Nitric oxide induces Zn2+ release from metallothionein by destroying zinc–sulphur clusters without concomitant formation of S-nitrosothiol

Abstract

The reaction of nitric oxide (NO) with metallothionein (MT) has been investigated at neutral pH under strictly anaerobic conditions. It is observed that NO mediates zinc release from MT by destroying zinc-sulphur clusters, but that it does not by itself Snitrosylate MT in contrast to common belief. Zinc release and loss of thiolate groups under anaerobic conditions is found to be much slower than under aerobic conditions. The observed percentage loss of Zn# + and thiolate groups after 3 h of NO treatment are 62 and 39 %, respectively. The reaction of NO with cysteine is reinvestigated and it is found that cysteine is quan-

Nitric oxide synthase inhibitors protect cerebellar Purkinje cells from zinc-induced cell loss in adult rat

“…It was found that NO can cause an obvious release of zinc from presynaptic buttons in vivo (Frederickson et al, 2002) and release from bound protein in vitro (Aravindakumar et al, 1999). Furthermore, Wei et al (2004) revealed that the inhibition of NOS with L-NAME, a broad-spectrum NOS inhibitor, blocked the increase in extracellular zinc accumulation during ischemia/ reperfusion.…”

An Insight of S‐Nitrosylation of Human GIF

“…This postulation was supported by certain previous work. Aravindakumar et al 36,37 have studied the reaction of cysteine, BSA and MT1 with NO and found that the reactivity was in this order: cysteine＞BSA>>MT1. The authors thought that the first attack of NO on a thiolate group was the rate-determining step.…”

Chronobiology and Effects of the Age on the Immune Function: Nutritional and Genetic Background

“…MT increase during stress and inflammation for a prompt immune response. Such an increment occurs in young-adult age during transient stress with zinc release by MT via reduced thiol groups or via Nitric Oxide (Aravindakumar et al, 1999). This phenomenon of intracellular zinc release is very limited in ageing because inflammation is made chronic by persistent high levels of IL-6 leading to impaired antioxidant activity and immune response.…”