Thermotolerance for Physiological and Endocrine Regulation of Embryo-Uterine Development

Introduction

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.