Paradoxically, prior acquisition of antioxidant activity enhances oxidative stress-induced cell death
Omer Murik and Aaron Kaplan
Department of Plant and Environmental Sciences, The Hebrew University of Jerusalem, 91904 Jerusalem, Israel.
Acquiring antioxidant capacity is thought to enhance the viability of cells challenged by a subsequent oxidative stress. Counter-intuitively, we show that in two phytoplankton species, Chlamydomonas reinhardtii and Peridinium gatunense, representing the green and red plastid lineages, oxidative stress induced cell death in cultures that already possessed high antioxidant activity but not in cells that exhibited low activity. Cell death of low antioxidant possessing cultures was markedly enhanced by the addition of dehydroascorbate (DHA), a product of ascorbate peroxidase (APX), but not of ascorbate or reduced glutathione, and was preceded by increased metacaspase expression and activity. These data suggested that the level of APX and its products, strongly upregulated by oxidative stress, serves as a possible surveillance signal reporting that the cells already experienced an earlier oxidative stress. A secondary oxidative burst consequent on the release of cytochrome oxidase has been implicated in the oxidative stress induced programmed cell death (PCD) in a wide variety of organisms. A mutant lacking complex III activity shows an altered oxidative stress-PCD response. Our data presents a novel role of APX and cytochrome oxidase in the response to oxidative stress and PCD induction in photosynthetic microorganisms. Elimination of cysts production by phytoplankton cells that were already damaged by oxidative stress (indicated by the rise in oxidized proteins) as the inoculum for the following year's population may be the evolutionary trigger for this phenomenon.
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