Wetested the hypothesis that hypoxia replicates effects of hyperthermia on reducing number and quality of sperm produced, whereas hyperoxia mitigates effects of hyperthermia. Forty-eight CD-1 mice (~50d old), inspired air with 13, 21, or 95% O2 and were exposed to ambient temperatures of 20 or 36 C(3 2 factorial, six groups) twice for 12h (separated by 12hat 20 C and 21% O2), with euthanasia 14 or 20d after first exposure. Combined for both post-exposure intervals, there were primarily main effects of temperature; mice exposed to 20 vs 36 C had differences in testis weight (110.2 vs 96.9mg, respectively; P<0.0001), daily sperm production (24.7 vs 21.1 106 sperm/g testes, P<0.03), motile sperm (54.5 vs 41.5%, P<0.002), morphologically normal sperm (59.9 vs 45.4%, P<0.002), morphologically abnormal heads (7.3 vs 22.0%, P<0.0001), seminiferous tubule diameter (183.4 vs 176.3mm, P<0.004) and altered elongated spermatids (2.2 vs 15.9, P<0.001). Increasing O2 (from 13 to 95%) affected morphologically abnormal heads (15.4, 10.8 and 17.6%, respectively; P<0.03), seminiferous tubule diameter (175.7, 185.6 and 178.4mm, P<0.003) and total altered spermatids (8.3, 3.3 and 15.2, P<0.05). Our hypothesis was not supported; hypoxia did not replicate effects of hyperthermia with regards to reducing number and quality of sperm produced and hyperoxia did not mitigate effects of hyperthermia. We concluded that hyperthermia per se and not secondary hypoxia was the fundamental cause of heat-induced effects on spermatogenesis and sperm. These findings are of interest to develop evidence-based efforts to mitigate effects of testicular hyperthermia, as efforts should be focused on hyperthermia per se and not on hyperthermia-induced hypoxia.
Kastelic, J.p., Wilde, R., Bielli, A., Genovese, P., Rizzoto, G., Thundathil, J.c. (2019). Hyperthermia is more important than hypoxia as a cause of disrupted spermatogenesis and abnormal sperm. THERIOGENOLOGY, 131, 177-181 [10.1016/j.theriogenology.2019.03.040].
Hyperthermia is more important than hypoxia as a cause of disrupted spermatogenesis and abnormal sperm
Rizzoto G;
2019
Abstract
Wetested the hypothesis that hypoxia replicates effects of hyperthermia on reducing number and quality of sperm produced, whereas hyperoxia mitigates effects of hyperthermia. Forty-eight CD-1 mice (~50d old), inspired air with 13, 21, or 95% O2 and were exposed to ambient temperatures of 20 or 36 C(3 2 factorial, six groups) twice for 12h (separated by 12hat 20 C and 21% O2), with euthanasia 14 or 20d after first exposure. Combined for both post-exposure intervals, there were primarily main effects of temperature; mice exposed to 20 vs 36 C had differences in testis weight (110.2 vs 96.9mg, respectively; P<0.0001), daily sperm production (24.7 vs 21.1 106 sperm/g testes, P<0.03), motile sperm (54.5 vs 41.5%, P<0.002), morphologically normal sperm (59.9 vs 45.4%, P<0.002), morphologically abnormal heads (7.3 vs 22.0%, P<0.0001), seminiferous tubule diameter (183.4 vs 176.3mm, P<0.004) and altered elongated spermatids (2.2 vs 15.9, P<0.001). Increasing O2 (from 13 to 95%) affected morphologically abnormal heads (15.4, 10.8 and 17.6%, respectively; P<0.03), seminiferous tubule diameter (175.7, 185.6 and 178.4mm, P<0.003) and total altered spermatids (8.3, 3.3 and 15.2, P<0.05). Our hypothesis was not supported; hypoxia did not replicate effects of hyperthermia with regards to reducing number and quality of sperm produced and hyperoxia did not mitigate effects of hyperthermia. We concluded that hyperthermia per se and not secondary hypoxia was the fundamental cause of heat-induced effects on spermatogenesis and sperm. These findings are of interest to develop evidence-based efforts to mitigate effects of testicular hyperthermia, as efforts should be focused on hyperthermia per se and not on hyperthermia-induced hypoxia.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
