A Histological and Immunohistochemically Study on the Possible Protective Action of Lithium Chloride on the Acrylamide Induced Toxicity During the Postnatal Development of Midbrain Red Nucleus in Male Albino Rats

Introduction: Acrylamide is considered as industrial product that is worldwide used . It is identified in humans as a neurotoxic agent.
Aim of the Work: Elucidate the influence of acrylamide on postnatal development of the midbrain red nucleus following maternal administration during pregnancy and lactating periods and the possible protective role of lithium chloride.
Materials and Methods: Thirty pregnant rats were divided into three groups ; Group I: Received distilled water orally daily from the 7th day of pregnancy until day 28 after delivery. Group II & III: Acrylamide ( 10 mg/kg/day ) was given orally to the rats from the 7th day of pregnancy until day 28 after delivery. Group III: Daily intraperitoneal injections of lithium chloride (85 mg/kg) was given concomitantly with acrylamide. The red nuclei specimens of the male pups at the following ages ; neonate ,7days ,21 days and 3 months of the three groups were taken and processed for further histological and Immunohistochemically techniques.
Results: The red nuclei of control rats at different age groups appeared as bilateral ovoid circumscribed collections of neurons on either side of the midline . It had two parts ; magnocellular and parvocellular . The acrylamide treated rats showed disturbed architecture of the red nuclei with darkly stained neurons . Immunohistochemically staining for GFAP showed increase in the number and size of GFAP-positive cells in the treated rats . Morphometric study showed that the mean number of the neurons in the treated group exhibited significant difference when compared with control group . Concomitant treatment with lithium chloride showed less obvious signs of degeneration in comparison with the acrylamide treated group.
Conclusion: Lithium chloride could be effective as a neuroprotective agent against acrylamide induced degenerative changes during the postnatal development of the midbrain red nucleus.