[2] PR toxin contains multiple functional groups, including acetoxy (CH3COO-), aldehyde (-CHO), α,β-unsaturated ketone (-C=C-CO) and two epoxides.

Aristolochene then gains an alcohol, a ketone, and an additional alkene, mediated by hydroxysterol oxidase and quinone oxidoreductase.

[3] Eremofortin C has been isolated from microbial sources and found to be in a spontaneous equilibrium between an open-chain hydroxy–ketone structure and a lactol form.

[4][6] Another interesting finding is the decreased activity of respiratory control and oxidative phosphorylation in the (isolated) mitochondria of the liver .

[6] Multiple experiments have shown the different effects of PR toxin: it can cause damage to the liver and kidney, can induce carcinogenicity, and can in vivo inhibit DNA replication, protein synthesis, and transcription.

[3][better source needed] Most experiments on the effect of the PR toxin focus on the inhibition of protein synthesis and impairment of the liver.

[1] The same study reported that ten minutes after an oral dose of 160 mg/kg, the animals experienced breathing problems that eventually led to death.

Toxic effects in mice and rats included abdominal writhing, decrease of motor activity and respiration rate, weakness of the hind legs and ataxia.

When the median lethal dose was ingested orally, the pathology was described as swollen-gas filled stomach and intestines as well as edema and congestion in the lungs.

If PR toxin was injected intraperitoneally, cats, mice and rats developed ascites fluid and edema of the lungs and scrotum.

This increased permeability lead to a decrease in blood volume and direct damage to the vital organs including lungs, kidneys, liver and heart.