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马兜铃酸(Aristolochic acids,AAs),主要是由来源于马兜铃科属植物的8-methoxy-6-nitro-phenanthro-(3,4-d)-1,3-dioxolo-5-carboxylic acid(Aristolochic acids I,AAI),6-nitro-phenanthro-(3,4-d)-1,3-dioxolo-5-carboxylic acid(Aristolochic acids II,AAII)组成的天然混合物,能够引起马兜铃酸肾病和上尿路上皮癌.本文概述了AAs及其衍生物的肾毒性及致癌性.AAs肾毒性能够诱导肾小管上皮细胞凋亡及氧化应激的发生,并能抑制水通道蛋白的表达.AAs还可以降低肾小管上皮细胞急性损伤后的修复能力,并通过TGF-β-Smad信号和促进巨噬细胞的迁移进一步促进肾脏纤维化.另外,AAs的致癌性可能是因为导致某些肿瘤抑癌基因或原癌基因突变的DNA加合物的形成,和不同个体的细胞色素P450在AAI代谢中的不同催化能力导致的.“,”Aristolochic acids (AAs), a natural mixture of 8-methoxy-6-nitro-phenanthro-(3,4-d)-1,3-dioxolo-5-carboxylic acid (AAI) and 6-nitro-phenanthro-(3,4-d)-1,3-dioxolo-5-carboxylic acid (AAII), derived from aristolochiaceae species, has been reported to cause AAS-induced nephropathy and upper urothelial cancer. In this review, we summarize the information on the nephrotoxicity and carcinogenesis of AAs and their derivatives. AAs nephrotoxicity can lead to apoptosis and oxidative stress of renal tubular cells, and inhibition of the expression of aquaporins. AAs can also reduce the capability for renal tubular epithelial cell repair after acute injury and further produce renal fibrosis by activating TGF-β-Smad signaling and promoting the migration of macrophages. Moreover, AAs-induced carcinogenesis may be due to the formation of covalent adducts with DNA which can lead to the mutation in certain tumor suppressor genes or proto-oncogenes and the different catalyzing capacity of the microsomal cytochrome P450 of individuals in AAI metabolism.