The bacterial toxin, tolaasin, causes brown blotch disease on the cultivated mushrooms by collapsing fungal and fruiting body structure of mushroom. Cytotoxicity of tolaasin was evaluated by measuring hemolytic activity because tolaasins form membrane pores on the red blood cells and destroy cell structure. While we investigated the inhibitions of hemolytic activity of tolaasin by $Zn^{2+}$ and $Cd^{2+}$, we found that $Ni^{2+}$ is another antagonist to block the toxicity of tolaasin. $Ni^{2+}$ inhibited the tolaasin-induced hemolysis in a dose-dependent manner and its Ki value was $sim10$ mM, implying that the inhibitory effect of $Ni^{2+}$ is stronger than that of $Cd^{2+}$. The hemolytic activity was completely inhibited by $Ni^{2+}$ at the concentration higher than 50 mM. The effect of $Ni^{2+}$ was reversible since it was removed by the addition of EDTA. When the tolaasin-induced hemolysis was suppressed by the addition of 20 mM $Ni^{2+}$, the subsequent addition of EDIA immediately initiated the hemolysis. Although the mechanism of $Ni^{2+}$ -induced inhibition on tolaasin toxicity is not known, $Ni^{2+}$ could inhibit any of fallowing processes of tolaasin action, membrane binding, molecular multimerization, pore formation, and massive ion transport through the membrane pore. Our results indicate that $Ni^{2+}$ inhibits the pore activity of tolaasin, the last step of the toxic process.