Michalopoulos G K, Eckl P M, Cruise J L, Novicki D L, Jirtle R L
Toxicol Ind Health. 1987 Jun;3(2):119-28. doi: 10.1177/074823378700300209.
Stimulation of DNA synthesis by peroxisome proliferators, including DEHP, should be viewed differently from the stimulation of DNA synthesis by xenobiotic chemicals which stimulate restorative hyperplasia after hepatic necrosis induced by the toxicity of the chemical. The emerging picture of the control mechanisms for hepatocyte proliferation suggests that rather few and distinct factors are involved. The stimulation of DNA synthesis by peroxisome proliferators should be examined in the context of the effects of these factors. Comparisons with other xenobiotics show that induction of DNA synthesis at rates comparable to those of peroxisome proliferators is not sufficient to explain the rates of carcinogenicity associated with peroxisome proliferators. These considerations lead to the conclusion that although DNA synthesis enhances the incidence of neoplasia, it should not be viewed as a complete carcinogen, nor should it be considered as resulting in initiation at rates that can explain the carcinogenic potency of compounds such as peroxisome proliferators.
过氧化物酶体增殖剂（包括邻苯二甲酸二（2-乙基己基）酯）对DNA合成的刺激作用，应与外源性化学物质对DNA合成的刺激作用区别看待。外源性化学物质在化学物质毒性诱导肝坏死之后刺激修复性增生。肝细胞增殖控制机制的新情况表明，涉及的因素相当少且各不相同。过氧化物酶体增殖剂对DNA合成的刺激作用，应结合这些因素的影响来研究。与其他外源性物质的比较表明，以与过氧化物酶体增殖剂相当的速率诱导DNA合成，不足以解释与过氧化物酶体增殖剂相关的致癌率。这些考虑得出的结论是，虽然DNA合成会增加肿瘤形成的发生率，但不应将其视为完全致癌物，也不应认为其引发肿瘤的速率能够解释诸如过氧化物酶体增殖剂这类化合物的致癌效力。
