Lin W C, Liao Y C, Liau M C, Lii C K, Sheen L Y
Department of Pharmacology, China Medical University, Taichung 404, Taiwan, ROC.
Food Chem Toxicol. 2006 Apr;44(4):546-51. doi: 10.1016/j.fct.2005.08.029. Epub 2005 Oct 17.
The effects of CDA-II (cell differentiation agent II; a urinary preparation) on both aflatoxin B(1) (AFB(1))-induced cell injury and DNA damage were investigated using cultured rat hepatocytes. CDA-II was able to suppress both the lipid peroxidation and lactate dehydrogenase leakage induced by AFB(1). Glutathione (GSH) depletion by AFB(1) was replenished by CDA-II treatment. Under these experimental conditions, CDA-II enhanced the activity of GSH peroxidase, but not GSH S-transferase. By evaluation of unscheduled DNA synthesis, CDA-II reduced AFB(1)-induced DNA damage in hepatocyte cultures. These findings suggest that CDA-II can inhibit cytotoxicity of AFB(1) through enhancing the activity of GSH peroxidase and preventing GSH depletion.
利用培养的大鼠肝细胞，研究了细胞分化因子II（CDA-II；一种尿液制剂）对黄曲霉毒素B1（AFB1）诱导的细胞损伤和DNA损伤的影响。CDA-II能够抑制AFB1诱导的脂质过氧化和乳酸脱氢酶泄漏。通过CDA-II处理可补充AFB1导致的谷胱甘肽（GSH）消耗。在这些实验条件下，CDA-II增强了GSH过氧化物酶的活性，但未增强GSH S-转移酶的活性。通过对非程序性DNA合成的评估，CDA-II减少了肝细胞培养物中AFB1诱导的DNA损伤。这些发现表明，CDA-II可通过增强GSH过氧化物酶的活性和防止GSH消耗来抑制AFB1的细胞毒性。
