Influence of aging on ethanol-induced oxidative stress in digestive tract of rats

Author:

Vučević D.1,Mladenović D1,Ninković M2,Stanković MN1,Jorgačević B1,Stanković MS1,de Luka S1,Radosavljević T.1

Affiliation:

1. Department of Pathophysiology, Faculty of Medicine, University of Belgrade, Belgrade, Serbia

2. Institute for Medical Research, Military Medical Academy, Belgrade, Serbia

Abstract

Aging and ethanol induce oxidative stress due to increased prooxidant production and decreased antioxidative capacity. The aim was to investigate the influence of aging on oxidative stress in liver, stomach and pancreas in acute ethanol intoxication. Adult (3 months) and old (18 months) male Wistar rats were divided into the following groups: control (control group rats aged 3 months (C3) and control group rats aged 18 months (C18)) and ethanol-treated groups (ethanol-treated 3-month-old rats (E3) and ethanol-treated 18-month-old rats (E18)). Ethanol was administered in five doses of 2 g/kg at 12-h intervals by orogastric tube. Tissue samples were collected for the determination of oxidative stress parameters. Malondialdehyde (MDA) concentration was increased in all the experimental groups and investigated organs versus C3 group (  p < 0.01). The highest MDA level was observed in the stomach in E18 group when compared with C18 and E3 groups (  p < 0.01). Activity of total superoxide dismutase (SOD) and its isoenzymes (copper-/zinc-SOD and manganese-SOD) in E18 group was significantly decreased when compared with E3 and C18 groups (  p < 0.01). Nitrates and nitrites (NO x) concentration was increased in stomach and pancreas for all the groups when compared with C3 group (  p < 0.01). Hepatic, gastric and pancreatic NO x level was significantly increased in E18 group when compared with E3 group (  p < 0.01). Moreover, level of NO x in liver and pancreas in E18 group was significantly increased when compared with C18 group (  p < 0.01). Aging potentiates ethanol-induced oxidative stress in liver, stomach and pancreas due to increased lipid peroxidation and nitrosative stress and decreased antioxidative tissue capacity.

Publisher

SAGE Publications

Subject

Health, Toxicology and Mutagenesis,Toxicology,General Medicine

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