Effect of chloramphenicol on hepatic mitochondrial and microsomal functions in protein-energy malnourishment.
In both protein-energy malnourished (PEM) and normal rats, chloramphenicol (7.5 mg/kg) competitively inhibits the activities of aniline hydroxylase and p-aminopyrine N-demethylase. The decrease in enzyme activities was very much less in PEM rats. In both groups of animals, chloramphenicol also lowered the respiratory control ratio (RCR) of mitochondria. However, as with the microsomal function, the decrease in mitochondrial RCR in PEM rats (18.2%) was much less than that (45.8%) in normal rats. These results suggest that the toxic effects of chloramphenicol could be less in PEM conditions.
D000633:Aminopyrine N-Demethylase / Q000037:antagonists & inhibitors; D000815:Aniline Hydroxylase / Q000037:antagonists & inhibitors; D000818:Animals; D002701:Chloramphenicol / Q000633:toxicity*; D008297:Male; D008862:Microsomes, Liver / Q000187:drug effects* / Q000378:metabolism; D008930:Mitochondria, Liver / Q000187:drug effects* / Q000378:metabolism; D010101:Oxygen Consumption; D011502:Protein-Energy Malnutrition / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D002701:Chloramphenicol; D000815:Aniline Hydroxylase; D000633:Aminopyrine N-Demethylase