Mechanisms of resistance to cis-diamminedichloroplatinum (II) in a rat ovarian carcinoma cell line |
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| Affiliation: | 1. College of Chemistry and Chemical Engineering, Shaanxi University of Science and Technology, Xi''an 710021, China;2. School of Information Science and Engineering, Ningbo Institute of Technology, Zhejiang University, Ningbo 315100, China;3. Institute of Advanced Electrochemical Energy & School of Materials Science and Engineering, Xi''an University of Technology, Xi''an 710048, China;4. Shaanxi International Joint Research Centre of Surface Technology for Energy Storage Materials, Xi''an, Shaanxi 710048, China;1. Kurnakov Institute of General and Inorganic Chemistry RAS, Leninsky pr., 31, Moscow 119991, Russia;2. Voronezh State University, Universitetskaya pl., 1, Voronezh 394018, Russia;3. Institut Européen des Membranes, UMR 5635, Université Montpellier, ENSCM, CNRS, CC047, 34095 Montpellier Cedex 5, France |
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| Abstract: | A cis-diamminedichloroplatinum(II) (cisplatin)-resistant subline (Cis-Ptr) demonstrated 20-fold greater resistance to the cytotoxic effects of cisplatin, compared with the parental cloned rat ovarian carcinoma cell line (ROT 68/C1). The uptake of cisplatin into the Cis-Ptr cells was identical to that into the ROT68/C1 cells in vitro and in vivo. Glutathione activity in a cytoplasmic extract was 1.4-fold and 1.8-fold greater in the Cis-PTr cells than in the ROT68/C1 cells in vitro and in vivo, respectively. There was no difference between the ROT68/C1 and Cis-PTr cells in 195mcisplatin binding per μg DNA. DNA repair of cisplatin DNA damage was increased in the Cis-PTr cells but not in the ROT68/C1 cells. These results suggest that the mechanism of resistance to cisplatin in rat ovarian carcinoma cells involve increased activity of the DNA repair system and increased cytosolic binding to thiols may also be involved. |
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