11月30日，据海外媒体报道，新加坡研究团队发现防晒霜等化妆品中常见的成分氧化锌以纳米微粒状态使用时，可能致癌。
氧化锌属于物理性防晒成分，可阻隔紫外线，常用于防晒霜等化妆品。化妆品厂商为改善氧化锌本身的白色粘厚质地，多在产品中添加微粒较小的氧化锌成分。
新加坡南洋理工大学和新加坡国立大学的研究人员研究化妆品中的纳米材料时发现，皮肤细胞吸收纳米级氧化锌微粒后，人体会产生蛋白质p53以防止损伤的细胞复制，从而避免致癌。但一些人体内无法产生这种蛋白质，或产生的量不足，就可能导致癌症发生。
这项研究成果发表在新一期学术期刊《生物材料》上。研究人员强调，该研究不一定表明氧化锌会致癌，人们没必要因此惊慌。不过，化妆品厂商在添加纳米级氧化锌时，需重新谨慎评估其后果。
doi:10.1016/j.biomaterials.2011.07.036
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The role of the tumor suppressor p53 pathway in the cellular DNA damage response to zinc oxide nanoparticles
Kee Woei Nga, Stella P.K. Khoob, Boon Chin Henga, Magdiel I. Setyawatic, Eng Chok Tanb, Xinxin Zhaoa, Sijing Xionga, Wanru Fangd, David T. Leongc, d, Corresponding Author Contact Information, E-mail The Corresponding Author, E-mail The Corresponding Author, Joachim S.C. Looa
In this paper, we explored how ZnO nanoparticles cross-interact with a critical tumor suppressive pathway centered around p53, which is one of the most important known tumor suppressors that protects cells from developing cancer phenotypes through its control over major pathways like apoptosis, senescence and cell cycle progression. We showed that the p53 pathway was activated in BJ cells (skin fibroblasts) upon ZnO nanoparticles treatment with a concomitant decrease in cell numbers. This suggests that cellular responses like apoptosis in the presence of ZnO nanoparticles require p53 as the molecular master switch towards programmed cell death. This also suggests that in cells without robust p53, protective response can be tipped towards carcinogenesis when stimulated by DNA damage inducing agents like ZnO nanoparticles. We observed this precarious tendency in the same BJ cells with p53 knocked down using endogeneous expressing shRNA. These p53 knocked down BJ cells became more resistant to ZnO nanoparticles induced cell death and increased cell progression. Collectively, our results suggest that cellular response towards specific nanoparticle induced cell toxicity and carcinogenesis is not only dependent on specific nanoparticle properties but also (perhaps more importantly) the endogenous genetic, transcriptomic and proteomic landscape of the target cells.
