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40 Age (days)
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Figure 9.2 Developmental pattern of serum glutathione S-transferase activity in female rats. (Adapted from H. Mukhtar and J. R. Bend, Life Sci. 21: 1277, 1977.)
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CHEMICAL AND PHYSIOLOGICAL INFLUENCES ON XENOBIOTIC METABOLISM
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of age, begins to decline some 250 days later, a decrease that may be associated with reduced levels of sex hormones. Glucuronidation also decreases in old animals, whereas monoamine oxidase activity increases. These changes in the monooxygenase activities are often re ected by changes in drug ef cacy or overall toxicity. In humans, age-related impairment of enzyme activity is highly controversial. Agerelated declines in activity were not detected with respect to the activity of CYP2C and CYP3A isoforms among 54 liver samples from donors ranging in age from 9 to 89 years. Studies involving an erythromycin breath test in humans also suggested that there were no age-related declines associated with CYP3A4 activity. However, a study of CYP content and antipyrine clearance in liver biopsies obtained from 226 closely matched subjects indicated that subjects older than 70 had signi cantly less activity and clearance than younger subjects. Likewise, in older subjects, clearance of the drug omeprazole, a CYP2C19 substrate, was nearly half the rates observed in younger subjects.
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9.3.2 Gender Differences
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Metabolism of xenobiotics may vary with the gender of the organism. Gender differences become apparent at puberty and are usually maintained throughout adult life. Adult male rats metabolize many compounds at rates higher than females, for example, hexobarbital hydroxylation, aminopyrine N -demethylation, glucuronidation of o-aminophenol, and glutathione conjugation of aryl substrates; however, with other substrates, such as aniline and zoxazolamine, no gender differences are seen. In other species, including humans, the gender difference in xenobiotic metabolism is less pronounced. The differences in microsomal monooxygenase activity between males and females have been shown to be under the control of sex hormones, at least in some species. Some enzyme activities are decreased by castration in the male and administration of androgens to castrated males increases the activity of these sex-dependent enzyme activities without affecting the independent ones. Procaine hydrolysis is faster in male than female rats, and this compound is less toxic to the male. Gender differences in enzyme activity may also vary from tissue to tissue. Hepatic microsomes from adult male guinea pigs are less active in the conjugation of p-nitrophenol than are those from females, but no such gender difference is seen in the microsomes from lung, kidney, and small intestines. Many differences in overall toxicity between males and females of various species are known (Table 9.1). Although it is not always known whether metabolism is the only or even the most important factor, such differences may be due to gender-related differences in metabolism. Hexobarbital is metabolized faster by male rats; thus female rats have longer sleeping times. Parathion is activated to the cholinesterase inhibitor paraoxon more rapidly in female than in male rats, and thus is more toxic to females. Presumably many of the gender-related differences, as with the developmental differences, are related to quantitative or qualitative differences in the isozymes of the xenobiotic-metabolizing enzymes that exist in multiple forms, but this aspect has not been investigated extensively. In the rat, sexually dimorphic P450s appear to arise by programming, or imprinting, that occurs in neonatal development. This imprinting is brought about by a surge of testosterone that occurs in the male, but not the female, neonate and appears to imprint the developing hypothalamus so that in later development the growth hormone
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PHYSIOLOGICAL EFFECTS
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Table 9.1 Species Rat
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Gender-Related Differences in Toxicity Toxicant EPN, warfarin, strychnine, hexobarbital, parathion Aldrin, lead, epinephrine, ergot alkaloids Dinitrophenol Benzene Folic acid Nicotine Digitoxin Susceptibility F >M M>F F F F M M > > > > > M M M F F
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