Effect of warm‐rearing and heat acclimation on pituitary‐gonadal axis in male rats

Abstract

Plasma gonadotrophic and testicular hormones concentrations in both immature and adult male rats exposed to 34 degrees C of ambient temperature were determined. In vitro steroidogenic ability of interstitial cells from experimental rats was also studied. Four groups of rats (n = 45) were used. Warm-reared (WR) males were housed in 34 degrees C and control-reared rats in 20 degrees C from birth to adulthood. The other groups were acclimated to 34 degrees C [warm-acclimated (WA) group] or 20 degrees C [deacclimated (DA) group] as adults. Decreased body weight and testis weight (p < 0.05) was found in heat-exposed groups, but relative testis weight was unchanged in WA and increased (p < 0.05) in WR and DA males. Plasma luteinizing hormone (LH) concentration increased in WA and DA males. Increased (p < 0.05) follicle-stimulating hormone (FSH) and prolactin plasma levels were found in DA and WR groups respectively. WA males had decreased testosterone (T) and WR rats androstenedione (A(4)) plasma concentration (p < 0.05). Interstitial cells (43% of them were Leydig cells by 3beta-hydroxysteroid dehydrogenase activity) from heat-exposed males secreted less (p < 0.05) T compared with the control group when incubated without LH (basal conditions). Androstenedione secretion decreased (p < 0.05) in WA rats. Secretion of estradiol-17beta (E(2)) was higher in WR and lower in DA cells under basal conditions. Weaker responsiveness to LH was observed in WR cells. Androgen synthesis from pregnenolone by interstitial cells increased (p < 0.05) in the WA group. We concluded that heat exposure of neonatal and adult male rats caused different pituitary-testicular axis adjustments. It seemed that long-term heat exposure of neonatal rats is less deleterious concerning the activity of pituitary-testicular axis than heat acclimation of adults.

Effect of two types of stress (heat shock/high temperature and malnutrition/serum deprivation) on porcine ovarian cell functions and their response to hormones

“…The reduction in ovarian cell proliferation and/or turnover and oversecretion of ovarian hormones can be causes of negative effects of heat stress on reproductive functions described previously (Christenson, 1980;Putney et al, 1989;Edwards and Hansen, 1997;Beere, 2004;Lawrence et al, 2004;Kunavongkrit et al, 2005;Rozenboim et al, 2007). They are in line with previous reports (Bridges et al, 2005;Kurowicka et al, 2006;Rozenboim et al, 2007) on the ability of heat stress to induce abnormal basal release of steroid hormones and to promote stimulatory effect of gonadotropin on steroid hormones output by cultured ovarian cells. Our observations represent the first data on the direct effect of high temperature on the proliferation and apoptosis of ovarian cells.…”

“…In ovarian cells, changes in the expression of heat shock proteins are associated with changes in the production of prostaglandins (Narayansingh et al, 2004) and receptors for steroid hormones (Salvetti et al, 2008). Furthermore, high ambient temperatures can either reduce or increase plasma folliclestimulating hormone (FSH), prolactin, progesterone, testosterone and estradiol levels (Kurowicka et al, 2006;Rozenboim et al, 2007), reduce androstenedione and estradiol, and increase basal and luteinizing hormone (LH)-induced progesterone production by ovarian cells in vitro (Bridges et al, 2005;Kurowicka et al, 2006). Therefore, high temperatures can suppress ovarian functions through changes in the release of reproductive hormones, and that consequently manipulation with these hormones can neutralize the negative effect of heat environment on reproduction.…”

“…Hot environments can increase blood, rectal and uterine temperatures, suppress puberty (Kurowicka et al, 2006), ovarian cyclicity (Christenson, 1980), ovulation (Rozenboim et al, 2007), spermatogenesis, fertility (Kunavongkrit et al, 2005), oogenesis and embryogenesis (Putney et al, 1989;Edwards and Hansen, 1997;Beere, 2004;Lawrence et al, 2004), and reduce conception and pregnancy rates (Christenson, 1980;Putney et al, 1989) in different domestic species.…”

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

“…Previously, we reported increased PRL and oestradiol-17β (E2) plasma levels and decreased androstenedione (A4) levels in male rats housed at a high ambient temperature from birth to adulthood [25]. Moreover, isolated Leydig cells from neonatal and adult heat-acclimated rat testes secreted less testosterone (T) compared with control rats [25].…”

“…Moreover, isolated Leydig cells from neonatal and adult heat-acclimated rat testes secreted less testosterone (T) compared with control rats [25]. …”