Ethanol‐induced alterations of the antioxidant defense system in rat kidney

Abstract

We report here the effects of chronic ethanol consumption on the antioxidant defense system in rat kidney. Thirty-two male Wistar rats were randomly divided in two identical groups and were treated as follows: control group (water for fluid) and the ethanol-fed group (2 g/kg body weight/24 h). The animals were sacrificed after 10 weeks, and respectively 30 weeks of ethanol consumption, and the renal tissue was isolated and analyzed. Results revealed that kidney alcohol dehydrogenase activities increased significantly after ethanol administration, but the electrophoretic pattern of alcohol dehydrogenase isoforms was unmodified. The SDS polyacrylamidegel electrophoretic study of kidney proteins has revealed the appearance of two new protein bands after long-term ethanol consumption. The kidney reduced glutathione/oxidized glutathione ratio decreased, indicating an oxidative stress response due to ethanol ingestion. The malondialdehyde contents and xanthine oxidase activities were unchanged. The antioxidant enzymatic defense system showed a different response during the two periods of ethanol administration. After 10 weeks, catalase, glutathione peroxidase, glutathione reductase, and glucose-6-phosphate dehydrogenase were activated, while superoxide dismutase, glutathione transferase, and gamma-glutamyltranspeptidase levels were stationary. After 30 weeks, superoxide dismutase and glutathione peroxidase activities were unmodified, but catalase, glutathione transferase, gamma-glutamyltranspeptidase, glutathione reductase, and glucose-6-phosphate dehydrogenase activities were significantly increased. Remarkable changes have been registered after 30 weeks of ethanol administration for glutathione reductase and glucose-6-phosphate dehydrogenase activities, including an increase by 106 and 216' of control values, respectively. These results showed specific changes in rat kidney antioxidant system and glutathione status as a consequence of long-term ethanol administration.

Protective Role of Crude Extract of Amorphophallus Campanulatus Against Ethanol-Induced Oxidative Renal Damage

“…As all the animals are maintained in the same condition and same room without showing any infection, the observed changes in biochemical and immunological parameters are due to ethanol and/or extract administration. It is well known that chronic alcohol consumption demonstrates a significant increase in free radical production and decrease in antioxidant status in the kidney of rats [6,32]. ROS accumulates in renal cortex and causes renal damage [33].…”

“…Besides, excess alcohol intake increases free radical or reactive oxygen species (ROS) production and causes oxidative stress by compromising the antioxidant defense system, production of the reactive product acetaldehyde, damage to mitochondria, and altered cytokine production [3][4][5]. ROS-induced altered antioxidant system causes continued damage to the vital biomolecules, and this condition ultimately gives way to impaired kidney function [6].…”

Are we over estimating serum oxidative stress/lipid peroxidation in alcoholic liver diseases? A review

“…[31] Acetaldehyde exerts nephrotoxic effects on the kidney [32] ROS generation may contribute to the oxidative stress in the kidneys. [31,32] ROS and oxidative stress mediated injury have been considered as primary cause of alcohol induced, swelling of glomerula and tubules, proliferation of mesangial cells and hyaline drops in tubular epithelial cells are seen in the kidney. [1,31,32] Ethanol metabolites -protein adducts and hyaline in the tubular epithelial cells are observed which precipitates alcohol related diseases.…”

“…[31,32] ROS and oxidative stress mediated injury have been considered as primary cause of alcohol induced, swelling of glomerula and tubules, proliferation of mesangial cells and hyaline drops in tubular epithelial cells are seen in the kidney. [1,31,32] Ethanol metabolites -protein adducts and hyaline in the tubular epithelial cells are observed which precipitates alcohol related diseases. [1,32] The role of free radicals in alcoholic renal disease is well established.…”

“…The long-term ethanol exposure increases enzyme activities related to the recycling and utilization of glutathione in the kidney. [31] Testis Chronic alcohol consumption results in oxidative stress followed by lipid peroxidation resulting in both endocrine and reproductive failure which in-turn alters the mechanism of testosterone production by inhibiting protein kinase C, a key enzyme in testosterone synthesis. [27] Testicular membranes are rich in polyenoic fatty acids that are prone for peroxidative decomposition, which may result in membrane injury leading to necrotic cell death and gonadal dysfunction that occurs in acute and chronic alcoholism.…”