Author/Authors :
Reiter, Russel J. University of Texas Health Science Center - Department of Cellular and Structural Biology, USA , Fuentes-Broto, Lorena University of Texas Health Science Center - Department of Cellular and Structural Biology, USA , Paredes, Sergio D. University of Texas Health Science Center - Department of Cellular and Structural Biology, USA , Tan, Dun-Xian University of Texas Health Science Center - Department of Cellular and Structural Biology, USA , Garcia, Joaquin J. University of Zaragoza - Department of Pharmacology and Physiology, Spain
Title Of Article :
Melatonin and the pathophysiology of cellular membranes
شماره ركورد :
18680
Abstract :
The ability of melatonin to influence the physiology of cell membranes is reviewed in this report. Publications related to this field from 1993 – present. Melatonin is a ubiquitously acting indoleamine which is associated with a variety of important functions within both unicellular and multicellular organisms. By virtue of its ability to protect lipids from free radical damage, melatonin is remarkably beneficial in preserving the morphological and functional integrity of cell membranes. In doing so, it reduces the quantity of oxidized lipids in membranes and maintains them at optimal fluidity, i.e., prevents them from becoming rigid. This contributes significantly to the function of proteins (receptors, channels, pores, etc.) in the cell membranes and helps in preserving the normal physiology of the cells. In addition to these indirect effects of melatonin on membrane function, there is evidence that this indoleamine also may act directly on channels assisting membranes in maintaining proper ion gradients and current. The role of melatonin in the functioning of membrane channels and pores is an area of research that should be experimentally exploited.
From Page :
1
NaturalLanguageKeyword :
Melatonin , cell membranes , lipid peroxidation , membrane channels , membrane pores , cell membrane receptors
JournalTitle :
Journal of Research in Pharmacy
To Page :
9
Link To Document :
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