Prenatal and perinatal acrylamide disrupts the development of cerebellum in rat: Biochemical and morphological studies.

Acrylamide is known to cause neurotoxicity in the experimental animals and humans. The literature on its neurotoxic effect in the adult animals is huge, but the effect of acrylamide on the embryonic and postnatal development is relatively less understood. The present study examined its effects on the development of external features and cerebellum in albino rats. Acrylamide was orally administered to non-anesthetized pregnant females by gastric intubation 10 mg/kg/day. The animals were divided into three groups as follows. (1) Group A, newborn from control animals; (2) Group B; newborns from mothers treated with acrylamide from day 7 (D7) of gestation till birth (prenatal intoxicated group); (3) Group C; newborns from mothers treated with acrylamide from D7 of gestation till D28 after birth (perinatally intoxicated group). Acrylamide administered either prenatally or perinatally has been shown to induce significant retardation in the newborns' body weights development, increase of thiobarbituric acid-reactive substances (TBARS) and oxidative stress (significant reductions in glutathione reduced [GSH], total thiols, superoxide dismutase [SOD] and peroxidase activities) in the developing cerebellum. Acrylamide treatment delayed the proliferation in the granular layer and delayed both cell migration and differentiation. Purkinje cell loss was also seen in acrylamide-treated animals. Ultrastructural studies of Purkinje cells in the perinatal group showed microvacuolations and cell loss. The results of this study show that prenatal and perinatal acrylamide or its metabolites disrupts the biochemical machinery, cause oxidative stress and induce structural changes in the developing rat cerebellum.