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为了探讨染发剂对DNA可能产生的损伤效应,采用SOS/Umu试验对氧化型染发剂的主要成分对苯二胺(PPD)和过氧化氢(H_2O_2)的遗传毒性进行了观察。结果表明:在无S_9存在的条件下,PPD在375～6000μg/管的剂量范围内与酶诱导率之间无剂量反应关系,H_2O_2在4～125μg/管的剂量范围内与酶诱导率之间有剂量反应关系(r=0.995,p<0.01),PPD被H_2O_2氧化后则显示出了遗传毒作用(r=0.988,p<0.01);4种氧化型染发剂(F、G、S及X牌)的1剂(主要含PPD)在39～1250μg/管的剂量范围内与酶诱导率之间无剂量反应关系,2剂(主要含H_2O_2)在9.8～312.5μg/管剂量范围内与酶诱导率之间有剂量反应关系(r_F=0.950,P<0.01;r_G=0.926,P<0.01;r_S=0.997,P<0.01;rx=0.993,P<0.01)。1剂和2剂按实用比例等量混和后在9.8～312.5μg/管(按PPD浓度计)剂量范围内有剂量反应关系(r_F=0.994,P<0.01;r_G=0.932,P<0.01;r_S=0.998,P<0.01;r_X=0.987,P<0.01)。在S_9存在的条件下,待测物在受试剂量范围内均未显示出遗传毒作用。结果提示,氧化型染发剂有DNA损伤作用,且其致突变性与氧化剂H_2O_2的作用有关。
In order to investigate the possible damage effect of hair dye on DNA, the genotoxicity of phenylenediamine (PPD) and hydrogen peroxide (H 2 O 2), the main component of oxidative hair dye, was observed by SOS / Umu assay. The results showed that there was no dose-response relationship between PPD and enzyme-induced rate in the range of 375-6000 μg / tube in the absence of S_9, and the dose-dependent relationship between PPD and enzyme-induced rate was observed in the range of 4 ~ 125 μg / (R = 0.995, p <0.01). After PPD was oxidized by H 2 O 2, it showed genotoxicity (r = 0.988, p <0.01). Four oxidative hair dyes (F, G, S and X (PPD) in the dose range of 39 ~ 1250μg / tube had no dose-response relationship with the induction rate of the enzyme. Two doses (mainly containing H_2O_2) had a dose-dependent relationship with the enzyme in the range of 9.8-312.5μg / There was a dose-response relationship between induction rate (r_F = 0.950, P <0.01; r_G = 0.926, P <0.01; r_S = 0.997, P <0.01; rx = 0.993, P <0.01). 1 dose and 2 dose according to the practical proportion of the same amount of mixture in 9.8 ~ 312.5μg / tube (by PPD concentration) dosage range dose-response relationship (r_F = 0.994, P <0.01; r_G = 0.932, P <0.01; r_S = 0.998, P <0.01; r_X = 0.987, P <0.01). In the presence of S_9, the analyte did not show genotoxic effects in the range of doses tested. The results suggest that oxidative hair dyes have DNA damage, and its mutagenicity and the role of oxidant H_2O_2.