Impact of Heat Stress on Bovine Sperm Quality and Competence (original) (raw)
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Heat stress effects on bovine sperm cells: a chronological approach to early findings
International Journal of Biometeorology, 2020
Testicular heat stress affects sperm quality and fertility. However, the chronology of these effects is not yet fully understood. This study aimed to establish the early sequential effects of heat stress in bull sperm quality. Semen and blood samples of Nellore breed bulls were collected and distributed into control and testicular heat stress (scrotal bags/96 h) groups. Semen samples were evaluated for sperm motility, abnormalities, plasma membrane integrity, acrosomal membrane integrity, mitochondrial membrane potential, sperm lipid peroxidation, seminal plasma lipid peroxidation, and DNA fragmentation. Blood plasma was also evaluated for lipid peroxidation. An increase in sperm abnormalities was observed 7 days following heat stress. After 14 days, sperm lipid peroxidation increased and mitochondrial membrane function, sperm motility, and plasma membrane integrity decreased. Heat stress effects were still observed after 21 days following heat stress. An increase in sperm DNA fragmentation was observed as a late effect after 28 days. Thus, the initial effects of heat stress (i.e., increasing sperm abnormalities and lipid peroxidation) suggest the presence of oxidative stress in the semen that alters mitochondrial function, sperm motility, plasma membrane integrity, and belatedly, DNA fragmentation. Although sperm abnormalities persisted and increased over time, sperm lipid peroxidation, in turn, increased only until 21 days after heat stress. In this regard, these findings provide a greater understanding of the chronological effects of experimentally induced heat stress on bovine sperm, providing valuable insights about spermatogenesis during the first 28 days following heat stress.
Heat exposure induces oxidative stress and DNA damage in the male germ line
Biology of reproduction, 2018
The reproductive consequences of global warming are not currently understood. In order to address this issue we have examined the reproductive consequences of exposing male mice to a mild heat stress. For this purpose, adult male mice were exposed to an elevated ambient temperature of 35°C under two exposure models. The first involved acute exposure for 24 hours, followed by recovery periods of between 1 day and 6 weeks. The alternative heating regimen involved a daily exposure of 8 hours for periods of 1 or 2 weeks. In our acute model, we identified elevated sperm mitochondrial ROS generation (p < 0.05), increased sperm membrane fluidity (p < 0.05), DNA damage in the form of single strand breaks (p < 0.001) and oxidative DNA damage (p < 0.05); characteristic of an oxidative stress cascade. This DNA damage was detected in pachytene spermatocytes (p < 0.001) and round spermatids (p < 0.001) isolated from testes after 1 day heat recovery. Despite these lesions, the s...
Oxidative Medicine and Cellular Longevity, 2016
Higher temperatures lead to an increase of testicular metabolism that results in spermatic damage. Oxidative stress is the main factor responsible for testicular damage caused by heat stress. The aim of this study was to evaluate lasting effects of heat stress on ejaculated sperm and immediate or long-term effects of heat stress on epididymal sperm. We observed decrease in motility and mass motility of ejaculated sperm, as well as an increase in the percentages of sperm showing major and minor defects, damaged plasma and acrosome membranes, and a decrease in the percentage of sperm with high mitochondrial membrane potential in the treated group until one spermatic cycle. An increased enzymatic activity of glutathione peroxidase and an increase of stressed cells were observed in ejaculated sperm of the treated group. A decrease in the percentage of epididymal sperm with high mitochondrial membrane potential was observed in the treated group. However, when comparing immediate and long...
Animal Production Science, 2017
Temperature is a crucial factor in mammalian spermatogenesis. The scrotum, pampiniform plexus, and cremaster and dartos muscles in mammals are specific adaptations to ensure sperm production in a regulated environment 4−6°C below internal body temperature. However, the limited endogenous antioxidant systems inherent in mammalian spermatozoa compounded by the loss of cytosolic repair mechanisms during spermatogenesis, make the DNA in these cells particularly vulnerable to oxidative damage. Boar sperm is likely to be more susceptible to the effects of heat stress and thus oxidative damage due to the relatively high unsaturated fatty acids in the plasma membrane, low antioxidant capacity in boar seminal plasma, and the boar’s non-pendulous scrotum. Heat stress has a significant negative impact on reproductive performance in piggeries, which manifests as summer infertility and results in productivity losses that amount to millions of dollars. This problem is particularly prevalent in tr...
