Pathogenesis of Heat-Induced Infertility in Male Mammals
Date
2020-09-04
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Abstract
Testicular temperature must be 3-5 ÂșC below body temperature for physiological spermatogenesis and testicular function. Therefore, increased testicular temperatures, either the entire body or just the testes, reduce sperm quality and fertility. Our understanding regarding the pathophysiology of testicular heat stress is unclear. There is a long-standing dogma that as testicular temperature increases, there is no change in blood flow, and the testes, which are regarded as physiologically functioning on the brink of hypoxia, undergo frank hypoxia. However, recent data challenged this dogma, indicating that temperature itself was the major pathological agent. Therefore, this thesis was developed to further investigate the subject. In a series of five studies, the overall aim was to investigate changes in testicular blood flow in response to testicular heat stress and its pathophysiology on testes and testicular function. In the first two studies, we investigated how heat stress and hypoxia affect testicular blood flow and metabolism in rams; both treatments increased testicular blood flow which supported metabolic needs, with no indications of hypoxia. The third study was a comparison of responses between Bos indicus and Bos taurus bulls to increased testicular temperature. Once again, testicular blood flow significantly increased, supporting metabolic needs, with no indications of hypoxia. These three studies provided new knowledge to debunk the previous dogma and to support the new understanding that temperature itself was the main pathological factor of testicular heat stress. In the last two studies, we investigated how heat stress modulates gene expression in bull and mouse testes. Heat stress caused modulation of gene P53 and components of the P53-dependent apoptotic pathway, also upregulation of genes associated with the antioxidant (GPX1) and chaperone systems (Hsp70) and downregulation of the StAR gene and reduced testosterone concentrations (impaired steroidogenesis). Collectively, these studies provided novel information regarding testicular vascular physiology under local heat stress and described several factors associated with its pathophysiology in the testes. Lastly, it is expected that these findings will serve as a strong base for new studies in this area, to elucidate in more detail, how heat stress affects reproduction in male mammals.
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Heat stress, testes, sperm, gene expression
Citation
Rizzoto, G. (2020). Pathogenesis of Heat-Induced Infertility in Male Mammals (Doctoral thesis, University of Calgary, Calgary, Canada). Retrieved from https://prism.ucalgary.ca.