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Drug Metabolism Letters


ISSN (Print): 1872-3128
ISSN (Online): 1874-0758

Review Article

Physiological and Pathophysiological Role of Cysteine Metabolism in Human Metabolic Syndrome

Author(s): Arunachalam Muthuraman*, Muthusamy Ramesh*, Sohrab A. Shaikh, Subramanian Aswinprakash and Dhamodharan Jagadeesh

Volume 14, Issue 3, 2021

Page: [177 - 192] Pages: 16

DOI: 10.2174/1872312814666211210111820

Price: $65


Abstract: Cysteine is one of the major intermediate products of cellular amino-acid metabolism. It is a semi-essential amino acid for protein synthesis. Besides, it is also employed in the regulation of major endogenous anti-oxidant molecule i.e., reduced glutathione (GSH). Further, it is a precursor of multiple sulfur-containing molecules like hydrogen sulfide, lanthionine, taurine, coenzyme A and biotin. It is also one of the key molecules for post-translational modifications of various cellular proteins. In physiological conditions, it is employed in the sulfhydration process and plays a key role in the physiology modification of the inflammatory process in various organs, including the neurological system. The catabolism of cysteine is regulated by cysteine dioxygenase enzyme activity. The dysregulated conditions of cysteine and cysteine-associated hydrogen sulfide metabolism are widely employed in the acceleration of the neurodegenerative process. Moreover, the upregulation of cysteine and hydrogen sulfide synthesis occurs via the reverse trans-sulfuration process. This process helps to manage the worsening of a pathological condition of a cellular system. Moreover, it is also employed in the accumulation of homocysteine contents. Further, both cysteine and homocysteine molecules are widely accepted as biomarkers for various types of diseases. Therefore, the targets involved in the regulation of cysteine have been considered as valid targets to treat various disorders like cardiac disease, ischemic stroke, diabetes, cancer, and renal dysfunction.

Keywords: Biomarker, homocysteine, hydrogen sulfide, reduced glutathione, stroke, metabolic syndrome.

Graphical Abstract
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