The toxicity of acetaldehyde and age related changes on oxidoreductases in the liver,brain, kidney, and musele of female albino rats (Wistar strain) were studied. The specific activities of lactate [LDH], isocitrate [ICDH (NAD/NADP)], succinate [SDH], malate [MDH], glutamate [GDH] and glucose-6-Phosphate [G-6-PDH] dehydrogenases were signifieantly inereased as a function of age. However, acetaldehyde treatment significantly inhibited oxidoreductases in the tissues of 21, 90 and 180 day old rats. Liver enzymes of young (21 days) rats exhibited greater sensitivity to acetaldehyde toxicity. Similar inhibition of oxidoreductases in brain and kidney of adult (180 days) rats treated with acetaldehyde was observed. LDH and GDH as compared to other enzymes studied showed higher susceptibility to acetaldehyde toxicity. The differential sensitivity of tissues and inhibition of oxidoreductases by acetaldehyde as a function of age could be attributed to hypoxic conditions, energy crisis, and mitochondrial structural changes. The results suggest that acetaldehyde affects oxidation of glucose via HMP shuni pathway, glycolytic pathway and Krebs cycle resulting in the impairment of carbohydrate metabolism The toxicity of acetaldehyde and age related changes on oxidoreductases in the liver, brain, kidney, and musele of female albino rats (Wistar strain) were studied. The specific activities of lactate [LDH], isocitrate [ICDH (NAD / NADP) succinate [SDH], malate [MDH], glutamate [GDH] and glucose-6-Phosphate [G-6-PDH] dehydrogenases were signifieantly inereased as a function of age. However, acetaldehyde treatment significantly inhibited oxidoreductases in the tissues of 21, 90 and 180 day old rats. Liver enzymes of young (21 days) Rats with greater sensitivity to acetaldehyde toxicity. Like inhibition of oxidoreductases in brain and kidney of adult (180 days) rats treated with acetaldehyde was observed. LDH and GDH as compared to other enzymes research showed higher susceptibility to acetaldehyde toxicity. The differential sensitivity of tissues and inhibition of oxidoreductases by acetaldehyde as a function of age could be attributed to hypoxic conditions, energy crisis, and mitoc hondrial structural changes. The results suggest that acetaldehyde affects oxidation of glucose via HMP shuni pathway, glycolytic pathway and Krebs cycle resulting in the impairment of carbohydrate metabolism