Ascorbic acid supplementation enhances recovery from ethanol induced inhibition of Leydig cell steroidogenesis than abstention in male guinea pigs

• Published in: European journal of pharmacology 2014-01, Vol.723, p.73-79
• Main Authors: Radhakrishnakartha, Harikrishnan, Appu, Abhilash Puthuvelvippel, Indira, Madambath
• Format: Article
• Language: English
• Subjects: 17-Hydroxysteroid Dehydrogenases - genetics; 17-Hydroxysteroid Dehydrogenases - metabolism; 3-Hydroxysteroid Dehydrogenases - genetics; 3-Hydroxysteroid Dehydrogenases - metabolism; Abstention; Alcoholism - drug therapy; Alcoholism - metabolism; Animals; Ascorbic Acid - pharmacology; Cells, Cultured; Cholesterol - metabolism; Cholesterol Side-Chain Cleavage Enzyme - genetics; Cholesterol Side-Chain Cleavage Enzyme - metabolism; Estradiol - blood; Ethanol - toxicity; Ethanol Ascorbic acid; Guinea Pigs; Leydig cell; Leydig Cells - drug effects; Leydig Cells - metabolism; Luteinizing Hormone - blood; Male; Phosphoproteins - genetics; Phosphoproteins - metabolism; Protective Agents - pharmacology; Receptors, LH - genetics; Receptors, LH - metabolism; Testosterone - antagonists & inhibitors; Testosterone - blood
• ISSN: 0014-2999; 1879-0712
• DOI: 10.1016/j.ejphar.2013.12.010

The impact of ascorbic acid supplementation against ethanol induced Leydig cell toxicity was studied in guinea pigs. Male guinea pigs were exposed to ethanol (4g/kgb.wt.) for 90 days. After 90 days, ethanol administration was completely stopped and animals in the ethanol group were divided into abstention group and ascorbic acid supplemented group (25mg/100gb.wt.) and those in control group were maintained as control and control+ascorbic acid group. Ethanol administration reduced the serum testosterone and LH (luteinising hormone) levels and elevated estradiol levels. Cholesterol levels in Leydig cell were increased whereas the mRNA and protein expressions of StAR (steroidogenic acute regulatory) protein, cytochrome P450scc (cytochrome p450side chain cleavage enzyme), 3β-HSD (3β-hydroxysteroid dehydrogenase), 17β-HSD (17β-hydroxysteroid dehydrogenase) and LH receptor were drastically reduced. Administration of ascorbic acid resulted in alteration of all these parameters indicating enhanced recovery from ethanol induced inhibition of Leydig cell steroidogenesis. Although abstention could also reduce the inhibition of steroidogenesis, this was lesser in comparison with ascorbic acid supplemented group.