![]() | Only 14 pages are availabe for public view |
Abstract Vitiligo is an idiopathic, acquired, circumscribed, hypomelanotic skin disorder, characterized by milky white patches of different sizes and shapes. It is due to the destruction of melanocytes resulting in the absence of pigment production of the skin and mucosal surfaces.The etiology of vitiligo is still not known but several theories have been proposed to explain the melanocyte destruction like genetic, neural, cytotoxic, and autoimmune theories. Various precipitating/ aggravating factors also play a role in etiopathogenesis of vitiligo like trauma (physical or emotional) or parasitic infection.Oxidative stress is reported to play a role in progress of vitiligo but there is conflicting evidence for the same. Some researchers report increased total antioxidant levels, others report no change or even decreased levels of these markers like Superoxide Dismutase(SOD), Glutathione peroxidase (GPx), Malondialdehyde (MDA),Nitric Oxide (NO), and Catalase.During oxidative stress, molecular oxygen (O2) is reduced to form superoxide radicals (O 2). Further, superoxide radical’s dismutase to hydrogen peroxide(H2O2) either spontaneously or by the action of Superoxide Dismutase (SOD).Nesfatin-1 was discovered by Oh-I and colleagues for the first time in 2006. They showed that nesfatin-1 is secreted from the hypothalamic nuclei, which are responsible for controlling appetite. |