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The present study tests the hypothesis that the effects of perinatal androgen administration on the development of the brain are brought about indirectly by a suppression of plasma gonadotropin (GTH) titers. Both castrated male and intact female rats were treated neonatally with 5 alpha-dihydrotestosterone propionate (DHTP) or testosterone propionate (TP) throughout the first ten postnatal days of life and the corresponding effects on neonatal plasma FSH and LH levels and the subsequent ability of the adult to exhibit cyclic GTH release and female sex behavior (lordosis) were determined. In males castrated within 24 h of birth, subcutaneous injections of DHTP (60 or 180 mug per 100 g average body weight) or TP (60 mug/100 g) given on day 2, 4, 6, 8 and 10 reduced plasma levels of FSH and LH as determined by radioimmunoassay 48 h following the first and last injections. However, TP but not DHTP masculinized the development of the regulation of GTH release as mesured by luteinization of subcutaneous ovarian grafts, and also suppressed the ability of adult neonatally castrated male primed with estradiol benzoate and progesterone to display lordosis behavior. In intact females, the same neonatal DHTP and TP injection regime lowered FSH and LH plasma levels following the last injection (day 12), while DHTP lowered LH, but not FSH, following the first injection (day 4). All TP treated females had ovaries devoid of CL by 45 days of age and showed prolonged vaginal cornification. However, DHTP failed to masculinize the pattern of GTH release in females since DHTP-treated females, like oil-treated females, possessed CL(days 45 and 100) and exhibited vaginal cycles (days 80-100). Lordosis quotients of females treated neonatally with DHTP were as high as those of oil-treated females and significantly higher than those of TP-treated females. These results demonstrate that the ability of TP to induce maculine differentiation of the neural regulation of GTH release and female sex behavior does not depend on its ability to depress circulating LH and FSH levels in the neonatal male, or LH levels in the neonatal female rat. 相似文献
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The rise in concentrations of FSH and LH in serum seen 24 h after castration was suppressed by the administration of an extract of bull seminal plasma or testosterone propionate at the time of castration. Whereas testosterone propionate preferentially suppressed LH, the seminal plasma extract suppressed FSH and LH equally. Small doses of bull seminal plasma extract and testosterone, that had little effect separately, acted synergistically to supress levels of FSH and LH to those found in intact animals, while combinations of larger doses had little further effect. This selective interaction suggests how inhibin and testosterone might together regulate concentrations of FSH and LH in the blood of the male rat. 相似文献
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T Ishikawa S McNeeley P M Steiner C J Glueck M Mellies P S Gartside C McMillin 《Metabolism: clinical and experimental》1978,27(1):89-96
Ten chlorinated hydrocarbons (tetradifon, Chlorobenzilate, Kepone, lindane, Kelthane, toxaphene, dieldrin, hexachlorobenzene, dienochlor, and Aroclor 1254; see below) were evaluated in rats to assess agents which might selectively elevate high-density lipoprotein cholesterol (C-HDL). Single, nontoxic doses of Aroclor, dieldrin, and Kepone elevated C-HDL at day 7 (31%, 26%, and 24%, respectively, p less than 0.05). The C-HDL elevations were maintained at days 21 and 60 (28% and 31%, p less than 0.01) in the Aroclor group, while C-HDL returned to baseline in the dieldrin and Kepone groups. Liver function tests were unchanged from control, suggesting that the changes in C-HDL were not the consequence of hepatotoxicity. The hepatic microsomal cytochrome P-450 content of animals receiving Aroclor, dieldrin, and Kepone was 67%, 56%, and 44% higher than control values (p less than 0.02), indicating probable hepatic enzyme induction. If HDL (an antiatherogenic lipoprotein) is also selectively elevated by chlorinated hydrocarbons in man, then analogues might potentially be developed as antiatherogenic pharmacologic agents. Alternatively, the implications of man's exposure to halogenated hydrocarbons may be better understood. 相似文献
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