Impact of thiamine supplementation in the reversal of ethanol induced toxicity in rats

Indian J Physiol Pharmacol. 2013 Oct-Dec;57(4):406-17.


One of the molecular mechanisms of alcohol induced toxicities is mediated by oxidative stress. Hence our studies were focused on the effect of thiamine (antioxidant) in the reversal of alcohol induced toxicity and comparison of the reversal with abstinence. Administration of ethanol at a dose of 4 g/kg body wt/day for 90 days to Sprague Dawley rats manifested chronic alcohol induced toxicity evidenced by decreased body weight, an increase in liver-body weight ratio, increase in activities of serum and liver aspartate transaminase (AST), alanine transaminase (ALT), gamma-glutamyl transpeptidase (GGT); decrease in the activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase in the liver and brain. The levels of inflammatory markers, fibrosis markers and DNA fragmentation were also elevated in the serum, liver and brain. After ethanol administration for 90 days, the reversal of the alcohol induced toxicity was studied by supplementing thiamine at a dose of 25 mg/100 g body wt/day. Duration of the reversal study was 30 days. The activities of AST, ALT, GGT, scavenging enzymes as well as markers of inflammation and fibrosis in serum, liver and brain were reversed to a certain extent by thiamine. Changes in neurotransmitter levels in brain were also reversed by thiamine supplementation. DNA damage was decreased and DNA content increased in thiamine supplemented group compared to abstinence group showing a faster regeneration. In short, histopathological and biochemical evaluations indicate that thiamine supplemented abstinent rats made a faster recovery of hepatic and neuronal damage than in the abstinence group.

MeSH terms

  • Alcohol-Induced Disorders, Nervous System / blood
  • Alcohol-Induced Disorders, Nervous System / drug therapy*
  • Alcohol-Induced Disorders, Nervous System / etiology
  • Alcohol-Induced Disorders, Nervous System / pathology
  • Animals
  • Antioxidants / pharmacology*
  • Biomarkers / blood
  • Body Weight
  • Brain / drug effects*
  • Brain / metabolism
  • Brain / pathology
  • DNA Damage
  • Disease Models, Animal
  • Ethanol*
  • Liver / drug effects*
  • Liver / metabolism
  • Liver / pathology
  • Liver Diseases, Alcoholic / blood
  • Liver Diseases, Alcoholic / drug therapy*
  • Liver Diseases, Alcoholic / etiology
  • Liver Diseases, Alcoholic / pathology
  • Male
  • Organ Size
  • Oxidative Stress / drug effects*
  • Rats
  • Rats, Sprague-Dawley
  • Thiamine / pharmacology*
  • Time Factors


  • Antioxidants
  • Biomarkers
  • Ethanol
  • Thiamine