Do chilling injury and heat stress share the same mechanism of injury in oocytes?

Chilling injury is the major limiting factor for successful cryopreservation of both human and animal oocytes. Maternal hyperthermia is the main reason for summer infertility in dairy cows. In this paper, we will present evidence for the involvement of membrane lipid composition and its thermotrophic behavior and the mechanism by which chilling injury and/or heat stress disrupt oocytes' developmental competence. Although oocyte and single zygote are similar in shape and size, the oocyte is known to be very sensitive to cryopreservation, whereas, the zygote is successfully cryopreserved. Recently, we have shown that the lipid-phase transition (LPT) in human MII oocytes occurs at about 20 degrees C, while the LPT temperature of zygotes is lower by 10 degrees C. Similarly, the LPT in oocytes collected from dairy cows was found to be elevated by 10 degrees C in the summer vs. the winter. This feature was associated with alterations in membrane lipid composition. In particular, during the winter, the oocyte membrane is composed mainly of mono- and polyunsaturated fatty acids while in the hot summer, it is composed of more saturated fatty acids. In another study, we showed that exposure of bovine oocytes to physiologically relevant heat shock increases the proportion of oocytes that undergo apoptosis, presumably via sphingomyelin hydrolysis and ceramide formation (i.e. the sphingomyelin apoptosis pathway). Using a mouse model, we have recently shown that hyperthermia of 1.5 degrees C affects the follicle enclosed oocyte as determined by lower developmental competence. Given the importance of the membrane's composition and integrity, it appears that alterations in the oocyte-membrane underlie the disruption of developmental competence in mammalian oocytes exposed to thermal stress (i.e. chilling injury or heat shock).