Mercury is a heavy metal which induced toxic effects. Diphenyl diselenide (PhSe)₂ and N-acetylcisteyne (NAC) are compounds with antioxidant or pro-oxidant properties. The objective of this work was evaluated the possible interaction between mercury plus (PhSe)₂ or mercury plus NAC. Therefore, we evaluated the in vitro effect of mercury on d -ALA-D activity and TBARS levels in liver of mice. We also verified a possible interaction between these compounds. Data were analyzed statistically by two-way ANOVA, followed by Duncan’s Multiple Range Test when appropriate.The results indicated that mercury (50 and 75 m M) inhibited d -ALA-D activity from liver. (PhSe)₂ (3, 5 and 10 m M) inhibited hepatic ALA-D activity. Simultaneous addition of mercury (50 and 75m M) and (PhSe)₂ (3, 5, 10 m M) increased the enzyme inhibition. However, (PhSe)₂ at 0.1 and 0.5 m M protected against d -ALA-D inhibition induced by mercury. We also observed that NAC (10-750 m M) did not modify d -ALA-D activity, but the interaction between mercury (25 and 50 m M ) and NAC (500 and 750 m M) caused reduction in d -ALA-D activity. Dithiothreitol was able to reactivate and to protect inhibited d -ALA-D. Mercury (50 and 200 m M) increased TBARS levels in liver. (PhSe)₂ increased TBARS levels at 20 m M and decreased at 100 m M. We verified that the increase in TBARS concentration caused by mercury was reduced by (PhSe)₂ (50 and 100 m M). NAC (500 m M) caused a reduction in TBARS levels. The increase observed in TBARS concentration by mercury at 50 m M was reverted by NAC 500 m M. These results suggested a interaction between mercury and (PhSe)₂ as well as mercury and NAC in liver of mice, and these effects were in a concentration-dependent manner.