Abstract

In the bioluminescent, marine dinoflagellate Lingulodinium polyedrum [syn. Gonyaulax polyedra ], light emission Is sensitive to oxidative stress in a dual way: (a) The nocturnal glow maximum, which depends on the melatonin metabolite 5-methoxytryptamine (5-MT), is decreased by 5-MT depletion following oxidation of its precursor melatonin, which easily undergoes radical reactions; attenuations of the glow maximum are typical for sublethal oxidative stress, (b) Since luciferin availability is triggered by proton translocation to the scintillons (bioluminescent microsources which form cytoplasmic intrusions into acidic vacuoles), lethal oxidative stress causes strong rises in bioluminescence (dying peaks) as a consequence of cytoplasmic acidification, which results from impaired proton pumping into vacuoles under ATP deficiency and/or proton leakage through damaged membranes. Sublethal concentrations of paraquat or buthionine sulfoximine decrease the circadian glow peak, in a dose-dependent fashion. These effects can be reverted by exogenous melatonin, although this indoleamine itself does not stimulate but rather slightly diminishes light emission. After a lethal dose of hydrogen peroxide, a dying peak appears, which can be rapidly terminated by adding catalase to the medium. Sublethal and lethal effects of the endogenous oxidotoxin 3-hydroxykynurenine can be distinguished on the basis of the differently timed glow and dying peaks.

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