ArticleActa pharmaceutica Sinica. B2022
Aristolochic acids exposure was not the main cause of liver tumorigenesis in adulthood.
Article in Acta pharmaceutica Sinica. B, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Role of immune dysregulation in aristolochic acid-induced multisystem toxicities: an insight from systems toxicology.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Aristolochic Acid and Hepatocellular Carcinoma: A Critical Review of Genotoxic and Inflammatory Mechanisms.International journal of molecular sciences · 2026Review
- Sex-specific toxicity targets of aristolochic acids: nephrotoxicity in males, hepatotoxicity in females.Archives of toxicology · 2026Article
- High incidence of intrahepatic cholangiocarcinoma in end-stage renal disease patients in Taiwan: analysis of a nationwide database with molecular insight of aristolochic acid exposure.Virchows Archiv : an international journal of pathology · 2026Article
- Whether aristolochic acid directly drives hepatocarcinogenesis: comprehensive investigations from mutational signatures to animal models.Archives of toxicology · 2025Review
- Article
- Aristolochic acids-hijacked p53 promotes liver cancer cell growth by inhibiting ferroptosis.Acta pharmacologica Sinica · 2025Article
- Unveiling correlations between aristolochic acids and liver cancer: spatiotemporal heterogeneity phenomenon.Chinese medicine · 2024Review
- Skullcapflavone II, a novel NQO1 inhibitor, alleviates aristolochic acid I-induced liver and kidney injury in mice.Acta pharmacologica Sinica · 2023Article
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Authors and funding
22 authors at 8 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aristolochic acids (AAs) have long been considered as a potent carcinogen due to its nephrotoxicity. Aristolochic acid I (AAI) reacts with DNA to form covalent aristolactam (AL)-DNA adducts, leading to subsequent A to T transversion mutation, commonly referred as AA mutational signature. Previous research inferred that AAs were widely implicated in liver cancer throughout Asia. In this study, we explored whether AAs exposure was the main cause of liver cancer in the context of HBV infection in mainland China. Totally 1256 liver cancer samples were randomly retrieved from 3 medical centers and a refined bioanalytical method was used to detect AAI-DNA adducts. 5.10% of these samples could be identified as AAI positive exposure. Whole genome sequencing suggested 8.41% of 107 liver cancer patients exhibited the dominant AA mutational signature, indicating a relatively low overall AAI exposure rate. In animal models, long-term administration of AAI barely increased liver tumorigenesis in adult mice, opposite from its tumor-inducing role when subjected to infant mice. Furthermore, AAI induced dose-dependent accumulation of AA-DNA adduct in target organs in adult mice, with the most detected in kidney instead of liver. Taken together, our data indicate that AA exposure was not the major threat of liver cancer in adulthood.
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