| Inhibition of selenite-induced cytotoxicity and apoptosis in human colonic carcinoma (HT-29) cells by copper. | |
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MedLine Citation:
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PMID: 10050269 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Selenite catalytically oxidizes reduced glutathione (GSH) with subsequent generation of superoxide. Our laboratory has previously shown that this selenite-catalyzed generation of superoxide is strongly inhibited by copper [as copper(II) sulfate]. In the present study we have demonstrated that exposure of human colonic carcinoma cells (HT-29) to selenite resulted in the induction of apoptosis, DNA fragmentation, an increase in intracellular levels of the antioxidant GSH, and cytotoxicity. Selenite-induced apoptosis, DNA fragmentation, increases in GSH levels, and cytotoxicity were inhibited by copper(II) sulfate. Copper only protected cells from selenite cytotoxicity when cells were exposed to selenite and copper simultaneously, not when cells were pretreated with copper, then washed before selenite exposure. This suggests that copper elicits its protective effect extracellularly. Previous data reported by this laboratory clearly demonstrated that copper inhibited selenite-catalyzed superoxide generation. Collectively, these data suggest that reactive oxygen species may play a role in selenite-induced cytotoxicity, apoptosis, and DNA fragmentation. |
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Authors:
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R L Davis; J E Spallholz; B C Pence |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Nutrition and cancer Volume: 32 ISSN: 0163-5581 ISO Abbreviation: Nutr Cancer Publication Date: 1998 |
Date Detail:
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Created Date: 1999-05-24 Completed Date: 1999-05-24 Revised Date: 2004-11-17 |
Medline Journal Info:
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Nlm Unique ID: 7905040 Medline TA: Nutr Cancer Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 181-9 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, Texas Tech University Health Sciences Center, Lubbock 79430, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Anticarcinogenic Agents
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pharmacology* Apoptosis* Cell Division / drug effects Cell Survival / drug effects Copper Sulfate / pharmacology* DNA Fragmentation* Glutathione / metabolism HT29 Cells / drug effects, metabolism, pathology* Humans In Situ Nick-End Labeling Reactive Oxygen Species / physiology Sodium Selenite / pharmacology* |
| Chemical | |
Reg. No./Substance:
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0/Anticarcinogenic Agents; 0/Reactive Oxygen Species; 10102-18-8/Sodium Selenite; 70-18-8/Glutathione; 7758-98-7/Copper Sulfate |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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