Comparative rates of formation, in vivo, of 16-androstenes, testosterone and androstenedione in boar testis

Abstract

Three mature Large White boars were anaesthetized and received [7(n)-3H]pregnenolone by continuous infusion into right and left spermatic arteries for up to 180 min. Spermatic venous blood flow was measured by separate timed collections of completely diverted outflow from each testis and blood not sampled was returned to the peripheral circulation. The total radioactivity in plasma from each testis increased markedly during the first 60 min of infusion to reach a plateau from 80 to 180 min. Radiolabelling of 5 alpha-androst-16-en-3-one, 5 alpha-androst-16-en-3 beta-ol and -3 alpha-ol showed similar patterns with ratios of mean radioactivity of 5:3:1 respectively between 80 and 180 min. In comparison, the amounts of tritiated 4,16-androstadien-3-one formed were very small. The radiolabelling of testosterone and 4-androstenedione occurred more rapidly than that of the 16-androstenes and reached maxima by 30 min. However the amounts were only one-fifth (testosterone) and one-tenth (4-androstenedione) those of the combined quantities of tritiated 16-androstenes. Addition of human chorionic gonadotrophin (hCG) to the infusate to one testis in each animal (so that 5000 i.u. hCG were delivered in 15-20 min) produced no change in the outputs of radiolabelled steroids although radioimmunoassay of spermatic venous plasma in samples from the third experiment showed a transient increase in the concentration of 4-androstene-3,17-dione during the hCG infusion. It is suggested the lack of response to hCG could be produced by saturation and down regulation of binding sites by the very high local concentrations of hCG.

Synthesis of free and sulphoconjugated 16-androstene steroids by the Leydig cells of the mature domestic boar

“…This is characteristic for animals at this stage of maturity [6]. A high concentration of 3␤-androstenol was found in both the unconjugated and sulphoconjugated fractions, in the 4 and 8 h incubations; however, 70% of the total amount of 3␤-androstenol existed in the sulphoconjugated form after incubation for 8 h with substrates such as pregnenolone, androstadienol or androstadienone.…”

“…The 5␣ reduced alcohols, including 5␣-androst-16-en-3␣-ol (3␣-androstenol) and 5␣-androst-16-en-3␤-ol (3␤-androstenol) have pheromonal properties [1,4,5]. In the mature animal, 3␤-androstenol is produced in three times greater amounts than 3␣-androstenol [6]. The high levels of these alcohols reflect the high activity of 4,5 isomerase, 5␣-reductase, 3␣-hydroxysteroid and 3␤-hydroxysteroid dehydrogenase (HSD) enzymes present in the testis [7,8].…”

Seasonal Variation in the Blood Concentration of 16-Androstenes in Adult Landrace Boars

“…The main cross-reacting steroids were 5a-androstenone (lN%) , Scy-androst-16-en-3B-ol (72%), 16-androstadien-3B-ol (12%) and 5cu-androst-16-en-3a-ol (10%); other closely related C19 5a-reduced metabolites did not cross react. Given that all four ofthese crossreacting steroids are produced by the testes (Bonneau 1982) and that all three 5o-reduced compounds are likely present in the peripheral blood circulation (Hurden et al 1984) and responsible for boar taint (Brennan et al 1986), our hormone values are reported as ng ml--r of 16 (month, P< 0.10) throughout the year and was not influenced by social environment at any time (Fig. 1).…”

The Pheromone Androstenol (5α-Androst-16-en-3α-ol) Is a Neurosteroid Positive Modulator of GABAA Receptors

“…The best studied site of androstenol synthesis is the testis (Gower and Haslewood, 1961;Hurden et al, 1984;Smals and Weusten, 1991). The crucial synthetic reaction is the conversion of pregnenolone (Brooksbank and Wilson, 1970;Hurden et al, 1984) to androstadienol by the recently described 16-ene-synthetase activity of cytochrome P450c17 (steroid 17␣-monooxygenase) (Soucy et al, 2003).…”

“…The best studied site of androstenol synthesis is the testis (Gower and Haslewood, 1961;Hurden et al, 1984;Smals and Weusten, 1991). The crucial synthetic reaction is the conversion of pregnenolone (Brooksbank and Wilson, 1970;Hurden et al, 1984) to androstadienol by the recently described 16-ene-synthetase activity of cytochrome P450c17 (steroid 17␣-monooxygenase) (Soucy et al, 2003). Androstadienol can then be sequentially converted to androstenol by 3␤-hydroxysteroid dehydrogenase, 5␣-reductase, and 3␣-hydroxysteroid dehydrogenase (Dufort et al, 2001), a series of reduction and oxidation steps analogous to the metabolic pathway for androgens in which dehydroepiandrosterone is converted to testosterone and then to androstanediol.…”