Acifluorfen, a protoporphyrinogen oxidase (PROTOX) inhibitor herbicide, promotes the accumulation of protoporphyrin IX (PPIX) and induces tumors in rodent livers. It causes significant photooxidative damage to pigments and lipids in sensitive plant species.

In order to assess the relationship between herbicide activity and endogenous antioxidants, the effect of Acifluorfen on glutathione and ascorbate levels in cucumber (Cucumis sativus L.) cotyledon discs is investigated. Acifluorfen decreases the levels of glutathione and ascorbate over 50% in discs exposed to less than 1.5 hours of white light (450 microeinsteins per square meter per second). Acifluorfen also causes the rapid depletion of ascorbate in far-red light grown plants which are photosynthetically incompetent [2].

Dietary treatment with 2500 ppm Acifluorfen for up to 13 weeks increases Cyp2b10 expression in the livers of wild-type mice, but not in CAR-knockout (CARKO) mice. Microscopically, Acifluorfen treatment-induces cytotoxic changes, including hepatocellular necrosis and inflammation, and causes regenerative changes accompanied by prolonged increases in the numbers of proliferating cell nuclear antigen-positive hepatocytes in WT mice [1]. These results indicated that prolonged cytotoxicity in the liver was a key factor for ACI-induced hepatocarcinogenesis, and that CAR played an important role in ACI-induced liver injury and tumor development in mice.