新華社華盛頓8月7日電（記者林小春）兩項(xiàng)7日發(fā)表在美國《科學(xué)－轉(zhuǎn)化醫(yī)學(xué)》雜志上的研究稱,，馬兜鈴酸會(huì)導(dǎo)致人體發(fā)生大量基因突變,，從而引發(fā)癌癥，其致癌性強(qiáng)于煙草和紫外線。
馬兜鈴酸天然存在于馬兜鈴、尋骨風(fēng)、天仙藤和朱砂蓮等馬兜鈴科植物中,。20多年前，含有這類成分的中草藥減肥藥被發(fā)現(xiàn)會(huì)導(dǎo)致腎損害,，后來人們又發(fā)現(xiàn)它還增加罹患尿路癌癥的風(fēng)險(xiǎn),。約10年前，世界衛(wèi)生組織下屬的國際癌癥研究中心將馬兜鈴酸列為一類致癌物,。
美國約翰斯·霍普金斯大學(xué)與紐約州立大學(xué)石溪分校等機(jī)構(gòu)研究人員在一項(xiàng)研究中報(bào)告說,，他們對(duì)接觸過馬兜鈴酸的19名上尿路癌癥患者以及沒有接觸這種毒物的另7名患者進(jìn)行了全外顯子組測序。結(jié)果發(fā)現(xiàn),，馬兜鈴酸接觸組每名患者平均發(fā)生753個(gè)基因突變,，而非馬兜鈴酸接觸組每名患者只有91個(gè)基因突變,。研究表明，馬兜鈴酸能引發(fā)的基因突變數(shù)量高于煙草和紫外線,。
另一項(xiàng)研究由來自新加坡,、美國與中國臺(tái)灣等多個(gè)醫(yī)學(xué)機(jī)構(gòu)的研究人員合作完成。他們利用全基因組和外顯子組測序技術(shù)證實(shí),，接觸馬兜鈴酸可能會(huì)引起過去被認(rèn)為由其他致癌因素導(dǎo)致的癌癥,。例如，一種過去被認(rèn)為是由吸煙引起的上尿路癌癥和一種過去被歸因于某種慢性肝炎感染所致的肝癌,，可能均與馬兜鈴酸有關(guān),。研究人員表示，這是首次證實(shí)馬兜鈴酸與肝癌之間的相關(guān)性,。
2004年,，中國國家食品藥品監(jiān)督管理局根據(jù)對(duì)含馬兜鈴酸藥材及其制劑不良反應(yīng)的報(bào)道以及毒副作用研究和結(jié)果的分析，決定加強(qiáng)對(duì)含馬兜鈴酸藥材及其制劑的監(jiān)督管理,，凡是含有馬兜鈴酸的中藥制劑一律嚴(yán)格按處方藥管理,。（生物谷Bioon.com）
生物谷推薦的英文摘要
Sci. Transl. Med. DOI: 10.1126/scitranslmed.3006200
Mutational Signature of Aristolochic Acid Exposure as Revealed by Whole-Exome Sequencing
Margaret L. Hoang1, Chung-Hsin Chen2, Viktoriya S. Sidorenko3, Jian He1, Kathleen G. Dickman3,4, Byeong Hwa Yun5, Masaaki Moriya3, Noushin Niknafs6, Christopher Douville6, Rachel Karchin6, Robert J. Turesky5, Yeong-Shiau Pu2, Bert Vogelstein1, Nickolas Papadopoulos1, Arthur P. Grollman3,4, Kenneth W. Kinzler1,* and Thomas A. Rosenquist3,*
In humans, exposure to aristolochic acid (AA) is associated with urothelial carcinoma of the upper urinary tract (UTUC). Exome sequencing of UTUCs from 19 individuals with documented exposure to AA revealed a remarkably large number of somatic mutations and an unusual mutational signature attributable to AA. Most of the mutations (72%) in these tumors were A:T-to-T:A transversions, located predominantly on the nontranscribed strand, with a strong preference for deoxyadenosine in a consensus sequence (T/CAG). This trinucleotide motif overlaps the canonical splice acceptor site, possibly accounting for the excess of splice site mutations observed in these tumors. The AA mutational fingerprint was found frequently in oncogenes and tumor suppressor genes in AA-associated UTUC. The AA mutational signature was observed in one patient’s tumor from a UTUC cohort without previous indication of AA exposure. Together, these results directly link an established environmental mutagen to cancer through genome-wide sequencing and highlight its power to reveal individual exposure to carcinogens.
