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Endocrinology, Vol 113, 1292-1298, Copyright © 1983 by Endocrine Society
ARTICLES |
SA Shain, JK Hilliard and C de Leon
We purified AXC rat hepatic S-adenosyl-L-methionine decarboxylase (AMDC) 4900-fold and obtained a preparation that was 75% AMDC. This material caused elaboration of rabbit antirat AMDC antibodies that essentially were monoprecipitating. Antibody from one rabbit was highly effective as an inactivator of prostatic AMDC activity and was used to evaluate the quantitative relationship between antigenic mass and AMDC activity in ventral and dorsolateral prostates of young mature (185-day- old) and aged (776-day-old) AXC rats. Although AMDC activity of aged AXC rat prostates was diminished (ventral, 68%; dorsolateral, 50%), the quantities of antibody required to inactivate 1 U AMDC activity in prostates of young mature and aged rats were identical. This antibody effectively recognized enzymatically inactive AMDC, which is antigenically similar to active AMDC. Therefore, the age-related reductions in prostatic AMDC activity are not due to the production of so-called altered AMDC. Four days of exogenous testosterone treatment of aged AXC rats failed to enhance ventral prostate AMDC activity, whereas AMDC activity in dorsolateral prostates was elevated 2.3-fold. New AMDC activity was antigenically identical to that in dorsolateral prostates of untreated young mature or aged AXC rats. Because we previously established that age-related reductions in AXC rat prostatic AMDC activity are due to neither trivial causes nor enhanced inactivation, our present studies imply that reductions in AMDC activity are due to decreased prostatic AMDC content. These studies are an initial demonstration of senescence-related quantitative reductions in the prostatic content of AMDC molecules, which appear to represent altered expression of a specific androgen-responsive prostatic gene.
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