Biological effects of selenium compounds with a particular attention to the ontogenetic development
Language English Country Czech Republic Media print
Document type Journal Article, Research Support, Non-U.S. Gov't, Review
PubMed
22827875
DOI
10.33549/physiolres.932327
PII: 932327
Knihovny.cz E-resources
- MeSH
- Myocardial Infarction pathology prevention & control MeSH
- Cardiotonic Agents pharmacology therapeutic use MeSH
- Cataract metabolism pathology MeSH
- Humans MeSH
- Lens, Crystalline drug effects pathology MeSH
- Oxidation-Reduction MeSH
- Myocardial Reperfusion Injury physiopathology prevention & control MeSH
- Selenium Compounds pharmacology toxicity MeSH
- Arrhythmias, Cardiac pathology prevention & control MeSH
- Age Factors MeSH
- Animals MeSH
- Check Tag
- Humans MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Review MeSH
- Names of Substances
- Cardiotonic Agents MeSH
- Selenium Compounds MeSH
Selenium is a trace element that is essential for living organism. Its beneficial effect is, however, expressed in a very narrow dosage range: the high and low doses of selenium are connected with pathological manifestations. The toxicity depends on the chemical form of selenium, state of organism, interactions with heavy metals and on the stage of ontogenetic development. Whereas one dose of sodium selenite (20 micromol/kg b.w.) is lethal in adult rats, suckling rats are entirely resistant. However, within one week after administration of the same dose, cataract of eye lens developed. The highest incidence of cataract was observed in 10-day-old animals and it decreased until day 20. From postnatal day 20 to day 40 the rats were resistant to both the lethal and cataractogenic effects of selenium. The incidence of cataract may be suppressed by premature weaning, lower hydration of suckling, change of water soluble/water insoluble lens protein ratio, thyroxine treatment, and by interaction with mercury. By means of its oxidative and reduction properties, selenium is involved in the maintenance of the cell redox homeostasis. Typical example is its possible cardioprotective effect: selenium decreased number of arrhythmias, reduced infarct size and improved the contractile recovery after ischemia/reperfusion injury. Selenium supplementation may thus increase cardiac tolerance to ischemic damage.
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