Influence of zinc sulfate intake on acute ethanol-induced liver injury in rats

Bolkent, Şehnaz; Arda-Pirincci, Pelin; Yanardağ, Refiye; Tunalı, Sevim; Yıldırım, Serkan

doi:10.3748/wjg.v12.i27.4345

Cited by 12 publications

(9 citation statements)

References 43 publications

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“…Free radicals and associated oxidative stress have been implicated in eliciting pathological changes, including atherosclerosis, diabetes mellitus, chronic alcohol toxicity, muscular dystrophy, aging, and other diseases (Senthilkumar, Viswanathan, and Nalini 2004). We showed the protective effects of antioxidants on ethanol-induced gastric mucosal, intestinal, and liver injuries in our other studies (Ozdil et al 2004a, 2004b; Koyuturk et al 2004; Bolkent et al 2006; Arda-Pirincci, Bolkent, and Yanardag 2006). Ethanol is also known to induce hyperlipidemia, leading to enhanced lipid peroxidation.…”

Section: Discussionsupporting

confidence: 58%

Combined Effects of Vitamin C, Vitamin E, and Sodium Selenate Supplementation on Absolute Ethanol-Induced Injury in Various Organs of Rats

et al. 2007

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In this study, the effect of combination of vitamin C (ascorbic acid), vitamin E (alpha -tocopherol), and selenium (sodium selenate) on ethanol-induced liver and intestine injury in rats was investigated. The ethanol-induced injury was produced by the administration of 1 ml of absolute ethanol to each rats. Animals received vitamin C (250 mg/kg), vitamin E (250 mg/kg), and sodium selenate (Se) (0.5 mg/kg) for 3 days; 1 h after the final antioxidant administration, they were sacrificed. Lipid peroxidation and glutathione levels, catalase (CAT), lactate dehydrogenase (LDH), superoxide dismutase (SOD), and glutathione peroxidase (GP(x)) activities were determined in liver and intestine tissues. Myeloperoxidase (MPO), aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), gamma-glutamyltransferase (GGT) were determined in liver tissue. Also, CAT activity, urea, creatinine, uric acid, and total lipid levels were determined in serum samples. In the ethanol group, serum urea, creatinine, uric acid, and total lipid levels; liver and intestine LDH; liver MPO, AST, ALP, ALT, and GGT activities; and liver and intestine LPO levels increased, whereas serum CAT activity, liver and intestine GSH levels, and CAT, SOD, and GP(x) activities decreased. On the other hand, treatment with vitamin C, vitamin E, and Se reversed these effects. As a result of these findings, we can say that the combination of vitamin C, vitamin E, and selenium has a protective effect on ethanol-induced changes in lipid peroxidation, glutathione levels, and antioxidant enzyme activities in liver and intestine tissues, and in some serum parameters of rats.

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Section: Discussionsupporting

confidence: 58%

Combined Effects of Vitamin C, Vitamin E, and Sodium Selenate Supplementation on Absolute Ethanol-Induced Injury in Various Organs of Rats

et al. 2007

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“…It was noted that the number of MT immunoreactive cells decreased in the duodenum of all animals of the group given only ethanol, but zinc sulfate administration to the ethanol group increased MT immunoreactivity remarkably when as compared to the group that received ethanol only. These results accord with our earlier findings on the liver 30) and gastric musosal tissue. 31) We found that MT is located predominantly in the Paneth cells at the base of the crypts of Lieberkühn in all the groups.…”

Section: Discussionsupporting

confidence: 94%

Effects of Zinc on Intestinal Injury and Some Serum Parameters in Ethanol-Administered Rats

Arda-Pirincci

Bilgin-Sokmen

Yanardağ

et al. 2009

Bioscience, Biotechnology, and Biochemistry

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This study was designed to determine the morphological and biochemical effects of zinc sulfate and the role of metallothionein in ethanol-induced intestinal injury. Rats received zinc sulfate (100 mg/kg/d) for 3 consecutive d, 2 h prior to the administration of ethanol by gavage. Ethanol administration caused intestinal injury as determined by increased serum lactate dehydrogenase activity, urea, creatinine, uric acid, and sialic acid levels, intestinal lipid peroxidation level, decreased serum catalase activity, intestinal glutathione level, and metallothionein expression. Zinc sulfate pretreatment of the ethanol group caused a decrease in histological damage, serum lactate dehydrogenase activity, urea, creatinine, uric acid, sialic acid levels, and intestinal lipid peroxidation level, but increases in serum catalase activity, intestinal glutathione level, and metallothionein expression. The present study indicates that zinc sulfate has a protective effect against ethanol-induced intestinal injury. In addition, the protective effect of zinc on ethanol-induced intestinal injury might be mediated by metallothionein, as well as having antioxidative potential.

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“…Zn supplementation attenuates ethanol-induced hepatic Zn depletion and suppresses ethanol-elevated cytochrome P450 2E1 activity, but increases the activity of alcohol dehydrogenase in the liver; an action that is likely to be responsible for Zn suppression of alcohol-induced oxidative stress. Intracellular Zn inhibits alcohol-induced hepatic apoptosis partially through the suppression of the Fas/FasL-mediated pathway [48]. Zn also enhances glutathione-related and superoxide-dismutase antioxidant capacity in the liver (unfortunately, the antioxidant tests applied in this study provide information about the overall antioxidant capacity and do not allow an insight into the alteration of the effect of this enzyme.…”

Section: Discussionmentioning

confidence: 87%

Sex-dependent alterations in erythrocyte trace element levels and antioxidant status after a month of moderate daily red wine consumption

Bekő¹,

Hagymási²,

Szentmihályi³

et al. 2010

European Journal of Gastroenterology &Amp; Hepatology

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Although no hepatotoxicity was observed, changes in trace element content were detected after 1 month of moderate red wine consumption. The most remarkable sex-specific alteration was the decrease of Zn levels and of the Zn/Cu ratio in women. Given the protective effect of Zn against liver damage, this finding suggests a possible contribution of decreased Zn levels to sex-dependent effects of red wine.

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Influence of zinc sulfate intake on acute ethanol-induced liver injury in rats

Abstract: Zinc sulfate has a protective effect on ethanol-induced liver injury. In addition, cell proliferation may be related to the increase in metallothionein immunoreactivity in the livers of rats administered ethanol + zinc sulfate.

Cited by 12 publications

References 43 publications

Combined Effects of Vitamin C, Vitamin E, and Sodium Selenate Supplementation on Absolute Ethanol-Induced Injury in Various Organs of Rats

Combined Effects of Vitamin C, Vitamin E, and Sodium Selenate Supplementation on Absolute Ethanol-Induced Injury in Various Organs of Rats

Effects of Zinc on Intestinal Injury and Some Serum Parameters in Ethanol-Administered Rats

Sex-dependent alterations in erythrocyte trace element levels and antioxidant status after a month of moderate daily red wine consumption

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