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Protective effect of some vitamins against the toxic action of ethanol on liver regeneration induced by partial hepatectomy in rats

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World Journal of Gastroenterology 2008年第6期14卷 899-907页

作者： Carlett Ramírez-Farías Eduardo Madrigal-Santillán José Gutiérrez-Salinas Nidia Rodríguez-Sánchez Maricela Martínez-Cruz Ilse Valle-Jones Ingrid Gramlich-Martínez Alejandra Hernández-Ceruelos José A Morales-González Unidad de Genética de la Nutrición Instituto Nacional de Pediatría México Instituto de Ciencias de la Salud Universidad Autónoma del Estado de Hidalgo México Laboratorio de Bioquímica y Medicina Experimental Unidad de Investigación Biomédica División de Investigación Centro Médico Nacional "20 de Noviembre" ISSSTE México Gatorade Sports Science Institute Mexico City México Escuela de Dietética y Nutrición ISSSTE México University of Ryerson Toronto

AIM: To investigate the effects of vitamins (A, C and E) on liver injury induced by ethanol administration during liver regeneration in rats. METHODS: Male Wistar rats subjected to 70% partial hepatectomy were divided into five groups (groups 1-5). During the experiment, animals of Group 1 drank only water. The other four groups (2-5) drank 30 mL of ethanol/L of water. Group 3 additionally received vitamin A, those of group 4 vitamin C and those of group 5 received vitamin E. Subsequently serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), albumin and bilirubin were measured colorimetrically. Lipid peroxidation (thiobarbituric-acid reactive substances, TBARS) both in plasma and liver was measured, as well as liver mass gain assessment and total DNA. RESULTS: Compared with sham group, serum AST and ALT increased significantly under ethanol treatment (43% and 93%, respectively, with P induced increases in ALT and AST activity. Ethanol treatment also decreased serum albumin concentration compared to sham group (3.1 ± 0.4 g/dL vs 4.5 ± 0.2 g/dL; P liver regeneration vitamins C and E significantly ameliorated liver injury for ethanol administration in hepatic lipid peroxidation (4.92 nmol/mg and 4.25 nmol/mg vs 14.78 nmol/mg, respectively, with P injury, ethanol administration caused a significant increase in both hepatic and plasma lipid peroxidation. Vitamins (C and E) treatment attenuated hepatic and plasma lipid peroxidation. CONCLUSION: Vitamins C and E protect against liver injury and dysfunction, attenuate lipid peroxidation, and thus appear to be significantly more effective than vitamin A against ethanol-mediated toxic effects during liver regeneration.

关键词： Lipid peroxidation Antioxidant vitamins alcohol-induced liver injury liver regeneration

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Camellia Seed Oil, a High-Quality Cooking Oil, Attenuates liver Oxidative Damage but Exacerbates Hepatic steatosis in alcohol-induced C57BL/6 Mice

Camellia Seed Oil, a High-Quality Cooking Oil, Attenuates Li...

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中国营养学会第十五届全国营养科学大会

作者： Rui Guo Jinyan Zhu Jiaomei Li Songtao Li Zhejiang Chinese Medical University

The purpose of this study was to compare the effect of camellia seed oil(CSO), a plant-derived monounsaturated fatty acid(MUFA), with corn oil(CO), a plant-derived n-6 polyunsaturated fatty acid(PUFA), on chronic alcohol consumption in C57 BL/6 mice. Methods 24 male SPF C57 BL/6 mice were randomly divided into four groups: pair-fed(PF)with CO group(PF/CO);alcohol-fed(AF) with CO group(AF/CO);PF with CSO group(PF/CSO);AF with CSO group(AF/CSO). Each group was fed traditional Lieber-De Carli liquid diets containing isocaloric maltose dextrin a control or alcohol with CO and CSO, respectively. After 5 weeks feeding, mice were euthanized and associated indications were investigated. Results Compared with CO, pretreatment with CSO drastically decreased the elevated activities of aspartate transaminase(AST), alanine transaminase(ALT), triglyceride(TG), and total cholesterol(TC) in plasma and the upregulated levels of malondialdehyde(MDA), 4-hydroxynonenal(4-HNE), tumor necrosis factor-α(TNF-α), and interleukin-6(IL-6) in liver, and significantly recovered the downregulated levels of hepatic antioxidants, such as superoxide dismutase(SOD) and glutathione peroxidase(GSH-Px), induced by alcohol intervention. Histopathological examination also revealed that CSO pretreatment obviously inhibited alcohol-induced liver injury. CSO appeared to act partly by inhibiting both c-Jun-N-terminal kinase(JNK) and P38 mitogen-activated protein kinase(MAPK) pathways in parallel. Unexpectedly, both CO and CSO significantly aggravated alcohol-induced hepatic steatosis. Conclusion The hepatoprotective effect exhibited by CSO on alcohol-induced liver oxidative injury may be due to its anti-oxidant and anti-inflammatory properties, and the accumulation of TG may be a protective mechanism to prevent progressive liver injury on chronic alcohol consumption.

关键词： camellia seed oil monounsaturated fatty acid alcohol-induced liver injury oxidative stress hepatic steatosis

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