Effects of whole-body heat on male germ cell development and sperm motility in the laboratory mouse

2016 ◽  
Vol 28 (5) ◽  
pp. 545 ◽  
Author(s):  
H. Wechalekar ◽  
B. P. Setchell ◽  
K. R. Pilkington ◽  
C. Leigh ◽  
W. G. Breed ◽  
...  

This study investigated the effects of high temperatures on male germ cell development and epididymal sperm motility of laboratory mice. In Experiment 1, adult males (n = 16) were exposed to whole-body heat of 37–38°C for 8 h day–1 for 3 consecutive days, whereas controls (n = 4) were left at 23–24°C. In Experiment 2, adult mice (n = 6) were exposed to 37–38°C for a single 8-h period with controls (n = 6) left at 23–24°C. Experiment 2 was conducted as a continuation of previous study that showed changes in spermatozoa 16 h after exposure to heat of 37–38°C for 8 h day–1 for 3 consecutive days. In the present study, in Experiment 1, high temperature reduced testes weights 16 h and 14 days after exposure, whereas by Day 21 testes weights were similar to those in the control group (P = 0.18). At 16 h, 7 and 14 days after exposure, an increase in germ cell apoptosis was noticeable in early and late stages (I–VI and XI–XII) of the cycle of the seminiferous epithelium. However, apoptosis in intermediate stages (VII–X) was evident 16 h after heat exposure (P < 0.05), without any change at other time periods. By 21 days, there were no significant differences between heat-treated groups and controls. Considerably more caspase-3-positive germ cells occurred in heat-treated mice 16 h after heat exposure compared with the control group (P < 0.0001), whereas 8 h after heat in Experiment 2, sperm motility was reduced with a higher percentage of spermatozoa showing membrane damage. In conclusion, the present study shows that whole-body heat of 37–38°C induces stage-specific germ cell apoptosis and membrane changes in spermatozoa; this may result in reduced fertility at particular times of exposure after heating.

2005 ◽  
Vol 337 (2) ◽  
pp. 663-669 ◽  
Author(s):  
Mark Castanares ◽  
Yanira Vera ◽  
Krista Erkkilä ◽  
Sauli Kyttänen ◽  
Yanhe Lue ◽  
...  

2006 ◽  
Vol 91 (2) ◽  
pp. 539-545 ◽  
Author(s):  
Yanhe Lue ◽  
Christina Wang ◽  
Yi-Xun Liu ◽  
Amiya P. Sinha Hikim ◽  
Xue-Sen Zhang ◽  
...  

Context: The context of the study was to examine whether combined testosterone (T) and heat (H) treatment have additive or synergistic effects on suppression of spermatogenesis. Objective: The objective of the study was to determine whether T+H induces a greater suppression of spermatogenesis than either treatment alone in monkeys. Design: The study was a randomized, placebo-controlled study. Setting: The study was conducted at a primate center in China. Participants: The study population was comprised of 32 adult cynomolgus monkeys. Interventions: Groups of eight adult monkeys were treated for 12 wk with: 1) two empty implants (C); 2) two T implants (T); 3) daily testicular heat exposure (43 C for 30 min) for 2 consecutive days (H); or 4) two T implants plus testicular heat exposure (T+H). Treatment was followed by an 8-wk recovery period. Main Outcome Measures: Measures included sperm counts and germ cell apoptosis. Results: Serum T levels were elevated in both the T and T+H groups during treatment but not in the C or H group. Sperm counts were transiently suppressed after heat to 16.4% of baseline at 4 wk and then returned to pretreatment levels. Sperm counts were suppressed slowly after T treatment to nadir of 6.4% of pretreatment levels at 12 wk. T+H rapidly suppressed sperm output as early as 4 wk to 3.9% of pretreatment levels that was maintained throughout treatment. The decreased sperm counts were due to increased germ cell apoptosis in all treatment groups. Sperm counts recovered to the pretreatment levels in all groups by 8 wk after treatment. Conclusion: This proof-of-concept study demonstrates that transient testicular warming enhances and hastens the effect of T implant on the suppression of spermatogenesis in monkeys.


APOPTOSIS ◽  
2007 ◽  
Vol 12 (6) ◽  
pp. 1085-1100 ◽  
Author(s):  
Tej K. Pareek ◽  
Ayesha R. Joshi ◽  
Amartya Sanyal ◽  
Rajan R. Dighe

2011 ◽  
Vol 1 (3) ◽  
pp. 195-208 ◽  
Author(s):  
Ricardo D. Moreno ◽  
Paulina Urriola-Muñoz ◽  
Raúl Lagos-Cabré

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Siyuan Hou ◽  
Li Xian ◽  
Peiliang Shi ◽  
Chaojun Li ◽  
Zhaoyu Lin ◽  
...  

FEBS Letters ◽  
2004 ◽  
Vol 575 (1-3) ◽  
pp. 41-51 ◽  
Author(s):  
Yun-Jung Choi ◽  
Do-Won Ok ◽  
Dueg-Nam Kwon ◽  
Jong-il Chung ◽  
Heung-Cheol Kim ◽  
...  

2003 ◽  
Vol 88 (11) ◽  
pp. 5572-5579 ◽  
Author(s):  
Laura Suomalainen ◽  
Jukka K. Hakala ◽  
Virve Pentikäinen ◽  
Marjut Otala ◽  
Krista Erkkilä ◽  
...  

2007 ◽  
Vol 92 (8) ◽  
pp. 3292-3304 ◽  
Author(s):  
Christina Wang ◽  
Yu-Gui Cui ◽  
Xing-Hai Wang ◽  
Yue Jia ◽  
Amiya Sinha Hikim ◽  
...  

Abstract Context: In rodents and monkeys, a combination of hormonal and physical agents accelerates germ cell death. Objective: A “proof of concept” study was performed to investigate whether addition of heat exposure or a progestin to an androgen induces germ cell death and more complete and rapid spermatogenesis suppression. Design and Settings: A randomized clinical trial was performed at academic medical centers. Participants: We treated four groups of healthy male volunteers (18 per group) for 18 wk: 1) testosterone undecanoate (TU) 1000 mg im (first dose), followed by 500 mg im every 6 wk; 2) submersion of scrota at 43 C in water for 30 min/d for 6 consecutive days; 3) TU plus heat; and 4) TU plus oral levonorgestrel (LNG) 250 μg/d. Main Outcome Measures: Semen parameters, testicular histology, and germ cell apoptosis were the main outcome measures. Results: Heat alone and TU plus heat suppressed sperm counts more than TU alone by wk 6. By wk 9, recovery began in the heat only group, whereas spermatogenesis remained suppressed in the TU plus heat group. Oral LNG plus TU suppressed spermatogenesis earlier and more severely than TU alone. At wk 2, significantly greater germ cell apoptosis occurred in heat and heat plus TU subjects, but not in subjects without heat treatment, compared with pretreatment subjects. By 9 wk, markedly smaller seminiferous tubule diameters and fewer spermatocytes and spermatids were noted in all 12 biopsies from men receiving TU, TU plus LNG, with most dramatic differences for the TU plus heat group, whereas no differences from pretreatment biopsies were observed in men who received heat treatment only. Conclusions: Heat causes a rapid and transient suppression of spermatogenesis. TU plus heat resulted in low-sperm output that was maintained by continuous treatment with TU. Addition of an oral progestin accelerated spermatogenesis suppression by TU alone. Increased germ cell apoptosis contributed to suppression of spermatogenesis.


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