Fomesafen

Fomesafen is an orally active herbicide. Fomesafen inhibits protoporphyrinogen oxidase (PPO). Fomesafen induces Apoptosis and increases ROS. Fomesafen exhibits developmental toxicity, immunotoxicity, and neurotoxicity. It induces precancerous lesions in the liver and hepaturoporphyria in mice. Fomesafen is used to control broadleaf weeds in soybean fields, rubber plantations, and orchards^{[1][2][3][4][5][6]}. In Vitro:Fomesafen (50-300 μg/L; 3 days) causes dose-dependent meristematic cell damage in Allium cepa roots, including epidermis cell damage, flattened cell nucleus, cortex cell damage, and thickening of cortex cell wall^[2].
Fomesafen (5-20 mg/L; from 6 h to 72 h post-fertilization) induces developmental toxicity, immunotoxicity, neurotoxicity, oxidative stress, and apoptosis in zebrafish embryos^[3].
Fomesafen (10-500 μg/kg in artificial soil; exposure for 3-28 days) causes oxidative stress in Eisenia fetida in the early exposure stage (3-14 days), with increased ROS level, which gradually recover in the later stage (21-28 days)^[6].
In Vivo:Fomesafen (0.25%; p.o. via diet; 18 weeks) induces hepatic uroporphyria in male DBA/2N mice^[4].
Fomesafen (0.23% in diet for C57BL/6J mice, 0.3% in diet for ICR mice; 14 months for C57BL/6J mice, 50 weeks for ICR mice) induces liver preneoplastic changes in mice^[5].