Factors for consideration in the interpretation of the adverse effects of elevated environmental temperatures on reproduction in the male rat

Abstract

ABSTRACT. --Continuous exposure of male rats to an elevated environmental temperature (33-35 ° C) for 3 weeks led to heat-acclimatized (HA) rats whose serum testosterone concentratrion was significantly lower (P < 0.01) than that of control (C) rats (20-22 ° C). The decrease in the androgen level was independent of major changes in serum FSH and LH concentrations, as well as hypothalamic content of thyrotropinreleasing hormone (TH R), gonadotropin-releasing hormone (GnRH) and prostaglandin E 2 (PGE2). However, the prostaglandin F2~(PGF2~) content of the hypothalamus of HA rats was significantly lower (P < 0.05) than that of C. The number of receptors for human chorionic gonadotropin (hCG) was significantly lower in testicular tissue of HA rats as compared to C males. Histological examination of t he testis disclosed t hat exposure to heat adversely affected the sperm production and integrity of the Sertoli cells. Activity of enzymes associated with testosterone biosynthesis in testicular tissue of rats incubated at temperatures similar to those prevailing in the scrotum of HA rats resembled the activity of these enzymes observed in HA animals. Catabolism of testosterone was enhanced when kidney and liver of C rats were incubated at temperatures similar to the deep-body temperatures of HA rats, supporting the thesis that acclimatization to heat is coupled, interalia, with increased androgen catabolism and excretion. It is suggested that the lower reproductive performance of H A rats is associated wit.h several phenomena: a low number of receptors for hCG in the testes, decreased testosterone production rate by the Leydig cells, increased catabolism and excretion of androgen, and partial atrophy of seminiferous tubules and Sertoli cells. These changes appear to be independent of either alteration in serum gonadotropin concentration or hypothalamic contents ofTRH, GnR H and PGE2. The physiological significance in the response of PGF:~ awaits further clarification.

Distinct Testicular Steroidogenic Response Mechanisms Between Neonatal and Adult Heat-Acclimated Male Rats

“…These results indicate that increased LH or PRL plasma concentrations were not directly associated with the steroid feedback mechanisms but occurred due to the effects of increased body temperature on pituitary cells as previously shown in heat-acclimated rats [11] or changes in thyrotrophic cell function as observed in farm animals during the summer conditions [35]. Heat acclimation-induced interstitial space enlargement was occasionally shown to be responsible for increased testicular steroid production [10]; however, in our case, no changes in the interstitial tissue morphology and gonado-somatic index (GSI) were found. The discrepancy between the plasma steroid levels and the in vitro steroid secretion ability by the testicular slices may be a result of increased steroid metabolism in adult heat-acclimated rats as previously shown [10].…”

“…Heat acclimation-induced interstitial space enlargement was occasionally shown to be responsible for increased testicular steroid production [10]; however, in our case, no changes in the interstitial tissue morphology and gonado-somatic index (GSI) were found. The discrepancy between the plasma steroid levels and the in vitro steroid secretion ability by the testicular slices may be a result of increased steroid metabolism in adult heat-acclimated rats as previously shown [10]. …”

“…Increased testicular HSD3B1 activity in adult heat-acclimated rats together with decreased CYP11A1 and increased CYP17A1 activity levels were observed in our AHA group. A previous study [9,10] showed that increased testicular HSD3B1 activity of adult heat-acclimated rats was accompanied by decreased intra-testicular testosterone production and serum concentration. Thus, the activity of steroidogenic enzymes without significant changes in their transcription rate may act as a molecular starting point for higher in vitro steroid production by testicular slices of adult heat-acclimated rats.…”

“…Elevated gonadal temperature is also suggested as a factor involved in the pathogenesis of human reproductive tract disorders such as fever [6], cryptorchidism [7] or varicocele [8]. The long-term effects of elevated ambient temperature on testicular steroidogenesis were primarily reported from the 1970s to the 1990s [9,10,11,12]. By contrast, recent transcriptome data obtained from the heat-acclimated rat hypothalami [13] and hearts [14] showed that short-term heat acclimation (two days) resembled a stress response, whereas long-term heat acclimation activated different sets of gene expression profiles and was characterised by the resumption of pre-acclimation stress response-related gene transcript levels.…”

Interrelationship between pituitary-testicular axis activity and raised environmental temperature in the rat

“…Recent reports indicate that the raised environmental temperature affects the activity of the axis at all levels of control Bedrak, Chap & Fried, 1980). Namely, it provokes a transient decrease in the hypothalamic content of gonadotrophin releasing hormone (GnRH), induces a similar response in the serum concentration of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) and decreases the capacity of the testis to synthesize testosterone.…”