Geschlechts- Und Altersabhängige Entwicklung Der Aktivitätsmuster Von Enzymen Des Steroidhormon-Stoffwechsels in Der Rattenleber Nach Neonatalem Eingriff in Die Sexuelle Differenzierung

Abstract

The influence of a single injection of 300 μg oestradiol-benzoate (OeB) or 1.25 mg testosterone-propionate (TP) shortly after birth (day 2 or 4 of life) on the age dependent and sex-specific development of the activity patterns of some liver enzymes involved in steroid metabolism (Δ4-5α-hydrogenase, steroid-hydroxylases, 3α- and 3β-hydroxysteriod-dehydrogenase and 20-keto-reductase) was studied in male and female rats. Female animals: The single neonatal injection of OeB or TP (day 2 or 4 of life) causes the mature animals to exhibit the typical morphological alterations of ovaries, uterus and adrenals. However, no effect on the sex-specific development of the activity patterns of the above mentioned enzymes could be observed, indicating that this treatment with TP cannot abolish the basic tendency of female livers to develop feminine activity patterns. This must be attributed to the antagonizing action of endogenous oestrogens. Male animals: A single injection of OeB on day 2 of life produces persistent feminization of enzyme activity patterns in mature animals. The development with age (day 30–180 of life) of the activities of particular enzymes is in every phase nearly or completely identical with that of sexually normal developed females. When TP is applied on day 2 of life, there is in no instance a complete adjustment of the enzyme activity to a female level, although some tendency to feminization is observed. However, 20-keto-reductase activity remains unchanged at the male level. If OeB is applied on day 4 of life the Δ4-5α-hydrogenase and the steroid-hydroxylases are the only enzymes whose activities show a considerable trend towards feminization.

Regulation of the Activities of the Enzymes Involved in the Metabolism of Steroid Hormones in Rat Liver: The Effect of Administration of Anterior Hypophyseal Hormones and Gonadotrophin Preparations to Hypophysectomized Rats

“…Three points in particular can be cited. First, neonatal hypothalamic damage is reported to lead to abnormally high PRL levels (Mallampati 8c Johnson 1974); it also leads to increased ¿d4-5a-hydrogenase activity in male rats (Schriefers et al 1972). Secondly, since pituitaries implanted under the kidney capsule secrete large amounts of PRL (Chen et al 1970), this may be responsible for inducing the very high level of z(4-5a-hydrogenase activity in hypophysectomized rats with pituitary im¬ plants (Denef 1974).…”

Neonatal Differentiation of Hepatic DHA 16α- and 7α-Hydroxylases

“…The basic pattern of sexual differentiation in the brain of rats appears to be that of a female-type cyclic gonadotropin release and sexual receptivity; androgen treatment of females or the presence of the testes in males promotes a defeminization or masculinization of the basic pattern to one of a non-cyclic (tonic) gonadropin release and male mounting be havior [26,27], Our data for hepatic mixed-function oxidases agree with those for oxidoreductases of corticosteroids [11][12][13][14][15], which appear to comply with this basic concept, since gonadectomy in neonatal males leads to adulthood activities identical to those of females. Masculinization of the characteristic feminine enzyme activities by testosterone propionate occurs in castrated neonates of either sex, but not in intact female neonates, as also do the gonadotropin secretion pattern and sexual behavior [24][25][26], A single injection of estradiol-17|3 benzoate to male neonates produces per sistent feminization of enzyme activity patterns in adulthood, however, the treatment of female neonates with testosterone propionate does not abolish the basic tendency to develop feminine activity patterns [28]. Fur thermore, male pseudohermaphroditic rats excrete urinary steroid meta bolites characteristic of normal females [29].…”

Differentiation of Steroid Metabolism in the Rat and Mechanisms of Neonatal Androgen Action

“…Taken from Denef and De Moor, 1968 (16). manently decreased to female levels in males treated with a high dose of estrogen at birth (28,70,71). The authors explain the phenomenon by postulating that estrogen blocks either the neonatal secretion or the action of testosterone.…”