Thermotolerance for Physiological and Endocrine Regulation of Embryo-Uterine Development

Thermotolerance for Physiological and Endocrine Regulation of Embryo-Uterine Development

Sameena Khanday, Rayees Ahmad, Guru Dutt Sharma
Copyright: © 2021 |Pages: 23
DOI: 10.4018/978-1-7998-4480-8.ch007
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Hyperthermia affects most aspects of reproductive performance in mammals by compromising the physiology of reproductive tract, through hormonal imbalance, disrupting the development and maturation of oocyte, causing embryonic mortality, abortion, growth retardation, and major developmental defects. Heat stress reduces the steroidogenic capacity of its theca and granulosa cells by altering the efficiency of follicular selection resulting in drop of luteinizing hormone and estradiol secretions from the dominant follicle in the plasma, reduced intensity, and duration of estrus expression. The mechanism for the developmental stage-dependent change in heat tolerance is considered to be the accumulation of antioxidants in embryos in response to heat-inducible production of reactive oxygen species. Morula or blastocysts can repair heat-induced misfolded or unfolded proteins or facilitate DNA damage induced apoptosis. Therefore, embryo transfer (ET) that can bypass the heat-sensitive stage could be a good solution to improve the conception rate under heat stress. However, further research is required to improve the reduction in pregnancy rates due to summer heat stress.
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Heat stress, also known as hypothermia is a condition in which the animal body temperature is elevated beyond normal temperature and is not able to sufficiently dissipate excess heat.It is a major significant factor contributing to reduced fertility in mammalians, which is a global issue and resulting in heavy economic losses. Researchers have secured major success and achievements mainly in reproductive technology; hormone levels, blood biochemical and immunological parameters and so on. This chapter reviews the effects and possible mechanisms of elevated maternal body temperature on reproductive efficiency of animals and humans. The early embryo–maternal dialogue that begins very early in the life of the embryo is criticalfor its own implantation. Successful embryo implantation involves the appropriate interaction between the receptive endometrium and an implantation-competent blastocyst, which occurs in a limited time period known as “the window of implantation” (Ma et al., 2003). A bidirectional communication is necessary for normal implantation thus the success of pregnancy, since disruptions will generate adverse development outcomes including decidualization and placentation, with potential loss of the pregnancy (Lim and Wang, 2010). Failure of implantation is an unsolved problem in reproductive medicine and is considered to be an important cause of infertility. Implantation is a complex biological process.

A disturbance in this complex embryo–maternal dialogue is the basic reasons for which majority of pregnancies are terminated at the end of the preimplantation period. This two way cumminication is precisely maintained by maternal hormones in particular, ovarian estrogens and progesterone (Conneely et al., 2002; Curtis Hewitt et al., 2002). The highly ordered events of cell migration, proliferation, specification or differentiation and programmed cell death (apoptosis) that illustrate the prenatal growth and development of the mammalian conceptus through to the potential effects of neo-natal and post-natal heat stress susceptibility. Maternal temperature elevations negatively affectseveral aspects related to pregnancy such as successful fertilization, establishment and maintenance of pregnancy such as production of reproductive hormones, uterine health, oocyte and embryo quality, and embryonic development. Earlier research has revealed that elevated maternal body temperatures induces embryonic and foetal mortality, growth retardation and developmental defects depends on the duration of the elevation in maternal body temperature and the specific phase of development during which the thermal dose is delivered. Direct heating of the embryo or foetus has shown a similar spectrum of effects signifying a direct effect of heat on development; disruption in maternal physiology may introduce additional factors complicating the overall interpretation. Studies have reported that raised maternal body temperatures in humans during pregnancy, either through fever or some other form of heating led to developmental defects. Two potential mechanisms associated with mitochondrial function-apoptosis and oxidative stress have been documented (for review, see Roth, 2017). Thermal stress not only affects cell function directly, but also leads to disruptions in the DNA or function of organelles by inducing oxidative stress (Roth, 2015; Lord and Averill, 2002). Oxidative stress agents like reactive oxygen species (ROS) is a major causative agent of DNA damage (leading to cell death), disrupt the mitochondrial function, lipid peroxidation, causing abnormal expression of genes and protein synthesis and ultimately result in apoptosis (Loven, 1998; Averill, 2002). Therefore, one factor that contrary influence the oocytes and embryos has been considered to be the increase of oxidative stress status originating from heat stress (Edwards et al., 2001; Hansen, 2007). Moreover, the change from maternal gene expression to zygotic/embryonic gene expression could be related with thermo tolerance in oocytes and embryos.

Key Terms in this Chapter

Reactive Oxygen Species (ROS): A phrase used to describe a number of reactive molecules and free radicals derived from molecular oxygen. ROS play a key role as a messenger in normal cell signal transduction and cell cycling.

Oxidative Stress: A condition where the levels of ROS significantly overwhelm the capacity of antioxidant defenses, leading to potential damage in a biological system.

Blastocyst: A thin–walled hollow structure in early embryonic development that contains a cluster of cells called the inner cell mass from which the embryo arises.

Hyperthermia: Abnormally high body temperature caused by a failure of the heat-regulating mechanisms of the body to deal with the heat coming from the environment.

Estradiol: A female sex hormone produced by the ovaries, adrenal gland, and also the placenta during pregnancy.

Prostaglandin F2-Alpha: A stable prostaglandin that stimulates the contraction of uterine and bronchial smooth muscle and produces vasoconstriction (tightening) in some blood vessels. It is used for the induction of abortion, for evacuation of the uterus after a missed abortion.

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