Role of Oxidative Stress and Antioxidants in Autism.

Autism spectrum disorder (ASD) is a heterogeneous group of neurodevelopmental disorders with poorly understood etiology that are defined exclusively on the basis of behavioral observations. This disorder has been linked to increased levels of oxidative stress and lower antioxidant capacity. 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). 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. Moreover, environmental and genetic risk factors may intensify vulnerability to oxidative stress in autism. Collectively, these studies suggest increased oxidative stress in autism that may contribute to the development of this disease both in terms of pathogenesis and clinical symptoms. Antioxidant supplementation, or ways to improve the altered metabolite levels in the interconnected transmethylation and transsulfuration pathways, has been associated with decreased autistic behaviors and severity. This chapter provides a conceptual framework on oxidative stress and antioxidants utility. These types of interventions should be further studied in order to determine their effectiveness at improving metabolic imbalances.

Effects of alpha-ketoglutarate on lipid peroxidation and antioxidant status during chronic ethanol administration in Wistar rats.

The effects of alpha-ketoglutarate (alpha-KG) on ethanol-induced hepatotoxicity were studied in biochemical experiments in rats. The levels of serum transaminases and thiobarbituric acid reactive substances were significantly increased in ethanol-treated rats. These levels were significantly decreased in alpha-KG- and ethanol-treated rats. Further, non-enzymatic (vitamins C and E) and enzymatic (superoxide dismutase and catalase) antioxidants were significantly decreased in ethanol-treated rats, and were increased in alpha-KG- and ethanol-treated rats. The biochemical alterations during alpha-KG treatment could be due to (i) the participation of alpha-KG in the non-enzymatic oxidative decarboxylation in the hydrogen peroxide decomposition process and (ii) enhancing the proper metabolism of fats which could suppress oxygen radical generation and thus prevent the lipid peroxidative damages in rats.

Safety evaluation of MMR vaccine during a primary school campaign in Saudi Arabia.

Monitoring of adverse events following the administration of MMR vaccine containing the Urabe mumps virus vaccine strain, to over 2 million schoolchildren (aged 6-13 years) revealed that the incidence of vaccine-associated aseptic meningitis was one case per 295 000 doses given. About 92 per cent of these children had had their primary immunization against MMR at 12 months of age and, therefore, were probably not immunologically naïve. It appears from our data that the use of the Urabe-based mumps vaccine in the booster-dose format induces much less adverse effects than usually observed following the primary immunization with it. Further studies are needed to prove this conclusively.