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Effect of chloramphenicol on hepatic mitochondrial and microsomal functions in protein-energy malnourishment
Abstract:
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.
Insights
Protein-energy malnutrition (PEM) may reduce the toxic effects of chloramphenicol by less significantly inhibiting key liver enzymes and mitochondrial function in rats. This suggests altered drug metabolism in malnourished states.
Area of Science:
- Biochemistry
- Toxicology
- Nutritional Science
Background:
- Chloramphenicol is an antibiotic with known toxic effects.
- Protein-energy malnutrition (PEM) can alter drug metabolism and toxicity.
- Microsomal and mitochondrial functions are crucial for drug detoxification.
Purpose of the Study:
- To investigate the effect of chloramphenicol on specific liver enzymes and mitochondrial function in protein-energy malnourished (PEM) rats compared to normal rats.
- To assess whether PEM alters the toxic effects of chloramphenicol.
Main Methods:
- Rats were divided into protein-energy malnourished (PEM) and normal groups.
- Chloramphenicol (7.5 mg/kg) was administered to both groups.
- Activities of aniline hydroxylase and p-aminopyrine N-demethylase were measured.
- Mitochondrial respiratory control ratio (RCR) was assessed.
Main Results:
- Chloramphenicol competitively inhibited aniline hydroxylase and p-aminopyrine N-demethylase in both groups.
- The reduction in enzyme activity was significantly less pronounced in PEM rats.
- Chloramphenicol decreased mitochondrial RCR in both groups, but to a lesser extent in PEM rats (18.2% decrease) compared to normal rats (45.8% decrease).
Conclusions:
- Protein-energy malnutrition (PEM) appears to mitigate the inhibitory effects of chloramphenicol on key drug-metabolizing enzymes.
- Mitochondrial function is less impaired by chloramphenicol in PEM rats.
- These findings suggest that chloramphenicol toxicity may be reduced in conditions of protein-energy malnutrition.