Fiorio R, Bronzetti G
Istituto di Mutagenesi e Differenziamento, CNR, Pisa, Italy.
Mutat Res. 1994 Jun;324(1-2):51-7. doi: 10.1016/0165-7992(94)90067-1.
The effects of the antimutagenic flavoring cinnamaldehyde on the induction of HGPRT- mutants by methyl methanesulfonate (MMS), N-nitroso-N-methylurea (MNU), ethyl methanesulfonate (EMS) and UV light was investigated in the Chinese hamster V79 cell line. Cinnamaldehyde did not show any mutagenic or toxic effects in this experimental system by itself and did not modify mutation frequency when given to cells simultaneously with chemical mutagens. Under these conditions, the cytotoxicity of MMS, but not that of MNU and EMS, was increased. Cell viability was also reduced in MNU-, EMS-, or UV light-pretreated cells when they were postincubated in the presence of cinnamaldehyde. Moreover, cinnamaldehyde reduced the frequency of mutations induced by MMS but not by the other mutagens. The results obtained suggest that cinnamaldehyde inhibits some cellular function(s) promoting the repair of a variety of different cytotoxic lesions. At the same time, stimulation by cinnamaldehyde of an error-free DNA repair mechanism acting on MMS-induced mutagenic damage was indicated.
在中国仓鼠V79细胞系中，研究了抗诱变剂肉桂醛对甲磺酸甲酯（MMS）、N-亚硝基-N-甲基脲（MNU）、甲磺酸乙酯（EMS）和紫外线诱导次黄嘌呤-鸟嘌呤磷酸核糖转移酶（HGPRT）突变体的影响。肉桂醛本身在该实验系统中未显示出任何诱变或毒性作用，并且当与化学诱变剂同时给予细胞时，也不会改变突变频率。在这些条件下，MMS的细胞毒性增加，而MNU和EMS的细胞毒性未增加。当MNU、EMS或紫外线预处理的细胞在肉桂醛存在下进行后培养时，细胞活力也会降低。此外，肉桂醛降低了MMS诱导的突变频率，但未降低其他诱变剂诱导的突变频率。所得结果表明，肉桂醛抑制了促进多种不同细胞毒性损伤修复的某些细胞功能。同时，表明肉桂醛刺激了作用于MMS诱导的诱变损伤的无差错DNA修复机制。
