The effect of the bleaching and non-bleaching phenylpyridazinones, norflurazon [4-chloro-5-(methylamino)-2-(α,α,α-trifluoro-m-tolyl)-3(2H)-pyridazinone] and BAS 29095 [4,5-dimethoxy-2-phenyl-3(2H)-pyridazinone], on chlorophyll fluorescence of the green alga,Scenedesmus acutus, was investigated and compared to other bleaching herbicides, difunon3[EMD-IT 5914, 5(dimethylamino-methylene)-2-oxo-4-phenyl-2,5-dihydrofuranecarbonitrile-(3)] and the diphenyl ether, oxyfluorfen [2-chloro-1-(3-ethoxy-4-nitrophenoxy)-4-(trifluoromethyl)benzene]. Following chlorophyll fluorescence during short-term cultivation in the presence of herbicides and comparing it to physiological parameters such as chlorophyll content and packed cell volume allowed for rapid screening to detect different primary herbicidal modes of action. Two primary bleaching effects caused by either inhibition of carotene biosynthesis (certain substituted pyridazinones and difunon) or peroxidative degradation of membrane lipids (certain diphenyl ethers) led to completely different fluorescence signals. Growth of algae in the presence of a carotene biosynthesis inhibitor resulted in a rapid rise to maximum fluorescence, followed by a single decay phase, whereas bleaching diphenyl ethers led to a rapid loss of total fluorescence. Non-bleaching phenylpyridazinones, which act as weak electron transport inhibitors, inhibited variable fluorescence. Detoxication during algal growth became evident by recovery of the fluorescence induction.
