The sulphurylation of [1,2 3H] deoxycorticosterone was studied in the 105000 x g supernatant fluid obtained from rat liver homogenates. The sulphurylating activity in newborn rats was high; it was considerably lower in rats 7 days of age. Between 7 and 28 days of age the sulphurylating activity did not change and it was the same in male and female rats. From about 28 days of age until the rats were about 56 days of age the sulphurylating activity increased in female rats but decreased in male rats so that finally female animals sulphurylated about five times more efficiently than male animals (P<0.001). Neonatal or postpubertal ovariectomy did not influence the hepatic sulphurylating activity in the adult female rats. Neonatal testectomy led to complete feminization of the sulphurylating activity in the adult male rats whereas postpubertal testectomy led to an increase in the hepatic sulphurylation but not complete feminization. Administration of testosterone propionate to postpubertally castrated male and female rats suppressed the hepatic sulphurylating activity in both sexes. Administration of estradiol benzoate did not affect the sulphurylating activity in female rat liver but feminized this activity in male rat liver. The conclusions drawn from all these findings are that the sulphurylating activity in female rats is normally regulated by nongonadal factors and that the sulphurylating activity in male rats is suppressed by testicular androgens in two ways; by irreversible 'imprinting' or programming of the liver during the neonatal period, and by reversible suppression postpubertally. The effects of estradiol benzoate treatment are probably best explained by 'de-imprinting' of the male liver back to the basal 'feminine' character with respect to sulphurylating activity.
|Original language||English (US)|
|Number of pages||6|
|Journal||European Journal of Biochemistry|
|State||Published - Jul 1973|
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