BENZOYL PEROXIDE INCREASES UVA-INDUCED PLASMA-MEMBRANE DAMAGE AND LIPID OXIDATION IN MURINE LEUKEMIA-L1210 CELLS

Ultraviolet A radiation induces oxidative stress and cell damage. The purpose of this investigation was to examine whether ultraviolet A-ind uced cell injury was amplified by the presence of a non-ultraviolet A absorbing molecule capable of generating free radicals. Benzoyl peroxi de was used as a lipid soluble potential radical-generating agent. Pla sma membrane permeability assessed by trypan blue uptake was used to m easure cell damage in murine leukemia L1210 cells. Cells were irradiat ed with a pulsed Nd/YAG laser at 355 nm using 0-160 J per cm(2). The r atio of the fluence-response slope in the presence of 40 mu M benzoyl peroxide to that of irradiated controls was 4.3 +/- 2.6, Benzoyl perox ide alone or benzoyl peroxide added after irradiation did not cause in creased trypan blue uptake. The ratio of the fluence-response slopes i n the presence of 40 mu M benzoyl peroxide to that of irradiated contr ols was 4.7 +/- 1.4 when cells were irradiated (0-43 J per cm(2)) with a xenon lamp, filtered to remove wavelengths <320 nm. The increased t rypan blue uptake in 355 nm-irradiated cells in the presence of benzoy l peroxide was inhibited in a concentration-dependent manner by butyla ted hydroxytoluene, vitamin E, and trolox, a water-soluble vitamin E d erivative. Lipid oxidation, assessed as thiobarbituric acid reactive s ubstances, was significantly increased in samples irradiated with ultr aviolet A in the presence of benzoyl peroxide at fluences >34 J per cm (2). The increased trypan blue uptake and thiobarbituric acid reactive substances were inhibited by butylated hydroxytoluene. These results suggest that agents not absorbing ultraviolet A radiation may enhance ultraviolet A-initiated oxidative stress in cells.