用户名: 密码: 验证码:
Metabonomic Analysis Reveals the CCl4-Induced Systems Alterations for Multiple Rat Organs
详细信息    查看全文
  • 作者:Limiao Jiang ; Jing Huang ; Yulan Wang ; Huiru Tang
  • 刊名:Journal of Proteome Research
  • 出版年:2012
  • 出版时间:July 6, 2012
  • 年:2012
  • 卷:11
  • 期:7
  • 页码:3848-3859
  • 全文大小:500K
  • 年卷期:v.11,no.7(July 6, 2012)
  • ISSN:1535-3907
文摘
CCl4-induced metabonomic changes have been extensively studied for mammalian liver, and such changes have not been reported for other organs. To investigate the CCl4 effects on other organs, we analyzed the CCl4-induced metabonomic changes in rat kidney, lung, and spleen using 1H NMR-based metabonomics approaches with complementary information on serum clinical chemistry and histopathology. We found that acute CCl4 exposure caused significant level elevation for creatine and decline for glucose, taurine, trimethylamine, uridine, and adenosine in rat kidney. CCl4-treatment also induced elevation of amino acids (isoleucine, leucine, valine, threonine, alanine, lysine, ornithine, methionine, tyrosine, phenylalanine, and histidine), creatine, and betaine in rat lung together with depletion of glycogen, glucose, taurine, glycine, and hypoxanthine. Furthermore, CCl4 caused elevation of lactate, alanine, betaine, and uracil in rat spleen accompanied with decline for glucose, choline, and hypoxanthine. These observations indicated that CCl4 caused oxidative stresses to multiple rat organs and alterations of their functions including renal osmotic regulations, accelerated glycolysis, and protein and nucleotide catabolism. These findings provide essential information on CCl4 toxicity to multiple rat organs and suggest that systems toxicological views are required for metabonomic studies of toxins by taking many other organs into consideration apart from so-called targeted ones.

Keywords:

carbon tetrachloride; metabonomics; systems toxicity; rat organs; NMR

© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号

地址:北京市海淀区学院路29号 邮编:100083

电话:办公室:(+86 10)66554848;文献借阅、咨询服务、科技查新:66554700