Selenocystine and cancer

Sougat Misra, Mikael Björnstedt

Research output: Chapter in Book/Report/Conference proceedingChapter

2 Scopus citations


The diselenide compound selenocystine is a selenium analog of cystine. It is more reactive compared to cystine due to intrinsic differences in chemical properties between sulfur and selenium. Thioredoxin reductase or excess cysteine and glutathione reduces selenocystine to highly reactive selenolate. When selenocystine is present at high concentration, selenolate-mediated biochemical reactions perturb cellular redox homeostasis and induce oxidative stress. Limited pharmacokinetic studies indicate rather long half-life and biphasic elimination kinetics of selenocystine. It is well tolerated in mice and rats with a narrow window between no observed effects and toxicity. Several preclinical studies have interrogated its redox modulatory effects as an anticancer modality. Reported cytotoxic effects include DNA damage, S-phase arrest, activation of P53, alteration of MAPK and PI3K-AKT signaling pathways, loss of mitochondrial membrane potential, and release of cytochrome C. So far, findings from published studies suggest limited antineoplastic effects of selenocystine in various animal models of cancer.

Original languageEnglish (US)
Title of host publicationMolecular and Integrative Toxicology
PublisherSpringer Science+Business Media B.V.
Number of pages16
StatePublished - 2018

Publication series

NameMolecular and Integrative Toxicology
ISSN (Print)2168-4219
ISSN (Electronic)2168-4235

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Pharmacology (medical)
  • Drug Discovery
  • Toxicology


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