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.