New Light on UV-B-Induced Effect in Skin

Excessive exposing to ultraviolet (UV-B) radiation is responsible for the majority of cutaneous damage and is considered to be the greatest in quantity important etiologic factor in human skin cancer. a great deal of of the adverse effects of UV-B particularly skin cancer, are mediated by means of its damage to the DNA and generation of reactive oxygen species (ROS) which proceeds in gene mutations and oxidative stres Skin is endowed with elaborate antioxidant defense mechanisms to cope with ROS-mediated oxidative damage. Among the cutaneous antioxidants, the tripeptide glutathione (GSH) plays an important part in protecting skin cells from ROS-mediated oxidative damage by the agency of directly scavenging ROS and serving as a coenzyme in GSH peroxidase- or GSH-S-transferase-catalyzed reaction and facilitating DNA repair and apoptosis. The molecular mechanism behind these diversified issues of GSH has been a subdue of many investigations but is still incompletely understood. In this issue (pp 191-196) Zhu and Bowden provide evidence that the primary mechanism by the agency of which UV-B irradiation of human keratinocytes causes GSH depletion is [i]or[/i] part of to the other inhibition of a cysteine transporter combination of parts to form a whole on the cell membrane. It remains to be seen whether these confined apartment culture data can be translated to UV-B-induced consequences in human skin and whether this knowledge could be useful in developing a strategy to preserve skin cells against UV-induced oxidant injury. single can envision the photochemopreventive approach with the use of topical supplementation of cysteine precursor for skin protection.

Hasan Mukhtar

Copyright American Society of Photobiology Sep/Oct 2004

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