Impaired Transsulfuration and Oxidative Stress in Autistic Children: Improvement with Targeted Nutritional Intervention
S. Jill James, PhD
DAN! Conference, 2003
The generation of reactive oxygen species (ROS) is an inevitable consequence of aerobic energy metabolism. A delicate oxidant-antioxidant balance within each cell maintains normal physiologic levels of ROS that serve as important signaling molecules for the activation of cGMP-dependent functions, for vasomotor tone, T cell activation, and normal gene expression 1,2. Oxidative stress occurs when cellular antioxidant defense mechanisms fail to counterbalance and control ROS production. Unopposed ROS can result in damage to mitochondrial and nuclear DNA, alteration in protein structure, and membrane lipid composition 3. Functionally, these aberrations translate into abnormal gene expression, membrane signal transduction, and altered rates of cell proliferation, differentiation, and apoptosis. A pro-oxidant microenvironment has been implicated in the etiology of numerous human diseases including cardiovascular disease, cancer, autoimmune disorders, and neurodegenerative conditions 4-8. The potential role of oxidative stress in the etiology of autism has received less research attention.