Aristolochic acids (English: /əˌrɪstəˈloʊkɪk/) are a family of carcinogenic, mutagenic, and nephrotoxic phytochemicals commonly found in the flowering plant family Aristolochiaceae (birthworts). Aristolochic acid (AA) I is the most abundant one. The family Aristolochiaceae includes the genera Aristolochia (birthwort) and Asarum (wild ginger), which are both commonly used in Chinese herbal medicine. Despite the host plants having a long history of use in traditional medicine, modern clinical research suggests aristolochic acids cause kidney and liver cancer. The FDA has issued warnings regarding consumption of AA-containing supplements. ^{[citation needed]}

Birthwort plants, and the aristolochic acids they contain, were quite common in ancient Greek and Roman medical texts, well-established as an herb there by the fifth century BC. Birthworts appeared in Ayurvedic texts by 400 AD, and in Chinese texts later in the fifth century. In these ancient times, it was used to treat kidney and urinary problems, as well as gout, snakebites, and a variety of other ailments. It was also considered to be an effective contraceptive. In many of these cases, birthworts were just some of the many ingredients used to create ointments or salves. In the early first century, in Roman texts, Aristolochia is first mentioned as a component of oral medicines that were used to treat things such as asthma, hiccups, muscle spasms and pains, and to assist in the expulsion of afterbirth.

Aristolochic acid poisoning was first diagnosed in the early 1990s at a clinic in Brussels, Belgium, when cases of nephritis leading to rapid kidney failure were seen in a group of women who had all taken the same weight-loss supplement, Aristolochia fangchi, which contained aristolochic acid. This nephritis was termed “Chinese herbs nephropathy” (CHN) due to the origin of the weight-loss supplement. A similar condition previously known as Balkan endemic nephropathy (BEN), first characterized in the 1950s in southeastern Europe, was later discovered to be also the result of aristolochic acid (AA) consumption. BEN is more slowly progressive than the nephritis that is seen in CHN, but is likely caused by low-level AA exposure, possibly from contamination of wheat flour seeds by a plant of the birthwort family, Aristolochia clematitis. CHN and BEN fall under the umbrella of what is now known as aristolochic acid nephropathy.

A study reported in the Science Translational Medicine journal in October 2017 reported high incidents of liver cancer in Asia, particularly Taiwan, which bore the "well-defined mutational signature" of aristolochic acids. The same link was found in Vietnam and other South-east Asian countries. This was compared with much lower rates found in Europe and North America.

The major components of the "aristolochic acid" mixture are aristolochic acid I (AA-I, 12) and aristolochic acid II (AA-II). AA-I biosynthesis begins with tyrosine (2), and proceeds via norlaudanosoline (6, a hydrogenated benzylisoquinoline) and the aporphine alkaloid stephanine (11):

This pathway is hardly surprising: the combination of an aryl carboxylic acid and an aryl nitro functionality (uncommon in natural products) suggests an apparent biogenetic relationship to the aporphines.

Proof, of course, comes from isotopic labeling studies. Feeding Aristolochia sipho (±)‑[3‑¹⁴C, ¹⁵N]-tyrosine, and isolating and degrading the resulting doubly-labeled AA-I evidences that the nitro group of AA-I originates from the amino group of tyrosine. Previous studies had already demonstrated that tyrosine is metabolized to norlaudanosoline, as follows. Tyrosine is metabolized to L-DOPA (3), and thence dopamine (4) and 3,4-dihydroxyphenylacetaldehyde (DOPAL, not shown — the decarboxylation product of 5). Norlaudanosoline synthetase then catalyzes a Pictet-Spengler-like condensation between dopamine and DOPAL.

Feeding A. sipho (±)‑[4‑¹⁴C]-norlaudanosoline forms ¹⁴C-labeled AA-I, and indeed the carbon atom at ring position C4 of norlaudanosoline is incorporated exclusively in the carboxylic acid moiety of AA-I. No labeled AA-I forms in the analogous experiment with [4‑¹⁴C]-tetrahydropapaverine; thus biosynthesis of AA-I from norlaudanosoline must require a phenol oxidation to aporphine intermediates.