Amelioration of behavioral aberrations and oxidative markers by green tea extract in valproate induced autism in animals.

Exposure to toxicants prenatally and postnatally could have deleterious consequences on the offspring. Postnatal exposure to valproate in mice pups is capable of inducing experimental autism resulting in neurobehavioral aberrations. Consumption of green tea has been associated with neuronal protection against the impact of toxicants. We investigated the role of green tea extract in reversing cardinal behavioral changes and aberrations in oxidative stress induced by valproate exposure. Young mice of both genders received a single dose of valproate (400mg/kg subcutaneously) on postnatal day 14 followed by a daily dose of green tea extract (75 and 300mg/kg) orally up to postnatal day 40. Mice pups were subjected to behavioral testing to assess motor co-ordination, nociceptive response, locomotion, anxiety, exploratory activity and cognition on various postnatal days up to postnatal day 40. At the end of behavioral testing, blood was withdrawn from the retro orbital plexus for the estimation of lipid peroxides. Animals were sacrificed on postnatal day 41 and whole brain was subjected to histopathological examination. Our studies revealed a significant improvement in behavioral assessments particularly with 300mg/kg of green tea extract. Formation of markers of oxidative stress was reduced at both dose levels. Histological findings confirm the neuroprotective effect of green tea at a dose of 300mg/kg. In conclusion it can be stated that green tea exerts neuronal cytoprotective action possibly due to anti-oxidant action and could be efficacious in the management of autism.