ArticleArchives of toxicology2023
N-acetyltransferase 2 genetic polymorphism modifies genotoxic and oxidative damage from new psychoactive substances.
Article in Archives of toxicology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Metabolism and genotoxicity of 4,4'-oxydianiline is dependent on N-acetyltransferase 2 genetic polymorphism.Environmental toxicology and pharmacology · 2025Article
- Article
- The effect of the rs1799931 G857A (G286E) polymorphism on N-acetyltransferase 2-mediated carcinogen metabolism and genotoxicity differs with heterocyclic amine exposure.Archives of toxicology · 2023Article
- G × E interactions as a basis for toxicological uncertainty.Archives of toxicology · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The use of new psychoactive substances (NPS) as drugs of abuse is common and increasingly popular, particularly among youth and neglected communities. Recent studies have reported acute toxic effects from these chemicals; however, their long-term toxicity is unknown. Genetic differences between individuals likely affect the toxicity risk. Arylamine N-acetyltransferase 2 (NAT2) capacity differs among individuals due to genetic inheritance. The goal of the present study is to investigate the gene-environment interaction between NAT2 polymorphism and toxicity after exposure to these chemicals. We measured N-acetylation by human NAT1 and NAT2 and found that N-acetylation of NPS is carried out exclusively by NAT2. Differences in N-acetylation between NAT2*4 (reference allele) and NAT2*5B (common variant allele) were highly significant (p < 0.0001). Using DNA repair-deficient genetically engineered Chinese hamster ovary (CHO cells), expressing human CYP1A2 and either NAT2*4 or NAT2*5B, we measured the induction of DNA double-strand breaks ([Formula: see text]H2Ax) following treatment of the CHO cells with increasing concentrations of NPS. The induction of [Formula: see text]H2Ax showed a NAT2 allele-dependent response, higher in the NAT2*4 vs NAT2*5B alleles (p < 0.05). Induction of oxidative stress (ROS/RNS) was evaluated; we observed NAT2 allele-dependent response for all compounds in concentrations as low as 10 [Formula: see text]M, where NAT2*4 showed increased ROS/RNS vs NAT2*5B (p < 0.05). In summary, NPS are N-acetylated by NAT2 at rates higher in cells expressing NAT2*4 than NAT2*5B. Exposure to psychoactive chemicals results in genotoxic and oxidative damage that is modified by the NAT2 genetic polymorphism.
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