Heat stress impact on bovine female reproduction
2022
Heat stress (HS), a harmful condition affecting animal production, reproduction, and welfare, occurs when an animal is exposed to temperatures that exceed its thermal comfort zone. Several nonspecific body responses involving neural, neuroendocrine, and immune systems are triggered to keep homeostasis in such conditions. These responses, primarily directed to cooling the body, also impact the hypothalamic-pituitary-gonadal axis, compromising the bovine female’s release of gonadotropins. Heat stress also promotes reactive oxygen species accumulation in ovarian cells, impairing protein folding and refolding, triggering antioxidant and DNA protection mechanisms. These mechanisms, directed to reduce cell metabolism and increase survival chances, are not always sufficient to protect the cell and result in apoptosis. Heat stress’s systemic and cellular consequences impact ovarian estradiol production, estrous behaviors, follicular development, oocytes and embryo competence, conception rat...
2014
Heat stress has long been recognised as a cause of subfertility in farm animals. The objectives of the present study were to elucidate the effect of heat stress on sperm function and involvement of the mitogen-activated protein kinase (MAPK) 14 signalling pathway. Spermatozoa incubated for 4 h at a physiological temperature (38.58C) exhibited significantly (P , 0.05) reduced motility, plasma membrane integrity and mitochondrial potential compared with nonincubated spermatozoa; the reductions in these parameters were more severe following incubation at a hyperthermic (418C) temperature (P , 0.01). Percentages of fertilisation and embryo development were highly affected in spermatozoa incubated at 418C compared with non-incubated spermatozoa (P , 0.01). Similarly, embryo quality was adversely affected by sperm incubation at 418C, as indicated by a higher apoptotic cell ratio in Day 7 blastocysts compared with that in the non-incubated control group (14.6% vs 6.7%, respectively; P , 0.01). Using SB203580 (10 mg mL À1 ), a specific inhibitor of the p38 MAPK pathway, during sperm hyperthermia reduced MAPK14 activation (24.9% vs 35.6%), increased sperm motility (45.8% vs 26.5%) and reduced DNA fragmentation (16.9% vs 23.4%) compared with the untreated control group, but did not improve subsequent fertilisation and embryo development. In conclusion, heat stress significantly affects the potential of spermatozoa to penetrate oocytes, as well as subsequent embryo development and quality. Notably, the data show that the MAPK14 signalling pathway is largely involved in heat-induced sperm damage. However, further research is needed to elucidate other signalling pathways possibly involved in heat-induced sperm damage.
Heat stress, a serious threat to reproductive function in animals and humans
Molecular Reproduction and Development
Global warming represents a major stressful environmental condition that compromises the reproductive efficiency of animals and humans via a rise of body temperature above its physiological homeothermic point (heat stress [HS]). The injuries caused by HS on reproductive function involves both male and female components, fertilization mechanisms as well as the early and late stages of embryofetal development. This occurrence causes great economic damage in livestock, and, in wild animals creates selective pressure towards the advantages of better-adapted genotypes to the detriment of others. Humans undergo several types of stress, including heat, and these represent putative causes of ongoing progressive decay in procreation; an increasing number of remedies in the form of antioxidant preparations are now being proposed to counteract the effects of stress. This review aims to describe the results of the most recent studies that aimed to highlight these effects and to draw information on the mechanisms acting as the basis of this problem from a comparative analysis.
Pathogenesis of Heat-Induced Infertility in Male Mammals
2020
Testicular temperature must be 3-5 ºC 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 iii 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.
141 Antioxidant Supplementation Alleviates DNA Damage in Boar Sperm Induced by Tropical Heat Stress
Reproduction, Fertility and Development, 2018
Seasonal heat stress is known to significantly diminish reproductive performance in pigs, particularly in the tropics, costing the industry millions in annual losses. The boar’s reduced capacity to sweat and non-pendulous scrotum, combined with the widespread use of European breeds in the tropics, makes this species particularly vulnerable to heat stress. Although heat stress is traditionally considered a sow problem, recent mouse studies demonstrate that heat stress-induced sperm DNA damage can result in arrested development and loss of early embryos. Our study investigated the impact of tropical summer heat stress on the quality and DNA integrity of boar sperm, and trialled antioxidant supplementation to alleviate the problem. Data, expressed as mean ± SEM, were analysed by one-way repeated-measures ANOVA with pairwise Bonferroni tests. Motility of sperm obtained from Large White boars (n = 5) housed in the dry tropics of Townsville, North Queensland, Australia, was characterised ...