Abstract
One of the expected effects of mammalian developmental defects is a rise in air temperature. Heat stress adversely affects embryo oogenesis, oocyte maturation, fertilization, and implantation. The number of defects caused by heat stress in all mammals is almost identical, but each species has its own particular sensitivity to specific defects. It suggests that genotype may have a significant effect on the type of defect, its occurrence, and its extent. By heat output and loss, the body temperature is usually preserved in a restricted range, but the equilibrium can be disrupted by illness, inadequate nutrition, and severe environmental temperature. Elevated maternal temperature during pregnancy, either by fever or any other means of heating, may result in embryo death, retarded development, abortion, and many embryonic defects such as cell proliferation, migration, differentiation and apoptosis or programmed cell death, structural and functional defects, and changes in maternal physiology. Maternal heat stress also reduces the levels of placental hormones. This chapter deals with the heat stress effect on reduction of reproductive function, implantation defects, etc. of different animals and humans.
TopEffects Of High Temperature
The closeness between a portion of the impacts of heat and the impacts of ionizing radiation, especially in their targeting of multiplying cells, have been accounted by Wanner and Edwards (1983). Also, harm to veins and the placenta will prompt further disturbance of developmental procedures. These impacts can be changed somewhat by the cell 'heat shock' reaction, which gives some security to uncovered undeveloped organisms. Various components can prompt premature birth and fetal development retardation. Killing of cells warmed during division is a significant element of the heat damaged embryonic brain and face and can be found immediately after short portion of heat. Close to a moderate rise of temperature (2-30C) given to guinea pig embryos during early stages of brain development (day 21 post-origination), mitotic cells show clustering of chromosomes and die. At higher heights (3-40C), cells in S-stage (DNA replication stage) die by apoptosis from 6 hours after exposure, significantly higher temperature may cause prominent degrees of this type of cell death. The imperfections coming about because of limited regions of cell death are normally very distorting and self-evident, for instance neural tube defects (NTD). Heat at later stages, for instance in day 21 guinea pig undeveloped organisms, causes a more extensive, progressively diffuse circulation of cell death and results in a proportional miniature of the normal brain (Edwards et al., 2003).