期刊
INDIAN JOURNAL OF CLINICAL BIOCHEMISTRY
卷 24, 期 3, 页码 301-306出版社
SPRINGER INDIA
DOI: 10.1007/s12291-009-0056-4
关键词
Ethanol; Glutathione; Liver function; Nitric oxide; Oxidative stress; Transforming growth factor; Vascular endothelial growth factor
资金
- Kerala State Council for Science, Technology and Environment (KSCSTE), Governtment of Kerala, India
- AACC VSF-CPOCT Division
Alcohol consumption and health outcomes are complex and multidimensional. Ethanol (1.6g/kg body weight/ day) exposure initially affects liver function followed by renal function of 16-18 week-old male albino rats of Wistar strain weighing 200-220 g. Chronic ethanol ingestion increased in thiobarbituric acid reactive substances level and glutathione s-transferase activity; while decreased reduced gluatathione content and activities of catalase, glutathione peroxidase and glutathione reductase in a time dependent manner in the hemolysate. Though superoxide dismutase activity increased initially might be due to adaptive response, but decreased later. Elevation of serum nitrite level and transforming growth factor-b 1 activity indicated that long-term ethanol consumption may cause hepatic fibrosis and can elicit pro-angiogenic factors. However, no alteration in vascular endothelial growth factor-C activity indicated that ethanol consumption is not associated with lymphangiogenesis. Therefore, we conclude that long-term ethanol-induced toxicity is linked to an oxidative stress, which may aggravate to fibrosis and elevate pro-angiogenic factors, but not associated with lymphangiogenesis.
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