Abstract
In animal models, neuronal apoptosis was induced by several anesthetics in the developing brain and this interruption could cause deficits in brain function in adulthood including social deficits. Recent research has revealed that exposure of the infant rhesus macaque brain to isoflurane causes widespread neuroapoptosis. However, inadequate human data exist to affirm the possibility that similar effects occur in human children. Previous studies showed many potential mechanisms of neuroapoptosis in immature animal brains but there are no promising therapeutic strategies to mitigate neurotoxicity. The purpose of this article is to discuss anesthesia-related neurotoxicity and the possible therapeutic applicability of molecular hydrogen as an antioxidant.
