Testicular function in boars exposed to elevated ambient temperature.

Pituitary-testicular function was examined in yearling boars exposed to 23 ± 1#{176}C (control) or 34.5 ± 1#{176}C for 8 h and 31 ± 1#{176}C for 16 h during each 24 h period (heat stressed). Plasma testosterone and immunoreactive LI concentrations were monitored throughout treatment and testes were removed after 13 weeks to quantify spermatogenesis and assess steroidogenesis by measuring the incorporation of E1�l 4C1 acetate into selected L� 4C1 androgens by slices of testicular tissue incubated in vitro. Plasma testosterone and LI concentrations were similar when control and heat stressed boars were bled infrequently during treatment. However, heat stress significantly altered androgen biosynthesis in vitro as evidenced by decreased amounts of II Cl associated with androstenedione, testosterone and dihydrotestosterone and increases in androsterone and androstanediol. Addition of LH and FSH to testicular incubates markedly enhanced the amount of (1-’ 4CI acetate incorporated into 1l 4C1 androgens but further differences between control and heat stressed boars were not apparent. In another experiment, plasma testosterone was quantified in the serum of boars every 30 mm for 12 h on Days 0, 7 and 14 during exposure to 23 ± 1#{176}C (control) or 34.5 ± 1#{176}C (heat stressed). Serum testosterone was reduced (P(0.10) after 7 days of heat stress. Elevated ambient temperature for 90 days significantly reduced the number of young spermatids in round cross sections of seminiferous tubules at stage 1 of the cycle of the seminiferous epithelium but failed to affect the number of type A spermatogonia or preleptotene and pachytene spermatocytes. The results demonstrate that heat stress can exert a transitory decline in plasma