These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


PUBMED FOR HANDHELDS

Search MEDLINE/PubMed


  • Title: Aging in the AXC rat: differential effects of chronic testosterone treatment on restoration of diminished prostate L-ornithine decarboxylase and S-adenosyl-L-methionine decarboxylase activities.
    Author: Shain SA, Moss AL.
    Journal: Endocrinology; 1981 Oct; 109(4):1184-91. PubMed ID: 7285866.
    Abstract:
    L-Ornithine decarboxylase (ODC) activity per 100 mg prostate was diminished 88% and S-adenosyl-L-methionine decarboxylase (AMDC) activity similarly ws diminished 57% in the ventral prostate of aged (26-month-old) as compared to that of young (3.8-month-old) AXC rats. Dorsolateral prostate ODC activity was too low to be reliably quantitated. Dorsolateral prostate AMDC activity per 100 mg prostate was diminished 55% in aged AXC rats. The age-related declines in prostate ODC and AMDC were not attributable to changes in the properties of the enzymes in aged AXC rats compared to young rats. There also was no evidence for an age-related production of inhibitors or inactivators of these prostate enzymes. The sensitivities of prostate ODC and AMDC to orchiectomy were comparable in young and aged AXC rats. Treatment of aged AXC rats with exogenous testosterone did not enhance ventral prostate AMDC activity per 100 micrograms DNA, but it did elevate dorsolateral prostate AMDC activity per 100 micrograms DNA to levels indistinguishable from those characteristic of untreated young AXC rats and caused a 303% increase in ventral prostate ODC activity per 100 micrograms DNA. However, ODC activity per 100 micrograms DNA in the ventral prostate of testosterone-treated aged rats was only 49% of that characteristic of untreated young AXC rats. We have identified three categories of age-related changes in prostatic enzyme activity: 1) decline fully reversible by exogenous testosterone, 2) decline partially reversible by exogenous testosterone, and 3) decline not reversible by exogenous testosterone. These alterations may reflect age-related changes in androgen-regulated prostate gene function.
    [Abstract] [Full Text] [Related] [New Search]