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Biomedical subjects

J Ellingboe

Publications and source records attributed to J Ellingboe.

7 recordsLinked to original sources

Ethanol inhibits testosterone biosynthesis by direct action on Leydig cells.

Ethanol was found to suppress gonadotropin-stimulated testosterone biosynthesis in sexually mature male rats in vivo and in intact Leydig cells in vitro. A similar ethanol dose-response inhibition curve was also observed when either whole or homogenized cells were stimulated by dibutyryl cyclic AMP. In the presence of pharmacologically relevant ethanol concentrations, added NAD+ restored testosterone production to stimulated control levels. These results demonstrate a direct inhibitory effect of ethanol on testicular testosterone synthesis. The site of inhibition is primarily intracellular and the mechanism is probably through a decrease in the NAD+/NADH ratio caused by ethanol oxidation.

Animals

Effects of chronic marihuana use on integrated plasma testosterone and luteinizing hormone levels.

Integrated plasma testosterone and luteinizing hormone levels were determined for 13 healthy adult males before, during and after a 21-day period of marihuana use. No significant relationships were found between antecedent or concurrent marihuana smoking and integrated plasma testosterone and luteinizing hormone levels. All values for all subjects obtained during the entire study were within normal limits for healthy adult males.

Adult

Effects of acute alcohol intake on pituitary-gonadal hormones in normal human males.

Plasma luteinizing hormone and testosterone levels were determined in 16 normal adult males during a period of acute alcohol intoxication. Plasma testosterone levels were in the normal range for adult males prior to alcohol administration. Plasma testosterone levels began to fall during the ascending phase of the blood alcohol curve but plasma luteinizing hormone levels did not change significantly. At peak blood alcohol levels [109 +/- 4.6 (S.D.) mg/100 ml], plasma testosterone was significantly depressed and a significant increase in plasma luteinizing hormone values occurred. During the descending phase of the blood alcohol curve, plasma testosterone levels remained depressed and plasma luteinizing hormone levels decreased toward base-line values. These data indicate that acute alcohol intake produces a suppression of plasma testosterone via peripheral mechanisms which regulate the biosynthesis and/or biotransformation of the steroid. The surge in luteinizing hormone values at peak levels of intoxication are most likely due to stimulation of gonadotropin secretion via "long loop" mechanisms associated with low levels of plasma testosterone.

Adult