115. WHOLE BODY HEAT EXPOSURE INDUCES APOPTOSIS IN MOUSE CAUDAL EPIDIDYMAL SPERMATOZOA

2009 ◽  
Vol 21 (9) ◽  
pp. 34 ◽  
Author(s):  
H. Wechalekar ◽  
B. P. Setchell ◽  
W. G. Breed ◽  
M. Ricci ◽  
C. Leigh ◽  
...  
Keyword(s):  
Actinomycin D ◽  
Heat Exposure ◽  
Annexin V ◽  
Whole Body ◽  
Sperm Number ◽  
Sperm Preparation ◽  
Heat Treated ◽  
Epididymal Spermatozoa ◽  
And Control ◽  
Body Heat

Introduction: The aim of the present study was to determine the immediate effects of whole body heating on sperm numbers, motility and apoptosis. Material and Methods: C57BL/6 mice (n=7) were exposed to 37-38oC (8 hours/day), for three consecutive days while control mice (n=7) were kept at 23-24oC. Caudal epididymal spermatozoa were collected from control and heat treated mice 16 hours after the last heat treatment to determine the sperm number and motility using a Neubauer haemocytometer and sperm apoptotic changes by dual colorflow cytometry using Annexin V/PE (Annexin V conjugated with phycoerythrin) and 7AAD (7-amino-actinomycin D) stains. Results: There were no significant differences (p>0.05) in sperm numbers between heat treated and control mice, however heating did result in a significant reduction in sperm motility (p<0.05). Apoptosis staining identified four different subpopulations of spermatozoa: (a) live spermatozoa (Annexin V-/7AAD-), (b) early apoptotic spermatozoa with exteriorized phosphotidylserine (PS) receptor and intact plasmalemma (Annexin V+/7AAD-), (c) late apoptotic spermatozoa with PS receptor translocation and leaky plasmalemma (Annexin V+/7AAD+) and (d) dead spermatozoa with damaged plasmalemma with no detectable PS receptor (Annexin V-/7AAD+). Heating resulted in significant reduction in the percentage of live spermatozoa (p<0.05), an increase in early apoptotic (p<0.05), late apoptotic (p<0.05), and dead spermatozoa (p<0.05). Conclusion: This study shows that mice exposed to whole body heat exposure of 37-38oC for 8 hours per day for three consecutive days exhibited early and late apoptotic changes to epididymal spermatozoa. These findings suggest possible adverse effects of exposure to high temperature on the viability of human spermatozoa in the epididymides. In addition, these findings reinforce the importance of temperature during sperm preparation procedures in infertility clinics, and research laboratories.

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 ◽  
...  
Keyword(s):  
Germ Cell ◽  
Sperm Motility ◽  
Cell Apoptosis ◽  
Heat Exposure ◽  
Male Germ Cell ◽  
Whole Body ◽  
Control Group ◽  
Germ Cell Apoptosis ◽  
Heat Treated ◽  
Body Heat

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.

Intermittent sequential pneumatic compression does not enhance whole-body heat loss in elderly adults during extreme heat exposure

2019 ◽  
Vol 44 (12) ◽  
pp. 1383-1386
Author(s):  
Andrew W. D’Souza ◽  
Sean R. Notley ◽  
Robert D. Meade ◽  
Glen P. Kenny
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Heat Loss ◽  
Lower Limb ◽  
Vascular Function ◽  
Heat Exposure ◽  
Extreme Heat ◽  
Whole Body ◽  
Elderly Adults ◽  
Body Heat

Lower-limb intermittent sequential pneumatic compression (ISPC) improves circulation and vascular function in elderly adults. We evaluated the hypothesis that ISPC would also augment whole-body heat loss (WBHL) in elderly adults (aged 69 ± 4 years) resting in extreme heat (40 °C). While ISPC increased mean arterial pressure (91 ± 9 mm Hg) relative to no-ISPC (83 ± 5 mm Hg; P = 0.013) at the end of the exposure, no influence on WBHL was observed (81 ± 7 and 86 ± 11 W for ISPC and no-ISPC, respectively, P = 0.310). Novelty When assessed in elderly adults during an extreme heat exposure, intermittent sequential pneumatic compression augmented mean arterial pressure but did not enhance whole-body heat loss.

scholarly journals The contribution of the mouse tail to thermoregulation is modest

2020 ◽  
Vol 319 (2) ◽  
pp. E438-E446
Author(s):  
Vojtěch Škop ◽  
Naili Liu ◽  
Juen Guo ◽  
Oksana Gavrilova ◽  
Marc L. Reitman
Keyword(s):  
Metabolic Rate ◽  
Heat Loss ◽  
Heat Dissipation ◽  
Whole Body ◽  
Total Heat Loss ◽  
Brown Adipose ◽  
Adrenergic Antagonist ◽  
Similar Body ◽  
And Control ◽  
Body Heat

