Cryostorage and oxidative stress in mammalian spermatozoa

Abstract

Although cryopreservation of ejaculated sperm has been in clinical and agricultural use for decades, it is not completely clear how the damage that sperm incur as a result of cryopreservation contributes to fertilization failure, or embryonic or fetal loss. Oxygen is required for life, but oxidative metabolism, particularly during low temperature storage, of biological molecules can be potentially toxic due to the formation of reactive oxygen species (ROS) that can modify cell functions or viability. A limited ability to store antioxidant enzymes combined with a membrane rich in unsaturated fatty acids makes spermatozoa particularly susceptible to oxidative stress and peroxidative attack by ROS, specifically superoxide anion and hydrogen peroxide. This chapter outlines the primary mechanisms of sperm damage during cryopreservation and loss of subsequent fertility and discusses the potential mechanisms of DNA/chromosomal fragmentation and damage, lipid peroxidation, and intracellular ice formation and associated cell damage. The origin of ROS in sperm is discussed as well as how ROS are processed and ultimately scavenged by sperm.