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NMR-based metabonomic analysis of the hepatotoxicity induced by combined exposure to PCBs and TCDD in rats

Lu, Chunfeng, Wang, Yimei, Sheng, Zhiguo, Liu, Gang, Fu, Ze, Zhao, Jing, Zhao, Jun, Yan, Xianzhong, Zhu, Benzhan, Peng, Shuangqing·2010·Toxicology and Applied Pharmacology
DOI 10.1016/j.taap.2010.07.020
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Abstract

A metabonomic approach using (1)H NMR spectroscopy was adopted to investigate the metabonomic pattern of rat urine after oral administration of environmental endocrine disruptors (EDs) polychlorinated biphenyls (PCBs) and 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) alone or in combination and to explore the possible hepatotoxic mechanisms of combined exposure to PCBs and TCDD. (1)H NMR spectra of urines collected 24h before and after exposure were analyzed via pattern recognition by using principal component analysis (PCA). Serum biochemistry and liver histopathology indicated significant hepatotoxicity in the rats of the combined group. The PCA scores plots of urinary (1)H NMR data showed that all the treatment groups could be easily distinguished from the control group, so could the PCBs or TCDD group and the combined group. The loadings plots of the PCA revealed remarkable increases in the levels of lactate, glucose, taurine, creatine, and 2-hydroxy-isovaleric acid and reductions in the levels of 2-oxoglutarate, citrate, succinate, hippurate, and trimethylamine-N-oxide in rat urine after exposure. These changes were more striking in the combined group. The changed metabolites may be considered possible biomarker for the hepatotoxicity. The present study demonstrates that combined exposure to PCBs and TCDD induced significant hepatotoxicity in rats, and mitochondrial dysfunction and fatty acid metabolism perturbations might contribute to the hepatotoxicity. There was good c…

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    “In addition, the increased levels of glucose and lactate in the urine from treated animals are consistent with mitochondrial impairment; this proposed inability may result from a lack of acetylCoA in themitochondria as a result of a reduction in the rate of oxidative phosphorylation and fatty acid β-oxidation (McGarry…”
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Metadata

Authors
Lu, C., Wang, Y., Sheng, Z., Liu, G., Fu, Z., Zhao, J., Zhao, J., Yan, X., Zhu, B., & Peng, S.
Venue
Toxicology and Applied Pharmacology
Publisher
Elsevier BV
Published
2010-11
Volume
248
Issue
3
Pages
178-184
ISSN
0041-008X
DOI
10.1016/j.taap.2010.07.020
Cited by
61
References
1
Language
en
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)

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