Asymmetric Dimethylarginine Synthesis and Degradation Under Physiological and Pathological Conditions

作者:Trocha Malgorzata*; Merwid Lad Anna; Szuba Andrzej; Sozanski Tomasz; Magdalan Jan; Szelag Adam
来源:Advances in Clinical and Experimental Medicine, 2010, 19(2): 233-243.

摘要

Asymmetric dimethylarginine (ADMA) is an endogenous methylated amino acid derived from arginine. ADMA can inhibit the activity of all isoforms of nitric oxide synthase (NOS). Protein arginine methyltransferases (PRMTs) catalyze the synthesis of ADMA and dimethylarginine dimethylaminohydrolase (DDAH) is responsible for the metabolism of this compound. ADMA enters cells through cationic amino-acid transporters (CATs), which are known to be y(+) carriers. Many factors can regulate the synthesis, transport, metabolism, or excretion of ADMA. In various pathological states such as hypercholesterolemia, hyperglycemia, hyperhomocysteinemia, hypertension, coronary artery disease, heart failure, and stroke, plasma levels of ADMA may increase two-or even tenfold, contributing to inhibition of NO synthesis and endothelial dysfunction. Impaired liver or renal function could also have an impact on the plasma concentration of ADMA. In some situations such as neurological disorders, decreased levels of ADMA are noted. It is very important to discover which states or drugs can increase or decrease the level of ADMA and what the mechanism of that action is (Adv Clin Exp Med 2010, 19, 233-243).

  • 出版日期2010