Copper(II)‐catalyzed lipid peroxidation in liposomes and erythrocyte membranes

Abstract

Cu++ was uniquely capable of catalyzing the peroxidation of rat erythrocyte membrane lipid in the presence of 10 mM H2O2, whereas several other transition metal ions were without significant effect. In contrast, peroxidation of soybean phospholipid liposomes could be catalyzed with decreasing efficiency by Co++, Cu++, Pb++, or Cr+++ also in the presence of H2O2. The effect of imidazole on Cu++- catalyzed lipid peroxidation was stimulatory in liposomes and inhibitory in membrane preparations, whereas EDTA, histidine, citrate and alanine inhibited peroxidation in both systems. EDTA could stop the peroxidation after initiation, but catalase could not, indicating that Cu++ alone was necessary for the propagation of the chain reaction. Competitive inhibition studies with various scavengers of hydroxyl radicals or singlet oxygen and the absence of significant reaction enhancement by D2O indicated that neither of these reactive oxygen species was a major mediator in the Cu++-H2O2 oxidative system. A copper-oxygen complex may be directly involved in the initiation of peroxidation. Normal erythrocyte membranes and phospholipid liposomes also differ in their sensitivities toward external oxidative stress. In the absence of H2O2, CU++ (0.2 mM) was capable of catalyzing lipid peroxidation in liposomes, aged erythrocyte membranes and membranes from vitamin-E-deficient rats; however, freshly prepared membranes from control rats and liposomes containing alpha-tocopherol required H2O2 greater than 2 mM for the catalytic effect of Cu++ to be observed.

Human Placenta as a Biomarker of Environmental Toxins Exposure – Long-Term Morphochemical Monitoring

“…With its ability to bind with nucleic acids, copper can cause permanent changes in their structure and thus alter their biological properties (KabataPendias & Pendias 1993). Copper and its ions have a very high affinity for sulfhydryl groups of various enzymes and a significant share in the creation of the reactive oxygen species that initiate the peroxidation of lipids in cell membranes, thus leading to the inactivation of enzymes associated with these membranes (Chan et al, 1982). Sokol et al (Sokol et al, 1993), especially in the mitochondrial lipid peroxidation induced by copper toxical action, which is considered the reason of the cytochrome c oxidase activity decrease.…”

In Vitro Studies on Pesticide-Induced Oxidative DNA Damage

“…Similar to iron, copper acts as a catalyst in the formation of reactive oxygen species and catalyzes peroxidation of membrane lipids (19). The metal ions present in some pesticides and fertilizers (20) may interfere with DNA repair and produce reactive oxygen species (ROS), leading to oxidative damage (6).…”

Testing the ‘photoinhibition’ model of coral bleaching using chemical inhibitors

“…There is a growing awareness that the toxicity of metals such as copper is associated with the generation of ROS (Stohs & Bagchi 1995). Copper (and iron) can act as catalysts for the generation of ROS such as the hydroxyl radical (HO _ ) by Fenton and HaberWeiss reactions (Halliwell & Gutteridge 1984), and initiate a self-propagating lipid peroxidation process (Chan et al 1982) that increases membrane permeability/leakiness. While it is not possible from the information reported here to identify the mechanism of copper-induced bleaching in Seriatopora hystrix, one can speculate that it is basically pathological and associated with the effect of copper on the host (animal) cells.…”