Summer-induced heat stress is the primary cause of fertility and has severe implications for livestock output, animal welfare, and overall health. Within the Thermoneutral zone (TNZ) range, animals maintain a physiological body temperature of 38.4ºC to 39.1ºC. Testicular tissue can become hypoxic and experience oxidative tissue stress if this is not accompanied by adequate blood flow to maintain an adequate amount of oxygenation. The awkwardness between generating reactive oxygen species (ROS) and detoxifying with antioxidants is known as oxidative stress. Almost all facets of cellular activity are impacted by reactive oxygen species (ROS). Oxidative stress is a major cause of heat stress in germ cells and leads to apoptosis, mostly in spermatocytes and early spermatids. There are correlations with decreased fertility due to DNA damage, early cell death, protein malfunction, and lipid peroxidation, all of which easily occur in spermatozoa if there is an oxidative stress condition. Heat stress affects different cellular components of the testis approximately 14–21 days after exposure. Testicular heat stress first causes an increase in morphological defects, followed by increased sperm lipid peroxidation, affecting mitochondrial membrane potential, sperm motility, plasma membrane integrity, and sperm DNA fragmentation.