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.
Acrylamide has been employed as an experimental probe to investigate biochemical and morphological changes in developing rat liver following toxin administration in pregnant rats. Non-anesthetized pregnant rats were given acrylamide by gastric intubation at a dose of 10 mg/kg/day. The pups were divided into three groups: Group A, mothers were treated with saline (control group); Group B, mothers were treated with acrylamide from day D7 of gestation till birth (prenatal intoxication); Group C, mothers were treated with acrylamide from D7 of gestation to D28 after birth (perinatal intoxication). Acrylamide-induced biochemical changes (in liver and serum) and morphological changes (in liver) were studied in control and acrylamide-treated developing pups. Prenatally and perinatally administered acrylamide significantly increased lipid peroxidation and reduced glutathione and total thiol levels in liver. Significant inhibition of peroxidase and superoxide dismutase activities was observed in liver tissue. Total lipids including cholesterol and triglycerides were significantly increased in the serum. Acrylamide treatment increased serum alanine aminotransferase and aspartate aminotransferase activities and inhibited alkaline phosphatase activity. Sodium and potassium concentrations were increased, but calcium, phosphorus and iron levels were significantly reduced in the serum. Acrylamide produced significant electrophoretic changes in serum proteins. The most noticeable change was splitting of beta-globulin into beta1- and beta2-globulins. Light microscopy showed acrylamide-induced fatty deposits, congested central vein, vacuolization and chromatolysis in hepatocytes. Ultrastructural studies revealed vacuolated cytoplasm, lipid droplets of variable size and mitochondria with damaged cristae and vacuolization. The nuclei in acrylamide-treated groups showed marked decrease in the staining of nuclear DNA.
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