Contrary to many other unicellular algae protected by cell walls or massive polysaccharide layers, mastigote dinoflagellates have the advantage of taking up numerous substances, whose effects can be easily studied. In bioluminescent species such as Lingulo-dinium polyedrum, different forms of cellular stress can be detected on the basis of light emission. Lumi-nescence is controlled by proton transfer from an acidic vacuole to the bioluminescent microsources. Therefore, stress related to proton leakage leads to rises in bioluminescent rates, in the extreme as a dying peak. Mild, sublethal oxidative stress exerts an opposite effect: Bioluminescence is decreased, in Lingulo-dinium polyedrum preferentially at the circadian glow maximum, which requires the presence of a melatonin metabolite, 5-methoxytryptamine; free radicals and other oxidants easily destroy melatonin, thereby causing a deficiency of its metabolite. Different forms of cellular stress are distinguished by specific light emission patterns: Lethal oxidative stress by hydrogen peroxide causes a dying peak, which can be prevented or terminated by catalase. Sublethal oxidative stress by buthionine sulfoximine or paraquat leads to suppres- sions of the glow peak, which is restored by melatonin. Transitions from sublethal to lethal oxidative stress can be followed under the influence of an endogenous oxidotoxin, 3-hydroxykynurenine. Oxidative formation of an ultratoxin deriving from the antioxidant indole-3-propionic acid is associated with stimulation of light emission and cell death. Stress by photocatalytic reactions of a pesticide metabolite, 2-hydroxyquin-oxaline, causes strong rises in bioluminescence during photophase and early scotophase of a day/night cycle, but not after recovery from phototoxicity.
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