OPPOSITE IMPACT OF INFLAMMATION AND OXIDATIVE STRESS ON VASCULAR GGT ACTIVITY

Gamma-glutamyltransferase (GGT) is involved in glutathione (GSH) and S-nitrosoglutathione catabolisms, allowing the recovery of precursor aminoacids and nitric oxide release. Increased GGT serum levels were correlated with cardiovascular diseases, including atherosclerosis or hypertension, two contexts of vascular wall inflammation and oxidative stress [1]. However, less is known concerning vascular wall GGT activity under these contexts. GGT activity (L-γ-glutamyl-3-carboxy-4-nitroanilide) and intracellular GSH concentrations (2,3-naphthalenedicarboxaldehide) were evaluated in a rat smooth muscle cell line (SMC A-10) stimulated with lipopolysaccharide (LPS; 20 µg/mL, 24 h) or 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH; 50 mM, 2 h), and in aortas, from Spontaneously Hypertensive Rats (SHR) compared to normotensive Wistar Kyoto rats (WKY). The GGT activity increased in the inflammatory A-10 LPS model, while it decreased with oxidative stress, both in A-10 AAPH and SHR aortas in parallel with a decrease in GSH content (n = 3-7; * p<0.05 vs control). Opposite GGT activity modulation under inflammation and oxidative stress need further investigation to determine the modulation mechanisms and links with the redox status (reactive oxygen and nitrogen species).