Studies on surfactant toxicity to the freshwater alga Chlorella fusca: a common mode of action?

Application of biosurfactant from Bacillus subtilis C9 for controlling cladoceran grazers in algal cultivation systems

“…It should be, however, noted that algal response to biosurfactant is closely dependent on the type of biosurfactant and the algal strains that are being cultivated 46 , 57 . Rieß and Grimme, for instance, reported that diethyleneglycol monohexadecylether (C16E2), a nonionic surfactant, was shown to act as an instantaneous inhibitor of cell growth and reproduction of Chlorella fusca , whereas a cationic surfactant cetyltrimethylammonium chloride (CTAC) was shown to induce only minor acute effects on photosynthesis and respiration 57 .…”

“…It should be, however, noted that algal response to biosurfactant is closely dependent on the type of biosurfactant and the algal strains that are being cultivated 46 , 57 . Rieß and Grimme, for instance, reported that diethyleneglycol monohexadecylether (C16E2), a nonionic surfactant, was shown to act as an instantaneous inhibitor of cell growth and reproduction of Chlorella fusca , whereas a cationic surfactant cetyltrimethylammonium chloride (CTAC) was shown to induce only minor acute effects on photosynthesis and respiration 57 . A recent study further tested the toxicity of alkylglucosides on the freshwater alga, Selenastrum capricornutum and reported that these non-ionic surfactants are relatively innocuous to Selenastrum after a 72-hour algal growth inhibition test, while substantial toxicity of these surfactants were confirmed with cladoceran Daphnia magna 46 .…”

Acute Toxicity of LAS Homologues in Marine Microalgae: Esterase Activity and Inhibition Growth as Endpoints of Toxicity

“…This behavior is characteristic of eukaryotic algae and cyanobacteria, which have high and species-speci"c sensitivities to surfactants in single species toxicity tests (Lewis, 1990). The lipophilic structure of the surfactant is responsible for the inhibition of cell growth (Rie and Grimme, 1993). The higher lipophilicity of C than C LAS homologues is responsible for the increase in the toxicity for both endpoints (growth cell and esterase activity).…”