Conaway C C, Tong C, Williams G M
Mutat Res. 1984 May;136(2):153-7. doi: 10.1016/0165-1218(84)90158-7.
Morpholine and a series of morpholine derivatives were assayed for the potential to induce DNA repair in the rat hepatocyte primary culture/DNA repair assay. Morpholine did not induce DNA repair at dose concentrations which were not toxic (0.0001-0.1 mg/ml). Two animal metabolites of morpholine, N- methylmorpholine oxide and N- hydroxymorpholine , also did not induce DNA repair at the non-toxic concentrations tested (0.0001-10 mg/ml and 0.0001-1 mg/ml, respectively). A putative metabolite of morpholine, 3- morpholinone , was inactive (0.001-10 mg/ml) and a polyurethane foam catalyst, N- butylmorpholine (0.0001-0.1 mg/ml) was also inactive. The chemical intermediate N- hydroxyethylmorpholine induced DNA repair in the dose range 1-5 mg/ml. It was concluded that genotoxicity of substituted morpholines is a function of the substituent moiety rather than morpholine itself.
在大鼠肝细胞原代培养/DNA修复试验中，对吗啉及一系列吗啉衍生物诱导DNA修复的潜力进行了测定。在无毒剂量浓度（0.0001 - 0.1毫克/毫升）下，吗啉未诱导DNA修复。吗啉的两种动物代谢产物，N - 甲基氧化吗啉和N - 羟基吗啉，在所测试的无毒浓度（分别为0.0001 - 10毫克/毫升和0.0001 - 1毫克/毫升）下也未诱导DNA修复。吗啉的一种假定代谢产物3 - 吗啉酮无活性（0.001 - 10毫克/毫升），一种聚氨酯泡沫催化剂N - 丁基吗啉（0.0001 - 0.1毫克/毫升）也无活性。化学中间体N - 羟乙基吗啉在1 - 5毫克/毫升的剂量范围内诱导DNA修复。得出的结论是，取代吗啉的遗传毒性是取代基部分的函数，而不是吗啉本身的函数。
