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Comparison of selenium and sulfur analogs in cancer prevention.

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TLDR
Compared to the sulfur structural analogs, selenium compounds are much more active in cancer protection and may have a multi-modal mechanism in preventing cellular transformation as well as in delaying or inhibiting the expression of malignancy after carcinogen exposure.
Abstract
Several organoselenium compounds have been shown to have powerful anticarcinogenic activity. In view of certain similarities between selenium and sulfur biochemistry, we have evaluated the chemopreventive efficacy of three pairs of analogs using the 7,12-dimethylbenz[a]anthracene (DMBA)-induced mammary tumor model in rats. The compounds tested were selenocystamine/cysteamine, Semethylselenocysteine/S-methylcysteine, selenobetaine/sulfobetaine. In the first study, each agent was added to the basal AIN-76A diet and was given before and continued after DMBA treatment until the end. All three selenium compounds were active; a 50% inhibition was achieved at approximately 25 x 10(-6) mol/kg with Se-methylselenocysteine and selenobetaine and at approximately 40 x 10(-6) mol/kg with selenocystamine. In the sulfur series, only cysteamine and S-methylcysteine produced anticancer activity, and the levels required for comparable responses were 500- to 750-fold higher compared to the corresponding selenium analogs. Sulfobetaine was inactive even when present at near maximally tolerated levels. In the second study, Se-methylselenocysteine and S-methylcysteine were chosen for further examination during the initiation and post-initiation phases of mammary carcinogenesis. Se-Methylselenocysteine was effective when it was given either before or after DMBA administration. In contrast, S-methylcysteine was effective only after DMBA treatment. Thus, compared to the sulfur structural analogs, selenium compounds are much more active in cancer protection and may have a multi-modal mechanism in preventing cellular transformation as well as in delaying or inhibiting the expression of malignancy after carcinogen exposure.

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Journal ArticleDOI

Organoselenium and Organotellurium Compounds: Toxicology and Pharmacology

TL;DR: The development of new organochalcogens with higher thiol-peroxidase activity that can use other non-toxic thiol reducing agents, such as N-acetylcysteine instead of glutathione, will permit the investigation of the co-administration of organochAlcogens and thiols as a formulation for antioxidant therapy.
Journal ArticleDOI

From selenium to selenoproteins: Synthesis, identity, and their role in human health

TL;DR: The function of most selenoproteins is currently unknown; however, thioredoxin reductases, glutathione peroxidases and thyroid hormone deiodinases are well characterised selenobroteins involved in redox regulation of intracellular signalling, redox homeostasis and thyroid hormones metabolism.
Journal ArticleDOI

Chemopreventive agents: selenium.

TL;DR: According to this two-stage model of the roles of Se in cancer prevention, individuals with nutritionally adequate Se intakes may benefit from Se supplementation and the development of the potential of Se compounds as cancer chemopreventive agents is facilitated.
Journal ArticleDOI

On the nature of selenium toxicity and carcinostatic activity.

TL;DR: The thesis presented here for scrutiny is that compounds of selenium are toxic owing to their prooxidant catalytic activity to produce superoxide (O2.-), hydrogen peroxide, and very likely other cascading oxyradicals.
Journal ArticleDOI

Selenium and its relationship to cancer: an update.

TL;DR: Even though SeMCYS was shown to be the most effective seleno-compound in the reduction of mammary tumours, it may not be the best choice for reduction of colon tumours because several mechanisms have been proposed on the mechanism whereby Se reduces tumours.
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