title: Reversal of alcohol induced testicular hyperlipidemia by supplementation of ascorbic acid and its comparison with abstention in male guinea pigs.
abstract: BACKGROUND
  Chronic ethanol exposure causes hyperlipidemia. The present study was designed to investigate the impact of ascorbic acid supplementation on ethanol induced hyperlipidemia in testis and to compare it with that of abstinence from taking alcohol.
  
  
  METHODS
  Thirty-six male guinea pigs were divided into two groups and were maintained for 90 days as follows (1) control (C) (2) ethanol treated group (E) (4 g/kg body wt/day). Ethanol was administered for 90 days and on 90th day, alanine amino transaminase (ALT), aspartate amino transaminase (AST) and γ-glutamyltransferase (GGT) in serum was assayed. The animals in the ethanol group were further divided into an ascorbic acid supplemented group (25 mg/100 g body wt/day) (E+AA) and an ethanol abstention group (EAG) and those in the control group were divided into a control group and a control+ascorbic acid group (C+AA).
  
  
  RESULTS
  There was significant increase in levels of testicular cholesterol, free fatty acid, phospholipids and triglycerides in the ethanol group. There was also a significant increase in the activity of HMG CoA reductase and decrease in activity of testicular glucose-6-phosphate dehydrogenase (G6PDH) and malic enzyme in ethanol-ingested animals that further led to decreased levels of serum testosterone. Alcohol administration also enhanced the activity of testicular alcohol dehydrogenase (ADH). Ascorbic acid supplementation and abstention altered all these parameters induced by chronic alcohol administration. Histological studies were also in line with the above results.
  
  
  CONCLUSIONS
  Ascorbic acid was able to reinstate the cholesterol homeostasis in testis which could have further restored the testicular steroidogenesis. The present study demonstrated that ascorbic acid is effective in reducing the hyperlipidemia induced by chronic alcohol administration and produced a better recovery than abstention.
authors.forename: Harikrishnan
authors.initials: H
authors.lastname: Radhakrishnakartha
authors.forename: Abhilash Puthuvelvippel
authors.initials: AP
authors.lastname: Appu
authors.forename: Indira
authors.initials: I
authors.lastname: Madambath
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D064829:Alcohol Abstinence; D000426:Alcohol Dehydrogenase / Q000378:metabolism; D000818:Animals; D001205:Ascorbic Acid / Q000494:pharmacology / Q000627:therapeutic use*; D001219:Aspartate Aminotransferases / Q000097:blood; D019587:Dietary Supplements; D000431:Ethanol / Q000009:adverse effects*; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D006168:Guinea Pigs; D006903:Hydroxymethylglutaryl CoA Reductases / Q000378:metabolism; D006949:Hyperlipidemias / Q000097:blood / Q000139:chemically induced / Q000178:diet therapy* / Q000378:metabolism; D008291:Malate Dehydrogenase / Q000378:metabolism; D008297:Male; D013737:Testis / Q000187:drug effects* / Q000378:metabolism; D013739:Testosterone / Q000097:blood; D005723:gamma-Glutamyltransferase / Q000097:blood
chemical_list: D000431:Ethanol; D013739:Testosterone; D006903:Hydroxymethylglutaryl CoA Reductases; D000426:Alcohol Dehydrogenase; D008291:Malate Dehydrogenase; D005954:Glucosephosphate Dehydrogenase; D005723:gamma-Glutamyltransferase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D001205:Ascorbic Acid