Increase of lipid peroxidation by cisplatin in WI38 cells but not in SV40‐transformed WI38 cells
Increase of lipid peroxidation by cisplatin in WI38 cells but not in SV40‐transformed WI38 cells
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顺铂在 WI38 细胞中增加脂质过氧化，但在 SV40 转化的 WI38 细胞中不增加
DOI：
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发表时间：
2003
影响因子：
3.6
通讯作者：
L. See
中科院分区：
文献类型：
--
作者：
H. Yen;C. Nien;H. Majima;Chia;Sz‐Yun Chen;Jeng Wei;L. See
顺铂(CPT)是一种对正常组织有蓄积性毒性的有效抗癌药物。有人认为，CPT通过引起氧化应激来损害正常细胞，但尚不清楚它是否会对肿瘤细胞造成类似的氧化损伤。本研究以正常人肺成纤维细胞(W138)和SV40转化的WI38(VA13)细胞为模型，比较了CPT对正常和肿瘤细胞的细胞毒性、细胞凋亡、脂质过氧化和线粒体基因表达的影响。CPT对VA13细胞的生长抑制作用更强，细胞凋亡率更高。然而，CPT可增加WI38细胞中两种特异性脂质过氧化产物--酯化F2-异前列腺素和4-羟基-2-壬烯醛的水平，而对VA13细胞则无影响。此外，CPT对两种细胞线粒体12S rRNA的转录水平均有上调作用，但对WI38细胞的作用更强。这些数据表明，在WI38细胞中，脂质过氧化与细胞毒性或线粒体转录水平增加之间存在相关性，而在VA13细胞中则不然。结果还表明，在转化的WI38细胞表型中，氧化损伤和线粒体基因调控对CPT的反应发生了变化。《威利期刊》，J Biochem Mol Toxicol 17：39-46,2003；在线发表在《威利国际科学》(www.intercience.wiley.com)上。DOI 10.1002/jbt.10059
Cisplatin (CPT) is an effective anticancer drug that causes cumulative toxicity to normal tissues. It has been suggested that CPT damages normal cells by causing oxidative stress, but it is not known whether it can induce similar oxidative damage to tumor cells. In this study, by using normal human lung fibroblast (W138) cells and SV40‐transformed WI38 (VA13) cells as a model, we compared the effect of CPT on cytotoxicity, apoptosis, lipid peroxidation, and mitochondrial gene expression, which could be regulated by oxidative stress, between normal and tumor cells. CPT induced greater growth inhibition and percentage of apoptotic cells in VA13 cells. However, levels of esterified F2‐isoprostanes and 4‐hydroxy‐2‐nonenal, two specific products of lipid peroxidation, were increased by CPT in WI38 cells, but not in VA13 cells. Furthermore, the transcript level of mitochondrial 12S rRNA was augmented by CPT in both cells, but to a higher degree in WI38 cells. The data suggest a correlation between lipid peroxidation and cytotoxicity or increased mitochondrial transcript levels in WI38 cells but not in VA13 cells. The results also indicate an altered response of oxidative damage and mitochondrial gene regulation to CPT in the transformed phenotype of WI38 cells. © 2003 Wiley Periodicals, Inc. J Biochem Mol Toxicol 17:39–46, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.10059
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DOI：
10.1093/toxsci/47.2.195
发表时间：
1999-02
期刊：
Toxicological sciences : an official journal of the Society of Toxicology
影响因子：
--
作者：
Leonard P. Rybak;K. Husain;C. Whitworth;Satu M. Somani
通讯作者：
Leonard P. Rybak;K. Husain;C. Whitworth;Satu M. Somani
顺铂诱导肾小管上皮细胞中 N-乙酰半胱氨酸可抑制的 F2-异前列腺素产生和损伤。
DOI：
10.1681/asn.v981448
发表时间：
1998
期刊：
Journal of the American Society of Nephrology : JASN
影响因子：
--
作者：
Salahudeen,A;Poovala,V;Parry,W;Pande,R;Kanji,V;Ansari,N;Morrow,J;Roberts2nd,J
通讯作者：
Roberts2nd,J
影响因子：
7.4
作者：
Roberts, LJ;Morrow, JD
通讯作者：
Morrow, JD
顺铂和双核铂络合物形成 DNA-DNA 链间交联的序列特异性。
影响因子：
2.9
作者：
Zou,Y;VanHouten,B;Farrell,N
通讯作者：
Farrell,N
DOI：
10.1073/pnas.89.22.10721
发表时间：
1992-11-15
影响因子：
11.1
作者：
MORROW, JD;AWAD, JA;ROBERTS, LJ
通讯作者：
ROBERTS, LJ