Abstract
Syrian hamsters were fed one of three levels of lactalbumin (10, 20, or 40%) from 4 weeks of age. Parents (F 0 generation) and their offspring (F 1 generation) remained for life on the parental diet. Randomly selected hamsters from both generations were killed at 0, 6, 18, 30, and 60 weeks to evaluate hepatic microsomal drug metabolism systems. Microsomal protein content rose with increased dietary protein in both generations of females at 30 and 60 weeks and in both generations of males at 18 weeks. Microsomal protein rose during life, but the timing and magnitude of the increase varied with sex, diet, and generation. Cytochrome P-450 content increased with elevation in dietary protein at most measurement times in females and at all measurement times in F 1 generation males. Hepatic aryl hydrocarbon hydroxylase (AHH) and aniline hydroxylase (ANH) activities were influenced by dietary protein, primarily at 6, 18, and 30 weeks, and these values tended to decline between maturity and senescence. AHH generally increased as dietary protein rose, except at 30 weeks, at which time the group fed the medium protein level usually had the highest activity. ANH activity was either elevated in groups fed the 20 or 40% lactalbumin levels or depressed in these groups at 6 and 18 weeks when these values were influenced by dietary protein. The effects depended upon sex and generation. Age effects on hepatic microsomal metabolism in hamsters varied by sex and dietary protein and were somewhat different than those reported for other rodents.
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