Influence of androgens on the transaminases and glutamic dehydrogenase of tissues

1959 ◽  
Vol 197 (1) ◽  
pp. 129-134 ◽  
Author(s):  
Charles D. Kochakian ◽  
Barbara R. Endahl ◽  
Gerald L. Endahl

Aspartic-glutamic and alanine-glutamic transaminase activities of the kidney and heart of the rat and mouse change in direct proportion with the changes in weight produced by castration and testosterone. The transaminase activities of the rat but not the mouse liver are decreased by castration and restored to normal by testosterone propionate administration. The glutamic dehydrogenase activity of the liver and kidney of the rat and the mouse is not altered by castration or androgen administration. An increase of the kidney weight above normal size by androgen, however, is accompanied by a proportionate increase in the enzyme.

1974 ◽  
Vol 142 (2) ◽  
pp. 273-277 ◽  
Author(s):  
Jan-Åke Gustafsson ◽  
Åke Pousette

The regulatory mechanisms involved in the control of the nuclear NADPH-dependent 3-ketosteroid 5α-reductase (5α-reductase) activity were studied in liver, kidney and prostate. The substrate used was [1,2-3H]androst-4-ene-3,17-dione (androstenedione) (for liver and kidney) or [4-14C]androstenedione (for prostate). The hepatic nuclear 5α-reductase activity was greater in female than in male rats, was greater in adult than in prepubertal female rats, increased after castration of male rats, but was not affected by treatment with testosterone propionate or oestradiol benzoate. These regulatory characteristics are in part different from those previously described for the hepatic microsomal 5α-reductase. The renal nuclear metabolism of androstenedione, i.e. 5α reduction and 17β-hydroxy steroid reduction, was relatively unaffected by sex, age, castration and treatment with testosterone propionate. However, treatment of castrated male rats with oestradiol benzoate led to a significant increase in the 5α-reductase activity and a significant decrease in the 17β-hydroxy steroid reductase activity. Finally, the nuclear 5α-reductase activity in prostate was androgen-dependent, decreasing after castration and increasing after treatment with testosterone propionate. In conclusion, the nuclear 5α-reductase activities in liver, kidney and prostate seem to be under the control of distinctly different regulatory mechanisms. The hypothesis is presented that whereas the prostatic nuclear 5α-reductase participates in the formation of a physiologically active androgen, 5α-dihydrotestosterone, this may not be the true function of the nuclear 5α-reductase in liver and kidney. These enzymes might rather serve to protect the androgen target sites in the chromatin from active androgens (e.g. testosterone) by transforming them into less active androgens (e.g. 5α-androstane-3,17-dione and/or 5α-dihydrotestosterone).


1970 ◽  
Vol 176 (1044) ◽  
pp. 277-285 ◽  

Chromatin (chromosomal nucleoprotein) from mammalian colls is used as a template for the synthesis of RNA which is characterized and compared with other RNA by RNA-DNA hybridization. It is found to be transcribed from a restricted set of sequences and cannot be distinguished from natural RNA from the same organ as the chromatin. In contrast, it is different from RNA from other organs. Hence, DNA is masked in an organ-specific way in vivo and the masking is preserved on isolation. When cell division is induced in mouse liver and kidney a very early event is a change in masking in chromatin. This precedes changes in RNA populations; both precede DNA synthesis. Chromatin can be accurately reconstructed from DNA, histones and non-histone proteins. Experiments using this system indicate that histones non-specifically mask DNA; non-histone proteins are essential to reverse masking in a specific way.


1990 ◽  
Vol 127 (2) ◽  
pp. 249-256 ◽  
Author(s):  
J. Klindt ◽  
J. J. Ford ◽  
G. J. Macdonald

ABSTRACT The effect of testosterone propionate (TP), alone and in combination with porcine GH, on the growth of hypophysectomized rats was investigated. An initial study determined doses of TP and GH which would result in a synergistic response. Hypophysectomized male rats, approximately 40 days of age, received GH at doses of 5, 25 and 62·5 μg/day administered in two injections/day at 08.00 and 16.00 h. At all doses of GH, administration of TP at 100 μg/day significantly enhanced the GH-stimulated rate of growth. This growth enhancement by TP was greatest in combination with GH at 25 μg/day. In a subsequent study, growth responses to 25 μg GH/day and 100 μg TP/day were examined in animals with differing degrees of sexual differentiation. Sex groups were: intact males, males castrated at 11 days of age and females administered 100 μg TP at 3 days of age (masculinized rats), and males castrated at 2 days of age and normal females (non-masculinized rats). In all sex groups, growth of hypophysectomized rats was stimulated by GH. Genetic sex and masculinization did not influence the response to GH. Masculinized hypophysectomized rats exhibited significantly greater rates of growth and final live, empty body, liver and kidney weights than non-masculinized hypophysectomized rats. All sex groups other than normal females responded synergistically to the combination treatment of GH plus TP. Rats that experienced neonatal exposure to testosterone became programmed to respond to testosterone and demonstrated greater rates of growth and body and organ weights when administered the combination of GH plus TP. These data indicate that TP synergizes with GH to promote growth of hypophysectomized rats appropriately programmed to respond. The ability to manifest a synergistic response is a differentiated trait dependent upon exposure to testosterone during the appropriate period of development. The time of differentiation of this ability to respond to testosterone occurs earlier than that for differentiation of body growth. Journal of Endocrinology (1990) 127, 249–256


Toxicon ◽  
1978 ◽  
Vol 16 (4) ◽  
pp. 351-359 ◽  
Author(s):  
Richard D. Phillips ◽  
A.Wallace Hayes
Keyword(s):  

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