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Testosterone modulation of N-acetylation in mouse kidney
T N Smolen1, J A Brewer, W W Weber
1Institute for Behavioral Genetics, University of Colorado, Boulder.
The Journal of Pharmacology and Experimental Therapeutics
|February 1, 1993
Summary
Kidney N-acetyltransferase (NAT) activity is higher in male mice due to androgenic control, influencing their susceptibility to certain chemical carcinogens.
Area of Science:
- Pharmacology
- Toxicology
- Biochemistry
Background:
- N-acetylation is crucial for metabolizing drugs and carcinogens.
- Variations in acetylation capacity affect chemical toxicity and carcinogenicity across species.
- Kidney N-acetyltransferase (NAT) plays a role in biotransformation.
Purpose of the Study:
- To investigate how genotype, age, and sex influence kidney NAT activity in mice.
- To understand the hormonal regulation of kidney NAT activity.
Main Methods:
- Assessed kidney N-acetyltransferase (NAT) activity using p-amino-benzoic acid (PABA) as a substrate.
- Compared NAT activity across different inbred mouse strains (C57BL/6J and A/J).
- Examined the effects of age, sex, castration, testosterone, and estradiol on NAT activity.
Main Results:
- No significant strain differences in kidney NAT activity were observed.
- Male mice exhibited significantly higher kidney NAT activity than females, starting from postnatal day 30.
- Androgen manipulation (castration, testosterone, estradiol) demonstrated androgenic control over male kidney NAT activity.
- Testosterone increased NAT activity in females, while estradiol decreased it in males.
Conclusions:
- Kidney NAT activity in male mice is developmentally regulated and under androgenic control.
- Hormonal influences on NAT activity may contribute to sex-based differences in susceptibility to chemical mutagens and carcinogens.