title: Ascorbic acid supplementation enhances recovery from ethanol induced inhibition of Leydig cell steroidogenesis than abstention in male guinea pigs.
abstract: 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.
authors: Department of Biochemistry, University of Kerala, Thiruvananthapuram-695581, India.
authors: Harikrishnan
authors: H
authors: Radhakrishnakartha
authors: Department of Biochemistry, University of Kerala, Thiruvananthapuram-695581, India.
authors: Abhilash Puthuvelvippel
authors: AP
authors: Appu
authors: Department of Biochemistry, University of Kerala, Thiruvananthapuram-695581, India. Electronic address: indiramadambath@gmail.com.
authors: Madambath
authors: M
authors: Indira
mesh_terms: D015067:17-Hydroxysteroid Dehydrogenases / Q000235:genetics / Q000378:metabolism; D015096:3-Hydroxysteroid Dehydrogenases / Q000235:genetics / Q000378:metabolism; D000437:Alcoholism / Q000188:drug therapy / Q000378:metabolism; D000818:Animals; D001205:Ascorbic Acid / Q000494:pharmacology*; D002478:Cells, Cultured; D002784:Cholesterol / Q000378:metabolism; D002786:Cholesterol Side-Chain Cleavage Enzyme / Q000235:genetics / Q000378:metabolism; D004958:Estradiol / Q000097:blood; D000431:Ethanol / Q000633:toxicity*; D006168:Guinea Pigs; D007985:Leydig Cells / Q000187:drug effects* / Q000378:metabolism; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D010750:Phosphoproteins / Q000235:genetics / Q000378:metabolism; D020011:Protective Agents / Q000494:pharmacology*; D011974:Receptors, LH / Q000235:genetics / Q000378:metabolism; D013739:Testosterone / Q000037:antagonists & inhibitors* / Q000097:blood; D000098682:Steroidogenic Acute Regulatory Protein
chemical_list: D010750:Phosphoproteins; D020011:Protective Agents; D011974:Receptors, LH; D000098682:Steroidogenic Acute Regulatory Protein; D000431:Ethanol; D013739:Testosterone; D004958:Estradiol; D007986:Luteinizing Hormone; D002784:Cholesterol; D015067:17-Hydroxysteroid Dehydrogenases; D015096:3-Hydroxysteroid Dehydrogenases; C044256:3 (or 17)-beta-hydroxysteroid dehydrogenase; D002786:Cholesterol Side-Chain Cleavage Enzyme; D001205:Ascorbic Acid
keywords: Abstention; Ethanol Ascorbic acid; Leydig cell