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| UDK 612.014.3 ; 615.32:582.573.36 |
ISSN 035-2899, 38(2013) br.1 p.30-34 |
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Review article Apoptosis induction as one of the mehanisms of cytotoxixity and antiproliferative action of hypericin Indukcija apoptoze jedan od mehanizama citotoksičnosti antiproliferativnog efekta hipericina
Tatjana Sokolović (1), Milica Lazović (2), Dušan Đurić (3), Vlada
Cekić (4) |
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| Summary: Life, growth and development of a multicellular organism depends on its ability to create new cells through the process of cell proliferation and destroy the old ones through the process of programmed cell death. The growth of tissue, whether it is normal or malignant, is determined by the quantitative relation between the rate of cell proliferation and the rate of cell death. Apoptosis is programmed cell death that is characterized by specific functional changes that are correlated with morphological changes in the nucleus and cytoplasm. The ultimate result of these changes is to create apoptotic bodies with preserved cell membrane integrity. The integrity of mitochondria is another hallmark of apoptosis. Mitochondria do not swell, and do not lose their function, namely they are functionally active in apoptotic small bodies. Once initiated programmed cell death (PCD) causes a cascade of biochemical reactions which eventually results in degradation and fragmentation of genomic DNA. The main carriers in biochemical reactions are proteases (caspases) and nuclease. Numerous studies point to the antiproliferative effects of active ingredients of some plants from the group of flavonoides, flavones, hyperoside and others. Hypericin - photosensitive, liposulubile perihinone derivate of Hypricum perforatum (St. John’ Wort) is one of the active ingredients of plants the antiproliferative and fotocytotoxicity effects of which have been subject of numerous in vitro and in vivo studies. The complexity of antproliferative effects induced by hypericin is the result of apoptosis induction and includes many biochemical mechanisms such as protein kinase C inhibition, suppression of Bcl-2 expression and/or change of oxidative status. Key words: cell proliferation, hipericin, apopotosis Napomena: kompletan tekst rada na srpskom jeziku Note: full text in Serbian |
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Corresponding Address: Tatjana Sokolović, Trgovačka 30/41, Beograd, Srbija; E-mail: tatjanasokolovic@teva.rs |
Paper received: 30. 3. 2012 Paper accepted: 1. 4. 2013 Paper Internet issues: 15. 7. 2013 |
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