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RESEARCH PRODUCT

Chronic aspartame intake causes deficient glutathione synthesis and induces cxcl1 up-regulation in mice liver

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Reduced glutathione (GSH) depletion and inflammation have been linked to chronic aspartame consumption. However, the cause of aspartame-induced GSH depletion and the role of pro- and anti-inflammatory cytokines in aspartame-triggered inflammation are still unknown. The aims of this research were to investigate if aspartame causes GSH depletion due to deficient synthesis and also which pro- and anti-inflammatory genes are involved in aspartame-related inflammation in mice liver. Mice were divided into three groups: control, aspartame (80 mg kg-1, v.o., 3 months), aspartame treated with N-acetylcysteine (NAC) (1 mmol kg-1, i.p., last month). Aspartame markedly reduced GSH, γ-glutamylcysteine and cysteine levels. It also triggered down-regulation of the catalytic unit of glutamate cysteine ligase (gclc). Moreover, aspartame produced liver inflammation as confirmed through histologic analysis. It also caused the up-regulation of cxcl1 (the equivalent in mouse to human il-8) and down-regulation of il-10. In conclusion, chronic aspartame intake generates GSH depletion due to decreased cysteine levels and gclc downregulation. Moreover, pro- (cxcl1) and anti-inflammatory (il-10) cytokines are involved in aspartame-related inflammation. NAC abrogated all aspartame-induced changes.