11月30日，據(jù)海外媒體報道,，新加坡研究團隊發(fā)現(xiàn)防曬霜等化妝品中常見的成分氧化鋅以納米微粒狀態(tài)使用時,，可能致癌,。
氧化鋅屬于物理性防曬成分,，可阻隔紫外線，常用于防曬霜等化妝品,。化妝品廠商為改善氧化鋅本身的白色粘厚質(zhì)地,，多在產(chǎn)品中添加微粒較小的氧化鋅成分,。
新加坡南洋理工大學和新加坡國立大學的研究人員研究化妝品中的納米材料時發(fā)現(xiàn),，皮膚細胞吸收納米級氧化鋅微粒后,，人體會產(chǎn)生蛋白質(zhì)p53以防止損傷的細胞復(fù)制,，從而避免致癌。但一些人體內(nèi)無法產(chǎn)生這種蛋白質(zhì),，或產(chǎn)生的量不足,，就可能導(dǎo)致癌癥發(fā)生,。
這項研究成果發(fā)表在新一期學術(shù)期刊《生物材料》上,。研究人員強調(diào),，該研究不一定表明氧化鋅會致癌,，人們沒必要因此驚慌,。不過,，化妝品廠商在添加納米級氧化鋅時,，需重新謹慎評估其后果,。
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.
