Document Detail

Mitochondrial changes during the apoptotic process of HeLa cells exposed to cisplatin.
MedLine Citation:
PMID:  10365247     Owner:  NLM     Status:  MEDLINE    
HeLa cells undergo apoptosis after exposure to cisplatin. Since mitochondria have recently been proposed as a probable effector of this type of cell death, we performed an analysis using the fluorescent cation rhodamine 123, which is transported actively by this organelle. Cisplatin induces a decrease in the mitochondrial staining, as assessed by cytofluorometric analysis. Microscopic analysis demonstrated that this effect was accompanied by damage of the mitochondria. These features were not exclusive of cisplatin, as other antineoplasic agents (taxol, etoposide) elicited similar effects. These results point toward the notion of a general effect of antineoplasic drugs over the mitochondria during induction of apoptotic cell death.
J Melendez-Zajgla; E Cruz; V Maldonado; A M Espinoza
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Biochemistry and molecular biology international     Volume:  47     ISSN:  1039-9712     ISO Abbreviation:  Biochem. Mol. Biol. Int.     Publication Date:  1999 May 
Date Detail:
Created Date:  1999-08-23     Completed Date:  1999-08-23     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  9306673     Medline TA:  Biochem Mol Biol Int     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  765-71     Citation Subset:  IM    
Laboratorio de Biología Molecular, Instituto Nacional de Cancerología, México, D. F.
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MeSH Terms
Antineoplastic Agents / pharmacology*
Antineoplastic Agents, Phytogenic / pharmacology
Cisplatin / pharmacology*
Etoposide / pharmacology
Flow Cytometry
Hela Cells
Mitochondria / drug effects*
Paclitaxel / pharmacology
Reg. No./Substance:
0/Antineoplastic Agents; 0/Antineoplastic Agents, Phytogenic; 15663-27-1/Cisplatin; 33069-62-4/Paclitaxel; 33419-42-0/Etoposide

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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