**5. Different cellular alteration induced by the heat stress in bovine oocyte**

The processes by which impact of high temperature affect physiology of oocyte is still not identified but some studies consider that it has been identified that high temperature can damage the cell structures and organelles depending on the basis of temperature [1]. In biological membranes, cytoplasmic and nuclear compartments, heat induce can cause cellular damage in bovine oocytes had been observed. However, evidence suggests that the cytoplasm of the oocyte is more vulnerable towards negative effects of high temperatures as compared to the nucleus [1]. Heat stress may also prevent oocytes from maturing their nuclei, resulting in a decline in polar body charge. Heat stress perhaps, can cause oocytes cytoskeletal structure to be disrupted [9]. In the cumulus oophorus complex however, heat stress controls the appearance of HSP70, the apoptotic gene caspase-3 and other antioxidant superoxide dismutase (SOD1), catalyse (CAT), and Complexin (CPX4). These changes in gene regulation resemble coefficient of coincidence (COC) self-defence mechanisms when they are exposed to heat stress. The 70 kilo Dalton heat shock proteins (HSP70) is a multiple effect factor that keeps the intracellular surroundings are stable and decline cell death [9]. By controlling Caspase-3 and cytochrome c, HSP70 expression can also defend cells from apoptosis [9]. The higher level of HSP70 appears to aid oocyte survival from heat stress by up regulating SPKH1, BCL-2, SOD1, CAT, and CPX4 while down adaptable p53. The changes can be brought by heat shock in bovine oocytes because of lack of nuclear maturation. The oocytes that entered metaphase II phase (MII) following In vitro maturation (IVM) was decreased germinal vesicle (GV) stage [1] and maturation *Adverse Impact of Heat Stress on Bovine Development: Causes and Strategies for Mitigation DOI: http://dx.doi.org/10.5772/intechopen.99307*

of oocytes [1]. By growing the amount of metaphase I (MI) in oocytes. Heat shock stopped meiotic progression. On the other hand, in one study it is demonstrated that heat shock at 41°c after 16 to 18 hours it increases the maturation of nuclear and also increasing amount of MII oocytes [1]. The high temperature can cause cellular harm in oocytes of bovine observed in the cellular compartment along with region of cytoplasmic and in nucleus. The cytoskeleton of oocyte gets affected when it comes in contact of high temperature. The Heat-induced shows interruption of microtubules and microfilaments affects chromosome segregation at the time of fertilisation and cell division, as well as the division of cellular structures like cortical granules and mitochondria. On the other hand, heat shock also causes affect to DNA fragmentation and lowers mitochondrial activity in bovine oocytes, implying that the heat-induced mitochondrial apoptotic pathway is activated for combat the low fertility caused by heat stress, a variety of methods have been used. In bovine oocytes, molecules like IGF-I, caspase inhibitors, and the sphingolipid (S1P) have recently been identified as thermoprotective factors. This factors improved oocyte developmental competence and rescued many cellular functions that had impaired by high temperatures. As a result, identifying and characterisation of cellular thermoprotective molecules may be a viable option for reducing the impact of elevated temperature on reproductive function.
