期刊
BIOCHEMICAL JOURNAL
卷 414, 期 -, 页码 93-102出版社
PORTLAND PRESS LTD
DOI: 10.1042/BJ20071615
关键词
anticancer drug toxicity; cisplatin; glutathione; mitochondrial DNA (mtDNA) metabolism; mitochondrial RNA (mtRNA); stability
资金
- Spanish Ministry of Education [SAF2006-00428]
- Health Institute Carlos III [REDEMETH-G03/054, REDDEN C03/06-Grupo RC-N34-3]
- European Union
- EUMITOCOMBAT [LSHM-CT-2004-503116]
- DGA (Diputacion General de Aragon) Research Group of Excellence grant [1355]
- DGA Consolidated Research Group grant [1333]
- ROSASNET [CSD2007-00020]
Cisplatin accumulates in mitochondria, which are a major target for this drug in cancer cells. Thus alterations in mitochondrial function have been implicated in cancer cell resistance to chemotherapeutic agents. Moreover, cisplatin toxic side effects seem to be associated with mitochondrial injury in vivo and in vitro. In order to clarify the potential effect of cisplatin in null (mitochondrial DNA) maintenance and expression, we have analysed rat liver mtDNA and mtRNA (mitochondrial RNA) synthesis as well as their stability under the influence of in vivo treatment on in vitro exposure to cisplatin. We show that cisplatin causes a direct and significant impairment of roll and mtRNA synthesis and decreases steady-state levels of mtRNAs in isolated mitochondria. Furthermore, in vivo treatment of the animals with cisplatin exerts a protective effect from the impairment of mtRNA metabolism caused by in vitro exposure to the drug, by means of increased mitochondrial GSH levels after in vivo cisplatin treatment.
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