Generation of free radicals during the death of Saccharomyces cerevisiae caused by lipid hydroperoxide

The exposure of Saccharomyces cerevisiae cells to 13-L-hydroperoxylinoleic acid (LOOH) caused their death, the degree of which was dependent on the gr owth phase of the cells. Pre-application of ethanol, hydrogen peroxide (H2O 2) and LOOH to S. cerevisiae cells reduced the effect of LOOH on the cells, showing the transient cross adaptation to LOOH. Antioxidants such as N,N', -diphenyl-p-phenylenediamine (DPPD), melatonin and vitamin E, and inhibitor s of permeability transition of mitochondria, cyclosporin A and trifluopera zine, inhibited the LOOH-triggered cell death, while an inhibitor of glutat hione synthetase, buthionine sulfoximine (BSO), enhanced the cell death by LOOH. Reactive oxygen species (ROS) were detected by flow cytometry, using the ROS-specific fluorescent indicator. A ferric iron chelator, deferoxamin e, inhibited the LOOH-triggered cell death, and peroxyl radicals (LOO .) we re detected by a spin trapping method. These reactive radicals possibly ind uced the death of S. cerevisiae cells. However, the DNA fragmentation chara cteristic of apoptosis was not observed in S. cerevisiae cells after exposu re to LOOH, staurosporine, dexamethasone or etoposide, which have been repo rted to cause apoptosis in mammalian cells.