Comparison of antioxidant activities of aminoguanidine, methylguanidine and guanidine by luminol‐enhanced chemiluminescence

Abstract

1 The objective of this study was to investigate the ability of aminoguanidine, methylguanidine and guanidine to inhibit free radicals or metabolites generated by either stimulated human leucocytes or cellfree systems using luminol-enhanced chemiluminescence (CL). 2 Aminoguanidine (0.1 mM ± 10 mM), methylguanidine (10 mM ± 10 mM) and guanidine (10 mM ± 10 mM) produced concentration-dependent inhibition (96+0.1%, n=7, 59+1.3%, n=6, and 62+3%, n=6, P50.05 at 10 mM, respectively) in FMLP-stimulated leucocytes CL. 3 In cell-free experiments, hydrogen peroxide (H 2 O 2 ), hypochlorous acid (HOCl), hydroxyl radical and peroxynitrite-induced CL responses were initiated by hydrogen peroxide (3.5 mM), NaOCl (50 mM), FeSO 4 (40 nM) and peroxynitrite (20 nM), respectively. Aminoguanidine, methylguanidine and guanidine produced concentration-dependent inhibition in H 2 O 2 -(69+0.7%, n=7, 26+1%, n=6, and 15+0.5%, n=6, at 1 mM, respectively) and HOCl-(84+0.3%, n=6, 50+1%, n=6, and 29+1%, n=7, at 1 mM, respectively) induced luminol CL. Peroxynitrite-induced CL was markedly attenuated in a concentrationdependent manner by aminoguanidine (99+0.1%, n=6, at 10 mM), methylguanidine (5+0.2%, n=6, at 10 mM) and guanidine (27+0.4%, n=7, at 10 mM). However, inhibition with aminoguanidine was found to be more marked than with methylguanidine and guanidine. Aminoguanidine (95+0.5%, n=6, at 1 mM) and methylguanidine (25+1%, n=6, at 1 mM), but not guanidine (2+1%, n=6, at 1 mM), signi®cantly decreased ferrous iron-induced CL. 4 Collectively, these data suggest that aminoguanidine and a high concentration (50.1 mM) of methylguanidine have direct scavenging activities against H 2 O 2 , HOCl, hydroxyl radical and peroxynitrite. Guanidine, at a high concentration (50.1 mM), scavenges H 2 O 2 , HOCl and peroxynitrite, but not the hydroxyl radical. These direct scavenging properties may contribute to inhibitory eects of these compounds on human leucocyte CL.

Aminoguanidine ameliorates radiation-induced oxidative lung damage in rats

“…27 Previous studies pointed out the beneficial antioxidant effects of AG and scavenger effects of ONOO -which is a reactive oxidant produced from NO and O 2-in various forms of tissue injury. 35 Yildiz et al 36 also found that AG had direct scavenging activities against HO. Recently, Giardino et al 37 reported that AG acts as an antioxidant in vivo, preventing ROS formation and lipid peroxidation in cells and tissues, thus preventing oxidant-induced apoptosis.…”

“…40 The beneficial effects of AG in various experimental models of inflammation have also been reported. 41 Recently, Mansour et al 36 reported that AG protects against nephrotoxicity induced by cisplatin (CDDP) in rats. The beneficial antioxidant effects of AG and the scavenger effects of ONOO -, which is a reactive oxidant produced from NO and superoxide (O -), have been observed in various forms of tissue injury.…”

Effect of sub-chronic intraperitoneal administration of aminoguanidine on the memory and hippocampal apoptosis-related genes in diabetic rats

“…Inhibition of iNOS by AG may ameliorate the cognitive defi cit induced by diabetes (38). Other neuroprotective mechanisms of AG may be related to its free radical scavenging properties (35,39). Also, a number of cellular metabolic pathways about AG neuroprotective functions relate to methylglyoxal (MG) inhibition (40).…”

Aminoguanidine impedes human pancreatic tumor growth and metastasis development in nude mice

“…GPx activity was slightly decreased after AG treatment in a model of liver injury in rat [31] . Chronic treatment with AG might cause a disruption of the cellular redox balance due to its capacity to scavenge oxidant reactive species [32] and to inhibit NO synthesis. This could explain the reduced expression of antioxidant enzymes as a compensatory mechanism.…”