ArticleRedox biology2017
Chronic aspartame intake causes changes in the trans-sulphuration pathway, glutathione depletion and liver damage in mice.
Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 60 citations in OpenAlex.
- New Insights into the Interplay Between Simple Sugars and Liver Diseases.Current issues in molecular biology · 2025Review
- Effects of Selected Food Additives on the Gut Microbiome and Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).Medicina (Kaunas, Lithuania) · 2025Review
- Effects of high dose aspartame-based sweetener on the gut microbiota and bone strength in young and aged mice.JBMR plus · 2024Article
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- Effects of long-term high dose aspartame on body mass, bone strength, femoral geometry, and microbiota composition in a young and aged cohort of male and female mice.bioRxiv : the preprint server for biology · 2024Article
- Daily Early-Life Exposures to Diet Soda and Aspartame Are Associated with Autism in Males: A Case-Control Study.Nutrients · 2023Article
- Is Glucose-6-Phosphate Dehydrogenase Deficiency a Risk Factor for Autoimmune Thyroid Disease? A Retrospective Case-Control Study.International journal of environmental research and public health · 2023Article
- Long-term intake of aspartame-induced cardiovascular toxicity is reflected in altered histochemical parameters, evokes oxidative stress, and trigger P53-dependent apoptosis in a mouse model.International journal of experimental pathology · 2022Article
- Ce doped polyaniline nanoparticles for absorption and photoacoustic imaging response to GSHBioactive materials · 2022Article
- Aspartame-True or False? Narrative Review of Safety Analysis of General Use in Products.Nutrients · 2021Review
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- Artificial Sweeteners: History and New Concepts on Inflammation.Frontiers in nutrition · 2021Review
- The in vitro cytotoxic, genotoxic, and oxidative damage potentials of the oral artificial sweetener aspartame on cultured human blood cellsTurkish journal of medical sciences · 2020Article
- Worsening of Oxidative Stress, DNA Damage, and Atherosclerotic Lesions in Aged LDLrOxidative medicine and cellular longevity · 2019Article
- Dietary Additives and Supplements Revisited: The Fewer, the Safer for Liver and Gut Health.Current pharmacology reports · 2019Article
- Chronic intake of 4-Methylimidazole induces Hyperinsulinemia and Hypoglycaemia via Pancreatic Beta Cell Hyperplasia and Glucose Dyshomeostasis.Scientific reports · 2018Article
- Dietary and Endocrine Regulation of Endogenous Hydrogen Sulfide Production: Implications for Longevity.Antioxidants & redox signaling · 2018Article
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Corrections and comments
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
No-caloric sweeteners, such as aspartame, are widely used in various food and beverages to prevent the increasing rates of obesity and diabetes mellitus, acting as tools in helping control caloric intake. Aspartame is metabolized to phenylalanine, aspartic acid, and methanol. Our aim was to study the effect of chronic administration of aspartame on glutathione redox status and on the trans-sulphuration pathway in mouse liver. Mice were divided into three groups: control; treated daily with aspartame for 90 days; and treated with aspartame plus N-acetylcysteine (NAC). Chronic administration of aspartame increased plasma alanine aminotransferase (ALT) and aspartate aminotransferase activities and caused liver injury as well as marked decreased hepatic levels of reduced glutathione (GSH), oxidized glutathione (GSSG), γ-glutamylcysteine (γ-GC), and most metabolites of the trans-sulphuration pathway, such as cysteine, S-adenosylmethionine (SAM), and S-adenosylhomocysteine (SAH). Aspartame also triggered a decrease in mRNA and protein levels of the catalytic subunit of glutamate cysteine ligase (GCLc) and cystathionine γ-lyase, and in protein levels of methionine adenosyltransferase 1A and 2A. N-acetylcysteine prevented the aspartame-induced liver injury and the increase in plasma ALT activity as well as the decrease in GSH, γ-GC, cysteine, SAM and SAH levels and GCLc protein levels. In conclusion, chronic administration of aspartame caused marked hepatic GSH depletion, which should be ascribed to GCLc down-regulation and decreased cysteine levels. Aspartame triggered blockade of the trans-sulphuration pathway at two steps, cystathionine γ-lyase and methionine adenosyltransferases. NAC restored glutathione levels as well as the impairment of the trans-sulphuration pathway.
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