The human body, with its innate sensitive ability, tries to keep the free radicals formed due to the natural production of the organism in a line known as oxidant-antioxidant balance. Disruption of this balance is called oxidative stress. The mitochondria constantly produce free oxygen radicals during the body's oxygen consumption. The free oxygen radicals released can be both harmful and beneficial. The role of oxidative stress in the pathogenesis of inflammatory, chronic, or degenerative diseases is known. Transient receptor potential (TRP) channels are non-selective cation channels essential in regulating calcium (Ca2+) concentration in various neuronal and non-neuronal cell types and tissues. It has been reported that excessive Ca2+ influx and oxidative stress caused by TRPM8 channel activation play a role in apoptosis. Therefore, the TRPM8 channel may help prevent oxidative stress-induced damage. Additionally, TRPM8 channels regulate Ca2+ cell homeostasis and function as a cellular sensor and cold temperature transducer. In this review, we examined the role of the TRPM8 cation channel in situations that may be caused by oxidative stress based on recent studies.
