- Yasuo Oyama (Laboratory of Cell Signaling, Institute of Socio-Arts and Sciences, The University of Tokushima / email@example.com)
1) Laboratory of Cell Signaling, Institute of Socio-Arts and Sciences, The University of Tokushima , 2) Tokushima Bunri University , 3) Kumamoto Health Science University
1,4-Naphthoquinone (NAPH) is found in diesel exhaust particles and it is an active metabolite of naphthalene, a fumigant insecticide. This compound is known to cause oxidative stress. Therefore, it is plausible to suggest that NAPH increases cell vulnerability to oxidative stress in an additive or synergistic manner. We tested this possibility using rat thymocytes with flow-cytometric techniques and appropriate fluorescent probes. NAPH attenuated the increase in cell lethality induced by hydrogen peroxide (H2O2). The combination of NAPH and H2O2 promoted the transition from normal cells to apoptotic living cells, but attenuated further transition to cell death. Thus, the process of cell death induced by H2O2 was not completed in the presence of NAPH. However, NAPH did not attenuate certain lethal cellular events such as decrease in the cellular content of non-protein thiols and increases in intracellular Ca2+ and Zn2+ levels, induced by H2O2. The inhibitory effect of NAPH on the increase in cell lethality induced by H2O2 was also observed when caspase activity was suppressed. In the present study, the mechanism underlying the NAPH-induced attenuation of cell death in cells affected by H2O2-generated oxidative stress was, however, not fully elucidated. Since both H2O2 and NAPH elevated intracellular Ca2+ and Zn2+ levels, and since Zn2+ is known to partly attenuate Ca2+-dependent cell death, the intracellular interaction between Ca2+ and Zn2+ may complicate the process of cell death induced by oxidative stress.