Abstract
We have previously reported that levels of phosphatidylethanolamine (PE) in the erythrocyte membrane and of ceruloplasmin, a copper-transport antioxidant protein, in the serum are lower in children with autism than in control subjects. In the present study, we report that (a) copper oxidizes and reduces the levels of membrane PE and (b) copper-mediated oxidation of PE is higher in lymphoblasts from autistic subjects than from control subjects. The effect of copper was examined on the oxidation of liposomes composed of brain lipids from mice and also on the lymphoblasts from autism and control subjects. Among the various metal cations (copper, iron, calcium, cadmium and zinc), only copper was found to oxidize and decrease the levels of PE. The metal cations did not affect the levels of other phospholipids. The action of copper on PE oxidation was time-dependent and concentration-dependent. No difference was observed between copper-mediated oxidation of diacyl-PE and alkenyl-PE (plasmalogen), suggesting that plasmalogenic and non-plasmalogenic PE are equally oxidized by copper. Together, these studies suggest that ceruloplasmin and copper may contribute to oxidative stress and to reduced levels of membrane PE in autism.
Highlights
IntroductionRecent evidence from our laboratory and others suggests that oxidative stress may be an important component in autism[1,2,3,4,5,6,7,8]
Autism is a severe neurodevelopmental disorder with a poorly understood etiology
We examined the effect of copper on the oxidation of brain lipids in the liposomes and on the lymphoblasts of autism and control subjects
Summary
Recent evidence from our laboratory and others suggests that oxidative stress may be an important component in autism[1,2,3,4,5,6,7,8]. We have reported that lipid peroxidation is greater in the plasma of children with autism than in developmentally normal siblings[5]. Increased urinary excretion of 8-hydroxy-2-deoxyguanosine (oxidative product of DNA) and 8-isoprostane-F2α (oxidative product of fatty acids) has been reported in children with autism[7]. An increased vulnerability to oxidative stress and decreased capacity for methylation has been reported by James et al[8]. Zoroglu et al reported altered activities of free radical scavenging enzymes in erythrocytes from autism[3]
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