Reprinted with the kind permission of Life Extension.
November 9, 2018. An article published on October 24, 2018 in Molecular Medicine Reports reveals improvements in lifespan and aging-associated changes in association with selenocysteine supplementation in the roundworm Caenorhabditis elegans.
“Selenocysteine, a sulfur‑containing amino acid, can modulate cellular oxidative stress defense systems by incorporating into antioxidant enzymes such as glutathione peroxidase and thioredoxin reductase.,” write So-Hyeon Kim and colleagues. “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.”
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The research involved normal C. elegans worms and genetically modified strains. Supplementation with selenocysteine increased the lifespan of normal worms as well as two of three strains of worms modified to live longer lives. Lack of a significant lifespan increase in association with selenocysteine supplementation in a third worm strain that was a model of dietary restriction suggested that the compound exerts its effects by similar mechanism. It was determined that selenocysteine requires the transcription factor SKN-1 (which is known to regulate responses to dietary restriction-induced lifespan in C. elegans) to extend life.
Further experimentation revealed that selenocysteine decreases the toxicity of amyloid beta, a protein that forms plaques in the brains of Alzheimer’s disease patients. Selenocysteine was also shown to decrease toxicity induced by high levels of glucose and cellular reactive oxygen species.
The research provides evidence for the development of dietary restriction mimetics utilizing selenocysteine. “Further studies focusing on the effect of selenocysteine on age‑related diseases such as Alzheimer’s disease Parkinson’s disease, and diabetes mellitus in mammalian disease models and the molecular basis of the effect of selenocysteine are necessary for the understanding of in vivo activity of selenocysteine,” the authors conclude.