFD without melatonin developed severe, grade Ⅲ, steatosis. Rats on HFD with concurrent use of melatonin showed significantly less steatosis, with grade Ⅲ steatosis observed in 1 of 29 (3.4%) rats on 10 mg/kg melatonin Hatzis G et al . Melatonin and fatty liver and in 3 of 27 (11.1%) rats on 5 mg/kg melatonin. Melatonin was ineffective in reversing established steatosis. Melatonin also had no effect on any of the common lipidemic serum markers, the levels of which did not differ significantly among the rats on HFD, irrespective of the use or not of melatonin. Liver cell necrosis was significantly less in rats on HFD receiving melatonin than in those not on melatonin, with the AST levels declining by a mean of 170 U/L (P = 0.01) and 224 U/L (P = 0.001), and the ALT levels declining by a mean of 62.9 U/L (P = 0.01) and 93.4 U/L (P < 0.001), for the 5 and 10 mg/kg melatonin dose, respectively. Melatonin mitigated l...

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“…Large doses of ethanol deplete hepatic GSH in vivo (9) and in vitro (10) by mechanisms that are not yet clear. It has been suggested that acute GSH depletion by ethanol is caused by an acetaldehyde adduct (10) or by impairing GSH synthesis (1 1, 12).…”

Section: Introductionmentioning

confidence: 99%

Effect of chronic ethanol feeding on rat hepatocytic glutathione. Compartmentation, efflux, and response to incubation with ethanol.

Fernández-Checa¹,

Ookhtens²,

Kaplowitz³

1987

J. Clin. Invest.

119

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Hepatocytes from rats that were fed ethanol chronically for 6-8 wk were found to have a modest decrease in cytosolic GSH (24%) and a marked decrease in mitochondrial GSH (65%) as compared with pair-fed controls. Incubation of hepatocytes from ethanol-fed rats for 4 h in modified Fisher's medium revealed a greater absolute and fractional GSH efflux rate than controls with maintenance of constant cellular GSH, indicating increased net GSH synthesis. Inhibition of y-glutamyltransferase had no effect on these results, which indicates that no degradation of GSH had occurred during these studies. Enhanced fractional efflux was also noted in the perfused livers from ethanol-fed rats. Incubation of hepatocytes in medium containing up to 50 mM ethanol had no effect on cellular GSH, accumulation of GSH in the medium, or cell viability. Thus, chronic ethanol feeding causes a modest fall in cytosolic and a marked fall in mitochondrial GSH. Fractional GSH efflux and therefore synthesis are increased under basal conditions by chronic ethanol feeding, whereas the cellular concentration of GSH drops to a lower steady state level. Incubation of hepatocytes with ethanol indicates that it has no direct, acute effect on hepatic GSH homeostasis.

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Effect of acute ethanol intoxication on the content of reduced glutathione of the liver in relation to its lipoperoxidative capacity in the rat

Cited by 123 publications

References 31 publications

An opium alkaloid-papaverine ameliorates ethanol-induced hepatotoxicity: Diminution of oxidative stress

An opium alkaloid-papaverine ameliorates ethanol-induced hepatotoxicity: Diminution of oxidative stress

Melatonin attenuates high fat diet-induced fatty liver disease in rats

Effect of chronic ethanol feeding on rat hepatocytic glutathione. Compartmentation, efflux, and response to incubation with ethanol.

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