Ameliorative effects of SLC22A2 gene polymorphism 808 G/T and cimetidine on cisplatin-induced nephrotoxicity in Chinese cancer patients

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• 作者：Jing Zhang^a ; Wen Zhou^b ; ^{wenzhou25@126.com}
• 关键词：Ala ; alanine ; AR ; androgen response ; GFR ; glomerular filtration rate ; OCT1 ; organic cation transporter 1 ; OCT2 ; organic cation transporter 2 ; PCR ; polymerase chain reaction ; rOCT2 ; rat organic cation transporters 2 ; ROS ; reactive oxygen species ; SCr ; seru
• 刊名：Food and Chemical Toxicology
• 出版年：2012
• 期刊代码：20_02786915
• 类别：pha
• 出版时间：July, 2012
• 卷：50
• 期：7
• 页码：2289-2293
• 文件大小：309 K

摘要

To investigate the roles of SLC22A2 gene polymorphism 808 G/T and cimetidine on cisplatin-induced nephrotoxicity, a total of 123 Chinese cancer patients treated with cisplatin alone (n = 55) or in combination with cimetidine (n = 68) were genotyped. The changes of serum creatinine (SCr), blood urea nitrogen (BUN) and cystatin C levels were used as biomarkers for the evaluation of cisplatin-induced nephrotoxicity. The changes of BUN and SCr levels showed no significant difference between groups divided by genotypes and treatments (P > 0.05). However, patients with mutant genotype (GT/TT) or with cimetidine treatment had smaller increase of the cystatin C levels compared to those with wild genotype (GG) or without cimetidine treatment (P < 0.05). In the non-cimetidine-treated group, the changes of cystatin C level in patients with mutant genotype (GT/TT) was significantly smaller than those with wild genotype (GG) (P = 0.043). In the wild type group, the cystatin C level change of patients without cimetidine treatment was significantly larger than those with cimetidine treatment (P = 0.007). These results suggested that SLC22A2 gene polymorphism 808 G/T and cimetidine could attenuate cisplatin nephrotoxicity in Chinese cancer patients. But the renoprotection mechanism of cimetidine might be damaged by the mutation.