Areas with high soil percolation by herbicides have higher incidence of low-grade non-Hodgkin lymphomas

Fazzi, Rita; Manetti, C.; Focosi, Daniele; Miligi, Lucia; Benvenuti, Alessandra; Bonari, E.; Barale, Roberto; Petrini, Mario

doi:10.1007/s00277-009-0898-0

Cited by 3 publications

(1 citation statement)

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“…CTU undergoes metabolic transformations, yielding N -dealkylated metabolites, benzyl alcohol metabolites, and phenol metabolites in various organisms. − Furthermore, its environmental residues pose a threat to human and biological safety, affecting organisms such as oysters and green algae. − Vigilance is essential for the protection of farm workers and consumers of CTU-treated products. Several studies have highlighted the toxic effects of CTU exposure, such as the induction of chromosomal aberrations and pathological changes in mouse testes. , Although existing toxicity data shed light on the effects of CTU on microorganisms and aquatic species, little attention has been paid to clarifying the biochemical basis of CTU toxicity in mammals .…”

Section: Introductionmentioning

confidence: 99%

CYP3A4-Mediated Metabolic Activation and Cytotoxicity of Chlortoluron

Guo,

Zhang,

et al. 2024

Chem. Res. Toxicol.

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Chlortoluron (CTU) is an herbicide extensively used in agricultural settings for crop cultivation. Its presence in water has been identified as a pollutant detrimental to aquatic species. The objective of the present study was to explore the metabolic activation and hepatotoxicity of CTU. Through human and rat liver microsomal incubations supplemented with CTU, nicotinamide adenine dinucleotide phosphate (NADPH), and either glutathione or N-acetyl cysteine, a benzylic alcohol metabolite (M1) was discerned, alongside a phenol metabolite (M2), a glutathione conjugate (M3), and an N-acetyl cysteine conjugate (M4). In rats exposed to CTU, biliary M3 and urinary M4 were detected in their bile and urine, respectively. The generation of M1 was detected in the presence of NADPH. The observation of M3 and M4 suggests the formation of an iminoquinone methide intermediate arising from the oxidation of M1. CYP3A4 was found to be the principal enzyme catalyzing the metabolic activation of CTU. Furthermore, CTU exhibited cytotoxic properties in cultured rat primary hepatocytes in a concentration-dependent pattern. Concomitant treatment of hepatocytes with ketoconazole mitigated their susceptibility to the cytotoxic effects of CTU.

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