NF kappa B, TNF-alpha, TGF-beta, thyoredoxin, nitric oxide, total oxidan status (TOS), total antioxidant status (TAS) levels and thyol dysulfide homeostasis in the androgenetic alopecia

Androgenetic alopecia is the most common cause of hair loss in men. The pathogenic role of DHT (Dihydrotestosterone) in AGA (Androgenetic Alopecia) has been discovered. But androgens affect other components that regulate the growth of the hair follicle. Follicular miniaturization plays a major role in AGA patagonesis. The miniaturization of terminal hairs was associated with periphonal lymphocytic infiltration and fibrosis. Exposure to oxidative stress is effective in the pathogenesis of AGA. Free oxygen radicals activate NF-κB and cause proinflammatory signal activation. NF-κB controls the expression of cytokines effective in inflammation. TNF-α is a proinflammatory cytokine, initiating the extrinsic cell death path and may also increase ROS (Reactive Oxygen Species) production. TGF-β has a key role in fibrosis. Thioredoxin has protection against reactive oxygen species and protection against oxidative stress. NO is a free radical produced from L-arginine by NOS enzymes. Total antioxidant status (TAS) and total oxidant status (TOS) are measured to evaluate oxidative stress globally. Thiols are compounds which can enter into oxidation and reduction reactions. Therefore, they have a critical role in preventing oxidative stress in cells. In our study, microinflammation, perifollicular fibrosis and oxidative stress were investigated in AGA. Serum samples were taken from the patient and control groups. Serum NF-κB, TNF-α, TGF-β1, Thioredoxin, NO, TOS, TAS and Thiol Disulfide Homeostasis were measured and evaluated. In conclusion, serum NF-κB, TNF-α, TGF-β1, Thioredoxin, NO, TOS serum levels were significantly higher in individuals with AGA. TAS, Native Thiol and Total Thiol and Disulfide serum levels were significantly lower in patients with AGA. In patients with androgenetic alopecia, we found that redox balance deteriorated, oxidant agents increased and antioxidant defense decreased. We evaluated the correlation and molecular relationships between the parameters. The androgens in AGA cause oxidative stress by increasing free oxygen radicals. It causes microinflammation and fibrosis. Thus, hair loss is accelerated in patients. Oxidative stress plays an active role in androgenetic alopecia. Understanding of the effects of androgens on the hair follicle cycle is important in terms of developing new and effective treatment methods. In this study, we tried to contribute to the understanding of AGA pathogenesis factors with biochemical oxidant and antioxidant parameters and apoptosis markers.