Effects of dose and human N-acetyltransferase 1 genetic polymorphism in benzidine metabolism and genotoxicity

Habil, Mariam R.; Hein, David W.

doi:10.1007/s00204-023-03497-1

Arch Toxicol

2023

DOI: 10.1007/s00204-023-03497-1

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Effects of dose and human N-acetyltransferase 1 genetic polymorphism in benzidine metabolism and genotoxicity

Mariam R. Habil

David W. Hein

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2024

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Cited by 3 publications

References 43 publications

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Efficient synergistic degradation of Congo red and omeprazole in wastewater using rGO/Ag@ZnO nanocomposite

Kousar,

Rasheed,

Yasmeen

et al. 2024

Journal of Water Process Engineering

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Efficient synergistic degradation of Congo red and omeprazole in wastewater using rGO/Ag@ZnO nanocomposite

Kousar,

Rasheed,

Yasmeen

et al. 2024

Journal of Water Process Engineering

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Bioactivation, Mutagenicity, DNA Damage, and Oxidative Stress Induced by 3,4-Dimethylaniline

Habil,

Salazar-González,

Doll

et al. 2024

Biomolecules

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3,4-Dimethylaniline (3,4-DMA) is present in cigarette smoke and widely used as an intermediate in dyes, drugs, and pesticides. Nucleotide excision repair-deficient Chinese hamster ovary (CHO) cells stably transfected with human CYP1A2 and N-acetyltransferase 1 (NAT1) alleles: NAT1*4 (reference allele) or NAT1*14B (the most common variant allele) were utilized to assess 3,4-DMA N-acetylation and hypoxanthine phosphoribosyl transferase (HPRT) mutations, double-strand DNA breaks and reactive oxygen species (ROS). CHO cells expressing NAT1*4 exhibited significantly (p < 0.001) higher 3,4-DMA N-acetylation rates than CHO cells expressing NAT1*14B both in vitro and in situ. In CHO cells expressing CYP1A2 and NAT1, 3,4-DMA caused concentration-dependent increases in reactive oxygen species (ROS), double-stranded DNA damage, and HPRT mutations. CHO cells expressing NAT1*4 and NAT1*14B exhibited concentration-dependent increases in ROS following treatment with 3,4-DMA (linear trend p < 0.001 and p < 0.0001 for NAT1*4 and NAT1*14B, respectively) that were lower than in CHO cells expressing CYP1A2 alone. DNA damage and oxidative stress induced by 3,4-DMA did not differ significantly (p >0.05) between CHO cells expressing NAT1*4 and NAT1*14B. CHO cells expressing NAT1*14B showed higher HPRT mutants (p < 0.05) than CHO cells expressing NAT1*4. These findings confirm 3,4-DMA genotoxicity consistent with potential carcinogenicity.

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Emodin inhibits benzidine‑enhanced survival and migration of upper urinary tract urothelial carcinoma cells by targeting the PKA/COX2 signaling pathway

Jin,

Wang,

Feng

et al. 2024

Int J Oncol

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The carcinogenic effects of benzidine (BZ) on bladder cancer are well documented, but its potential for promoting upper urinary tract urothelial carcinoma (UTUC) remains unclear. The ability of emodin, a natural pharmaceutical compound, to prevent BZ-associated UTUC has not been previously explored. To the best of our knowledge, the present study is the first to reveal that BZ significantly enhanced the survival and migration of UTUC cell lines in vitro . Furthermore, in vivo experiments demonstrated that BZ promoted an increase in the size of subcutaneous tumors in nude mice. Further investigation revealed that BZ upregulated the expression of protein kinase A (PKA) and cyclooxygenase 2 (COX2), along with downstream matrix metalloproteinase 9 (MMP9) and vascular endothelial growth factor (VEGF), in UTUC cells. Moreover, BZ increased the levels of cyclic adenosine monophosphate (cAMP) and prostaglandin E2 (PGE2) in cell lysates. By contrast, emodin reduced the PKA and COX2 expression levels compared with the BZ-treated group. Similarly, the in vivo experiments demonstrated that emodin significantly inhibited tumor growth in BZ-pretreated nude mice, accompanied by reductions in the cAMP, PGE2, MMP9 and VEGF levels. These findings elucidated the role of BZ in promoting UTUC progression. Additionally, emodin has emerged as a novel inhibitor of BZ-induced UTUC development through PKA/COX2 inhibition, suggesting its potential as a natural therapeutic agent against BZ-associated UTUC.

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Effects of dose and human N-acetyltransferase 1 genetic polymorphism in benzidine metabolism and genotoxicity

Cited by 3 publications

References 43 publications

Efficient synergistic degradation of Congo red and omeprazole in wastewater using rGO/Ag@ZnO nanocomposite

Efficient synergistic degradation of Congo red and omeprazole in wastewater using rGO/Ag@ZnO nanocomposite

Bioactivation, Mutagenicity, DNA Damage, and Oxidative Stress Induced by 3,4-Dimethylaniline

Emodin inhibits benzidine‑enhanced survival and migration of upper urinary tract urothelial carcinoma cells by targeting the PKA/COX2 signaling pathway

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