Disruption of redox homeostasis in liver function and activation of apoptosis on consumption of aspartame in folate deficient rat model

摘要: Abstract This study assesses the effect of long-term intake aspartame on liver function and apoptosis signaling pathway in Wistar albino rats. Several reports have suggested that methanol is one major metabolites Aspartame. Non-primate animals are usually resistant to methanol-induced metabolic acidosis due high levels hepatic folate content; hence a deficiency model was induced by treating with methotrexate (MTX) prior exposure. The treated MTX exhibited marked significant increase alanine transaminase (ALT), aspartate (AST), alkaline phosphatase (ALP) lactic acid dehydrogenase (LDH) activity compared controls. Aspartame additionally down-regulation genes namely B-cell lymphoma 2 (Bcl2) expression up-regulation Bcl-2-associated X protein (Bax), Fas-associated death domain (FADD) Caspase 3, 9 apoptotic expression, indicating augmentation apoptosis. Nuclear condensation, micro vacuole formation cytoplasm necrosis were observed histopathology evaluation. Additionally, Immunohistochemical analysis revealed positive cells expressing Fas, FADD, Bax protein, an liver. Thus, may act as chemical stressor which alters functional status liver, leading hepatotoxicity.