Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

Erythrocyte oxidant/antioxidant status in essential hyperhidrosis.

Authors: Karaca, S  Kulac, M  Uz, E  Mollaoglu, H  Yilmaz, HR 
Citation: Karaca S, etal., Mol Cell Biochem. 2006 Oct;290(1-2):131-5. Epub 2006 May 23.
Pubmed: (View Article at PubMed) PMID:16718367
DOI: Full-text: DOI:10.1007/s11010-006-9177-8

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.


Disease Annotations
Objects Annotated

Additional Information

CRRD Object Information
CRRD ID: 9479745
Created: 2014-09-08
Species: All species
Last Modified: 2014-09-08
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.