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      Effects of heat stress on mammalian reproduction.

      Philosophical Transactions of the Royal Society B: Biological Sciences
      Adaptation, Physiological, Animals, Body Temperature Regulation, Hot Temperature, Mammals, physiology, Stress, Physiological

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          Abstract

          Heat stress can have large effects on most aspects of reproductive function in mammals. These include disruptions in spermatogenesis and oocyte development, oocyte maturation, early embryonic development, foetal and placental growth and lactation. These deleterious effects of heat stress are the result of either the hyperthermia associated with heat stress or the physiological adjustments made by the heat-stressed animal to regulate body temperature. Many effects of elevated temperature on gametes and the early embryo involve increased production of reactive oxygen species. Genetic adaptation to heat stress is possible both with respect to regulation of body temperature and cellular resistance to elevated temperature.

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          Natural hypometabolism during hibernation and daily torpor in mammals.

          Daily torpor and hibernation are the most powerful measures of endotherms to reduce their energy expenditure. During entrance into these torpid states metabolic rate is suppressed to a fraction of euthermic metabolism, paralleled by reductions in ventilation and heart rate. Body temperature gradually decreases towards the level of ambient temperature. In deep torpor body temperature as well as metabolic rate are controlled at a hypothermic and hypometabolic level. Torpid states are terminated by an arousal where metabolic rate spontaneously returns to normal levels again and euthermic body temperature is established by a burst of heat production. In recent years some of the cellular mechanisms which contribute to hypometabolism have been disclosed. Transcription, translation, as well as protein synthesis are largely suppressed. Cell proliferation in highly proliferating epithelia like the intestine is suspended. ATP production from glucose is reduced and lipids serve as the major substrate for remaining energy requirements. All these changes are rapidly reverted to normometabolism during arousal. Hibernation and daily torpor are found in small mammals inhabiting temperate as well as tropical climates. It indicates that this behaviour is not primarily aimed for cold defense, instead points to a general role of hypometabolism, as a measure to cope with a timely limited or seasonal bottleneck of energy supply.
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            Scrotal heat stress effects on sperm viability, sperm DNA integrity, and the offspring sex ratio in mice.

            Evidence exists to suggest detrimental effects of heat stress on male fertility. This study was designed to assess the effects of scrotal heat stress on mature and developing sperm in a mouse model. After receiving shock heat treatment (42 degrees C for 30 min), mature spermatozoa were recovered from the epididymis hours (6) or Days (7, 14, 21, 28, 60) later, to determine the variables: number of spermatozoa, sperm viability, motility and progressive motility, sperm DNA integrity as established by the TUNEL method, embryo implantation rate, and sex ratio of the fetuses conceived using the heat-exposed spermatozoa. Our results indicate that transient mild heat treatment does not affect in the same way the different types of male germ cells. Spermatocytes present within the testis at the time of heat stress resulted into a lower concentration of spermatozoa with reduced viability and low motility. Even though, DNA integrity of spermatozoa resulting from spermatocytes was also compromised by heat stress, the higher degree of DNA damage was found among spermatozoa resulting from spermatids present within the testis at the time of heat stress. At last, heat shock effect on spermatozoa present in the epididymis at the time of thermal stress resulted into a sex ratio distortion. These findings point to a higher sensitivity of spermatocytes to heat exposure and also suggest a different response of X and Y chromosome-bearing spermatozoa to heat stress that warrants further investigation. (c) 2007 Wiley-Liss, Inc.
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              A single, mild, transient scrotal heat stress causes hypoxia and oxidative stress in mouse testes, which induces germ cell death.

              Spermatogenesis is a temperature-dependent process, and increases in scrotal temperature can disrupt its progression. We previously showed that heat stress causes DNA damage in germ cells, an increase in germ cell death (as seen on TUNEL staining), and subfertility. The present study evaluated the stress response in mouse testes following a single mild transient scrotal heat exposure (40 degrees C or 42 degrees C for 30 min). We investigated markers of three types of stress response, namely, hypoxia, oxidative stress, and apoptosis. Heat stress caused an increase in expression of hypoxia-inducible factor 1 alpha (Hif1a) mRNA expression and translocation of HIF1A protein to the germ cell nucleus, consistent with hypoxic stress. Increased expression of heme oxygenase 1 (Hmox1) and the antioxidant enzymes glutathione peroxidase 1 (GPX1) and glutathione S-transferase alpha (GSTA) was consistent with a robust oxidative stress response. Germ cell death was associated with an increase in expression of the effector caspase cleaved caspase 3 and a decrease in expression of the protein inhibitor of caspase-activated DNase (ICAD). Reduced expression of ICAD contributes to increased activity of caspase-activated DNase and is consistent with the increased rates of DNA fragmentation that have been detected previously using TUNEL staining. These studies confirmed that transient mild testicular hyperthermia results in temperature-dependent germ cell death and demonstrated that elevated temperature results in a complex stress response, including induction of genes associated with oxidative stress and hypoxia.
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                Author and article information

                Journal
                19833646
                2781849
                10.1098/rstb.2009.0131

                Chemistry
                Adaptation, Physiological,Animals,Body Temperature Regulation,Hot Temperature,Mammals,physiology,Stress, Physiological

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