Several commercial and experimental herbicides such as p-nitrodiphenyl ethers, oxadiazoles, and cyclic imides inhibit protoporphyrinogen IX oxidase (Protox), the enzyme that converts protoporphyrinogen IX to protoporphyrin IX (Proto). This leads to uncontrolled autooxidation of the substrate and results in accumulation of Proto. Blockage of the porphyrin pathway at this site inhibits synthesis of both chlorophylls and heme. Heme is a feedback regulator of the porphyrin pathway. Thus, inhibition of Protox also deregulates the pathway, causing increased carbon flow to the accumulating pool of Proto. Proto is a potent photosensitizer that generates high levels of singlet oxygen in the presence of molecular oxygen and light. In plants treated with these herbicides, damage is light dependent and closely correlated with the level of Proto that accumulates. Proto accumulation is apparently largely extraplastidic, resulting in rapid photodynamic damage to the plasmalemma and tonoplast. After high levels of Proto accumulate in response to these herbicides, protochlorophyllide (PChlide) levels can increase also; however, Proto appears to be the primary photodynamic pigment responsible for the herbicidal activity.

Oxadiazon (10 μM) caused rapid, light-dependent membrane damage to cucumber cotyledon discs. Electrolyte leakage was detected within 1 h of exposure to light, as were cytoplasmic vesiculation and breakage of the tonoplast and plasmalemma. The ultrastructure of chloroplasts was not affected until the cytoplasm was dispersed. Photosynthetic inhibitors had no effect on activity and, after a period of dark incubation with oxadiazon, there was little effect of temperature on the light-caused membrane destruction. Porphyrin synthesis inhibitors (gabaculine and 4,6-dioxoheptanoic acid) almost completely prevented the herbicidal activity of oxadiazon. Oxadiazon treatment caused accumulation of protoporphyrin IX, a photodynamic pigment. Oxadiazon caused physiological effects on cucumber cotyledons that were virtually identical to those of p-nitro-diphenyl ether herbicides like acifluorfen and its methyl ester, which have recently been shown to also cause protoporphyrin IX accumulation.

The effect of 1.0 ppmw fluridone {1-methyl-3-phenyl-5-[3-trifluoromethyl)phenyl]-4(1H)-pyridinone} on growth of American pondweed (Potamogeton nodosus Poir.) and sago pondweed (Potamogeton pectinatus L.) was examined in plants kept in darkness or under various numbers of 12-h photoperiods. When plants were exposed to 1.0 ppmw fluridone for 1 to 10 12-h days, no stunting of American pondweed occurred until 21 days after treatment. Thirtythree days after treatment, plants that had received 4 to 10 days' exposure were most stunted. Sago pondweed was slightly more susceptible than American pondweed (87% and 50% reduction in length, respectively) 37 days after a 10-day exposure. Chlorophylls a and b were significantly lower in both species 14 days after all fluridone treatments. American pondweed plants exposed to fluridone continuously (1.0 ppmw) for 15 days, but given 0, 3, 6, 9, 12, or 15 12-h days were stunted only after having received at least six photoperiods. Stunting in sago pondweed was only slightly light-dependent. Neither species absorbed significantly more 14C-labeled fluridone after 2, 4, or 14 photoperiods compared to plants kept in darkness for the same time.