ArticleMolecular medicine reports2018
Selenocysteine mimics the effect of dietary restriction on lifespan via SKN‑1 and retards age‑associated pathophysiological changes in Caenorhabditis elegans.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
- The impact of cysteine on lifespan in three model organisms: A systematic review and meta-analysis.Aging cell · 2025Pooled it
- Article
- Effects of Combining Biofactors on Bioenergetic Parameters, Aβ Levels and Survival in Alzheimer Model Organisms.International journal of molecular sciences · 2022Article
- Natural Bioactive Products and Alzheimer's Disease Pathology: Lessons fromDiseases (Basel, Switzerland) · 2022Review
- The Relevance of Selenium Status in Rheumatoid Arthritis.Nutrients · 2020Review
- Phosphatidylcholine Extends Lifespan via DAF-16 and Reduces Amyloid-Beta-Induced Toxicity inOxidative medicine and cellular longevity · 2019Article
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3 authors at 1 institution in 1 country.
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Abstract
Selenocysteine, a sulfur‑containing amino acid, can modulate cellular oxidative stress defense systems by incorporating into anti‑oxidant enzymes such as glutathione peroxidase and thioredoxin reductase. Selenocysteine can also prevent cancer, neurodegenerative diseases and cardiovascular diseases. A recent study revealed that dietary supplementation with selenocysteine can increase the resistance of Caenorhabditis elegans to environmental stressors and its lifespan. The objective of the present study was to identify the underlying mechanism involved in the lifespan‑extending effect of selenocysteine and the effect of selenocysteine on age‑associated pathophysiological changes. Lifespan assays with known long‑lived mutants of age‑1 (the ortholog of the phosphoinositide 3-kinase), clk‑1 (the ortholog of demethoxyubiquinone hydroxylase) and eat‑2 (a ligand-gated ion channel subunit) revealed that the effect of selenocysteine on lifespan specifically overlapped with that of the eat‑2 mutation, a genetic model of dietary restriction (DR). Selenocysteine mimicked the effect of DR on the bacterial dilution method. It required SKN-1 (the ortholog of mammalian nuclear factor-erythroid-related factor) for lifespan extension. In addition, selenocysteine significantly delayed the paralysis induced by human amyloid‑β gene, positively correlated with the incidence of Alzheimer's disease. The effect of selenocysteine on amyloid‑β‑induced toxicity was dependent on the nuclear localization of DAF‑16. Reduced survival caused by high‑glucose‑diet was recovered by selenocysteine. Selenocysteine also reduced the cellular level of reactive oxygen species known to be increased by high‑glucose‑diet. The results of the present study suggested that selenocysteine can mimic the effect of DR on lifespan and age‑associated pathophysiological alterations, providing scientific evidence for the development of DR mimetics using selenocysteine.
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