ABSTRACT
The effect of a mega dose of ascorbic acid (200 mg/100 g body wt.) on alcohol-induced toxicity in rats was evaluated. In rats administered alcohol and ascorbic acid, malondialdehyde (MDA), hydroperoxide and conjugated dienes decreased in comparison with that given alcohol alone. The reduced activities of scavenging enzymes, e.g. superoxide dismutase (SOD) and catalase, in ethanol-administered rats were also enhanced by the co-administration of ascorbic acid and ethanol. Co-administration of ethanol and ascorbic acid reduced phospholipids and MDA levels of the erythrocyte membrane in comparison with that of the ethanol fed rats. The reduction in the activities of glutamic oxaloacetic transaminase (GOT), glutamic-pyruvic transaminase (GPT), gamaglutamyl transpeptidase (GGT) and the decrease in triglycerides levels also clearly showed the protective action of ascorbic acid in reducing ethanol induced toxicity.
Subject(s)
Animals , Antioxidants/pharmacology , Ascorbic Acid/blood , Catalase/drug effects , Central Nervous System Depressants/toxicity , Cholesterol/blood , Ethanol/toxicity , Fatty Acids, Nonesterified , Glutathione/drug effects , Lipid Peroxidation/drug effects , Male , Malondialdehyde/blood , Phospholipids/blood , Rats , Rats, Sprague-Dawley , Superoxide Dismutase/metabolism , Triglycerides/metabolismABSTRACT
The objective of this study was to determine the effects of a country liquor (Arrack) and the equivalent quantity of ethanol on liver function and lipid metabolism in utero. Female rats of average weight 125 g were exposed to Arrack (12 ml/kg body weight/day) and ethanol (3.2 ml/kg body weight/day) for 15 days before conception and throughout gestation. On 13th day and 19th day of gestation, altered liver function and hyperlipidemia was seen in the fetus of both the treated groups. Altered liver function was evidenced by the increased activity of alcohol dehydrogenase and glutamic pyruvic transaminase or alanine amino transferase (GPT). Hyperlipidemia was caused by increased biosynthesis since the incorporation of 14C acetate to lipids and activities of HMG CoA reductase and lipogenic enzymes were elevated. Arrack seemed to potentiate the toxicity induced by alcohol indicating the role of non ethanolic portion. Hepatic functions of the 13th day fetuses were effected to a lesser degree than the 19th day hepatic liver.
Subject(s)
Alcoholic Beverages/toxicity , Animals , Ethanol/toxicity , Female , Fetus/drug effects , Hydroxymethylglutaryl CoA Reductases/metabolism , Lipid Metabolism , Liver/drug effects , Pregnancy , Rats , Rats, Sprague-DawleyABSTRACT
Female rats were exposed to arrack (12.0 ml/kg body weight/day) and ethanol (4.0 g/kg body weight/day) before conception and throughout gestation and lactation. On 19th day of gestation and 21st day of lactation there was increase in the cholesterol phospholipids, triglycerides and free fatty acids in the mammary gland of rats administered arrack/ethanol in comparison with the controls. The lipoprotein lipase activity showed significant increase in the treated groups, in which the activity decreased on 21st day in comparison with 19th day. The absolute and relative weight of mammary gland also showed a significant decrease in ethanol/arrack treated group. The biochemical alterations produced in the mammary gland by arrack and its equivalent alcohol were different showing that non-alcoholic portion of arrack interferes with the toxicity induced by alcohol. Arrack was found to be a potent hyperlipidemic agent than ethanol.
Subject(s)
Alcoholic Beverages/toxicity , Animals , Cholesterol/metabolism , Ethanol/toxicity , Fatty Acids, Nonesterified/metabolism , Female , Lactation/drug effects , Lipid Metabolism , Mammary Glands, Animal/drug effects , Organ Size/drug effects , Phospholipids/metabolism , Pregnancy , Pregnancy, Animal/drug effects , Rats , Rats, Sprague-Dawley , Triglycerides/metabolismABSTRACT
Influence of excessive intake of ascorbic acid (AA) on alcohol induced hyperlipidemia was investigated. In the present study four groups of male guinea pigs were maintained for 30 days as follows: (1) Control group (1 mg AA/100 g body wt). (2) Ethanol group (I mg AA + 9 g ethanol/100 g body wt). (3) AA group (25 mg AA/100 g body wt). (4) AA + Ethanol group (25 mg AA/100 g body wt + 9 g ethanol 100 g body wt). It was shown that tissue ascorbic acid concentration increased with the intake of mega dose of AA. Alcohol administration depleted tissue ascorbic acid content. But coadministration of AA and alcohol enhanced AA levels in comparison with the ethanol group. Alcohol induced hyperlipidemia was reduced in almost all the tissues by the intake of ascorbic acid. This was observed to be due to increased hepatic catabolism of cholesterol to bile acids. However cholesterogenesis was enhanced as evidenced by the increased HMG CoA activity. Thus the results indicate that the mega dose of AA ingestion is beneficial in reducing alcohol induced hyperlipidemia and AA deficiency.