Metabolic profiling study on potential toxicity and immunotoxicity-biomarker discovery in rats treated with cyclophosphamide using HPLC-ESI-IT-TOF-MS.
Metabolic profiling study on potential toxicity and immunotoxicity-biomarker discovery in rats treated with cyclophosphamide using HPLC-ESI-IT-TOF-MS.
复制标题
使用 HPLC-ESI-IT-TOF-MS 对环磷酰胺治疗的大鼠进行潜在毒性和免疫毒性生物标志物发现的代谢谱研究。
DOI:
10.1002/bmc.3355
复制
发表时间:
2015
期刊:
影响因子:
--
通讯作者:
Xiaomei Ling
中科院分区:
文献类型:
--
作者:
Jing Li;Wensi Lin;Weiwei Lin;P. Xu;Jianmei Zhang;Haisong Yang;Xiaomei Ling
Despite the recent advances in understanding toxicity mechanism of cyclophosphamide (CTX), the development of biomarkers is still essential. CTX-induced immunotoxicity in rats by a metabonomics approach was investigated using high-performance liquid chromatography coupled with ion trap time-of-flight mass spectrometry (HPLC-ESI-IT-TOF-MS). The rats were orally administered CTX (30 mg/kg/day) for five consecutive days, and on the fifth day samples of urine, thymus and spleen were collected and analyzed. A significant difference in metabolic profiling was observed between the CTX-treated group and the control group by partial least squares-discriminant analysis (PLS-DA), which indicated that metabolic disturbances of immunotoxicity in CTX-treated rats had occurred. One potential biomarker in spleen, three in urine and three in thymus were identified. It is suggested that the CTX-toxicity mechanism may involve the modulation of tryptophan metabolism, phospholipid metabolism and energy metabolism. This research can help to elucidate the CTX-influenced pathways at a low dose and can further help to indicate the patients' pathological status at earlier stages of toxicological progression after drug administration.
影响因子:
4.3
作者:
Salem, Mohamed L.;Al-Khami, Amir A.;El-Nagaar, Sabry A.;Zidan, Abdel-Aziz A.;Al-Sharkawi, Ismail M.;Diaz-Montero, C. Marcela;Cole, David J.
通讯作者:
Cole, David J.
影响因子:
5.8
作者:
Li, Fei;Patterson, Andrew D.;Hoefer, Constance C.;Krausz, Kristopher W.;Gonzalez, Frank J.;Idle, Jeffrey R.
通讯作者:
Idle, Jeffrey R.