Understanding mouse thermal physiology informs the usefulness of mice as models of human disease. It is widely assumed that the mouse tail contributes greatly to heat loss (as it does in rat), but this has not been quantitated. We studied C57BL/6J mice after tail amputation. Tailless mice housed at 22°C did not differ from littermate controls in body weight, lean or fat content, or energy expenditure. With acute changes in ambient temperature from 19 to 39°C, tailless and control mice demonstrated similar body temperatures (Tb), metabolic rates, and heat conductances and no difference in thermoneutral point. Treatment with prazosin, an α1-adrenergic antagonist and vasodilator, increased tail temperature in control mice by up to 4.8 ± 0.8°C. Comparing prazosin treatment in tailless and control mice suggested that the tail’s contribution to total heat loss was a nonsignificant 3.4%. Major heat stress produced by treatment at 30°C with CL316243, a β3-adrenergic agonist, increased metabolic rate and Tb and, at a matched increase in metabolic rate, the tailless mice showed a 0.72 ± 0.14°C greater Tb increase and 7.6% lower whole body heat conductance. Thus, the mouse tail is a useful biomarker of vasodilation and thermoregulation, but in our experiments contributes only 5–8% of whole body heat dissipation, less than the 17% reported for rat. Heat dissipation through the tail is important under extreme scenarios such as pharmacological activation of brown adipose tissue; however, non-tail contributions to heat loss may have been underestimated in the mouse.

The effect of whole body heat exposure and of cooling the hypothalamus on antibody titre in the rat

1981 ◽  
Vol 391 (1) ◽  
pp. 25-27 ◽  
Author(s):  
M. Banet ◽  
D. Fischer ◽  
K. U. Hartmann ◽  
H. Hensel ◽  
Ursula Hilling
Keyword(s):  
Antibody Titre ◽  
Heat Exposure ◽  
Whole Body ◽  
Body Heat

scholarly journals Whole-body heat exposure induces membrane changes in spermatozoa from the cauda epididymidis of laboratory mice

2010 ◽  
Vol 12 (4) ◽  
pp. 591-598 ◽  
Author(s):  
Harsha Wechalekar ◽  
Brian P. Setchell ◽  
Eleanor J. Peirce ◽  
Mario Ricci ◽  
Chris Leigh ◽  
...  
Keyword(s):  
Heat Exposure ◽  
Whole Body ◽  
Laboratory Mice ◽  
Membrane Changes ◽  
Cauda Epididymidis ◽  
Body Heat

437. Whole body heat stress induces selective germ cell apoptosis in mice

2008 ◽  
Vol 20 (9) ◽  
pp. 117 ◽  
Author(s):  
H. Wechalekar ◽  
B. P. Setchell ◽  
W. G. Breed ◽  
M. Ricci ◽  
C. Leigh ◽  
...  
Keyword(s):  
Heat Stress ◽  
Germ Cell ◽  
Germ Cells ◽  
Wilcoxon Test ◽  
Whole Body ◽  
Seminiferous Tubules ◽  
Heat Treated ◽  
Significant Difference ◽  
Whole Body Heat Stress ◽  
Body Heat

Introduction: In scrotal mammals, heat stress (43°C/ 20 min) to the scrotum results in germ cell death in the testes1, abnormal spermatozoa, and infertility2 whereas two days of whole body heating (36°C, 12 h/ day) reduces testes weight, sperm numbers and fertility3. The aim of the present study was to determine the intratesticular effects of whole body heating on germ cell maturation and apoptosis. Methods: C57BL/6 mice (n = 16) were housed at 37–38°C for 8 h/ day for 3 days while controls (n = 4) were kept at 23–24°C. Animals from heat treated (n = 4), and control groups (n = 1) were sacrificed at 16 h, 7, 14 and 21 days post exposure to heat. Testes were weighed and analysed by t-test. In testes from each animal, two sections 70µm apart were end labelled for TdT-mediated-dUTP nick (TUNEL). Apoptosis was determined in 200 seminiferous tubules by a colour threshold set in the particle analysis program (Olympus).The tubules were staged as I-VI (early), VII-VIII, IX-X and XI-XII (late) and results analysed using Wilcoxon test. Results: The weights of testes were significantly reduced in heat-treated animals (P < 0.05) at 16 h, 7 and 14 days with no significant difference at 21 days. Apoptosis was significantly higher in the heat-treated group in stages I-VI and XI-XII at 16 h, 7 and 14 days (P < 0.05). In addition, in stages VII-VIII and IX-X apoptosis was significantly higher at 16 h (P < 0.05) with no statistical difference between other time intervals. By day 21, the levels of apoptosis did not differ significantly from the controls in any of the stages (P > 0.05).Conclusion: Whole body heat stress can induce stage and cell specific degeneration of the germ cells in the seminiferous epithelium. The germ cells undergoing apoptosis are spermatogonia, primary spermatocytes and early spermatids. In addition, heat stress produces significant apoptosis of germ cells in the hormone dependent stages VII-VIII immediately after heat stress. (1) Rockett, J.C. et al. (2001) Biol. Reprod. 65:229–239. (2) Banks, S. et al. (2005) Reproduction 129:505–514. (3) Yaeram, J. et al. (2006) Reprod. Fert. Dev. 18:647–653.

scholarly journals Whole body heat exposure modulates acute glucose metabolism

2018 ◽  
Vol 35 (1) ◽  
pp. 644-651 ◽  
Author(s):  
Amy L. Kimball ◽  
Patrick M. McCue ◽  
Michael A. Petrie ◽  
Richard K. Shields
Keyword(s):  
Glucose Metabolism ◽  
Heat Exposure ◽  
Whole Body ◽  
Body Heat
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