The involvement of transition metal ions on iron-dependent lipid peroxidation

Abstract

The metals iron (Fe) and copper (Cu) are considered trace elements, and the metals cobalt (Co) and nickel (Ni) are known as ultra-trace elements, considering their presence in low to very low quantity in humans. The biologic activity of these transition metals is associated with the presence of unpaired electrons that favor their participation in redox reactions. They are part of important enzymes involved in vital biologic processes. However, these transition metals become toxic to cells when they reach elevated tissue concentrations and produce cellular oxidative damage. Phospholipid liposomes (0.5 mg/ml, phosphatidylcholine (PC)/phosphatidylserine (PS), 60/40) were incubated for 60 min at 37 degrees C with 25 microM of Fe2+ in the absence and in the presence of Cu2+, Co2+, and Ni2+ (0-100 microM) with and without the addition of hydrogen peroxide (H2O2, 5-50 microM). Iron-dependent lipid peroxidation in PC/PS liposomes was assessed by thiobarbituric acid-reactive substances (TBARS) production. Metal transition ions promoted lipid peroxidation by H2O2 decomposition and direct homolysis of endogenous hydroperoxides. The Fe2+-H2O2-mediated lipid peroxidation takes place by a pseudo-second order process, and the Cu2+-mediated process by a pseudo-first order reaction. Co2+ and Ni2+ alone do not induce lipid peroxidation. Nevertheless, when they are combined with Fe2+, Fe2+-H2O2-mediated lipid peroxidation was stimulated in the presence of Ni2+ and was inhibited in the presence of Co2+. The understanding of the effects of transition metal ions on phospholipids is relevant to the prevention of oxidative damage in biologic systems.

Evaluation of trace elements and oxidative stress levels in the liver and kidney of streptozotocin-induced experimental diabetic rat model

“…The studies on diabetes patients and diabetic patient models reported that lipid peroxidation significantly increases in liver and kidney, which is compatible with the findings of the present study (Kakkar et al1998;Obrosova et al 2003). As indicated in the previous studies, free radical production is considered as one of the major mechanisms responsible for the toxicity of transition metals ions such as Cu and Fe (Repetto et al 2010). Intake and excretion of Fe and Cu, essential for organism, are required for a balanced organism.…”

“…The contribution of other factors, including the alternations in the homeostasis ions of some trace and transition elements as Fe and Cu on the occurrence and progression of the disease is still being discussed in literature (Eaton and Qian 2002;Viktorínová et al 2009). In the presence of certain metals (particularly iron or copper ions), a hydroxyl radical, which is the most powerful ROS, can be produced via the Fenton or the metal-catalyzed HaberWeiss reaction (Repetto et al 2010). These two chemical reactions appear to account for most of the hydroxyl radical production in biological systems and explain, at least in part, why metals such as Fe and Cu produce oxidative stress and ROS-induced injury in cells.…”

Lipid Peroxidation: Chemical Mechanism, Biological Implications and Analytical Determination

“…Enzymatic lipid peroxidation is catalyzed by the lipoxygenases family, a family of lipid peroxidation enzymes that oxygenates free and esterified PUFA generating as a consequence, peroxy radicals. Non enzymatic lipid peroxidation and formation of lipidperoxides are initiated by the presence of molecular oxygen and is facilitated by Fe 2+ ions (Repetto et al, 2010a).…”

“…generation), b) direct autoxidation of lipids, c) intermediates of the nitric oxide metabolism, and d) modifications of lipid membrane surface structure (Fridovich & Porter, 1981;Repetto et al, 2010a;).…”

Nanotoxicology and oxidative stress control: cutting-edge topics in toxicology

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