Autism is a severe developmental disorder with poorly understood etiology. Oxidative
stress in autism has been studied at the membrane level and also by measuring products
of lipid peroxidation, detoxifying agents (such as glutathione), and antioxidants
involved in the defense system against reactive oxygen species (ROS). Lipid peroxidation
markers are elevated in autism, indicating that oxidative stress is increased in this
disease. Levels of major antioxidant serum proteins, namely transferrin (iron-binding
protein) and ceruloplasmin (copper-binding protein), are decreased in children with
autism. There is a positive correlation between reduced levels of these proteins and
loss of previously acquired language skills in children with autism. The alterations
in ceruloplasmin and transferrin levels may lead to abnormal iron and copper metabolism
in autism. The membrane phospholipids, the prime target of ROS, are also altered in
autism. The levels of phosphatidylethanolamine (PE) are decreased, and phosphatidylserine
(PS) levels are increased in the erythrocyte membrane of children with autism as compared
to their unaffected siblings. Several studies have suggested alterations in the activities
of antioxidant enzymes such as superoxide dismutase, glutathione peroxidase, and catalase
in autism. Additionally, altered glutathione levels and homocysteine/methionine metabolism,
increased inflammation, excitotoxicity, as well as mitochondrial and immune dysfunction
have been suggested in autism. Furthermore, environmental and genetic factors may
increase vulnerability to oxidative stress in autism. Taken together, these studies
suggest increased oxidative stress in autism that may contribute to the development
of this disease. A mechanism linking oxidative stress with membrane lipid abnormalities,
inflammation, aberrant immune response, impaired energy metabolism and excitotoxicity,
leading to clinical symptoms and pathogenesis of autism is proposed.