Erythrocyte oxidant/antioxidant status in essential hyperhidrosis


Karaca S., Kulac M., Uz E. , Mollaoglu H., Yilmaz H. R.

MOLECULAR AND CELLULAR BIOCHEMISTRY, vol.290, pp.131-135, 2006 (Journal Indexed in SCI) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 290
  • Publication Date: 2006
  • Doi Number: 10.1007/s11010-006-9177-8
  • Title of Journal : MOLECULAR AND CELLULAR BIOCHEMISTRY
  • Page Numbers: pp.131-135
  • Keywords: essential hyperhidrosis, catalase, superoxide dismutase, glutathione peroxidase, malondialdehyde, NITRIC-OXIDE SYNTHASE, SUPEROXIDE-DISMUTASE, GLUTATHIONE-PEROXIDASE, SWEAT GLAND, CATALASE, MACROPHAGES

Abstract

Essential Hyperhidrosis is a disorder of excessive, bilateral, and relatively symmetric sweating occurring in the axillae, palms, soles, or craniofacial region without obvious etiology. Nitric oxide may play a physiological part in the production and/or excretion of sweat in skin eccrine glands. Tempol, a SOD mimetic, increases the half-life of NO and results in vasodilatation, hypotension, and reflex activation of sympathetic nervous system. Reactive oxygen species (ROS) may directly activate both central and peripheral sympathetic nervous system activity. We assessed the levels of malondialdehyde (MDA), the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) of red blood cells in patients with essential hyperhidrosis (n = 31) compared to age-and sex-matched healthy controls (n = 28). Erythrocyte activities of SOD and level of MDA were detected significantly higher (p = 0.020, p = 0.004 and respectively) and activities of CAT and GSH-Px were significantly lower (p = 0.0001, p = 0.0001 respectively) in patients than controls. Our results support the hypothesis that oxidative damage resulting from increased ROS production along with insufficient capacity of antioxidant mechanisms may be involved in pathogenesis of EH.