Mercuric ion, a well-known nephrotoxin, promotes oxidative tissue damage to kidney cells. One principal toxic action of Hg(I1) is the disruption of mitochondrial functions, although the exact significance of this effect with regard to Hg(I1) toxicity is poorly understood. In studies of the effects of Hg(I1) on superoxide (0%) and hydrogen peroxide (H,O,) production by rat kidney mitochondria, Hg(I1) (1-6 pM), in the presence of antimycin A, caused a concentration-dependent increase (up to fivefold) in mitochondrial H202 production but an apparent decrease in mitochondrial 0,-production. Hg(I1) also inhibited 0,-dependent cytochrome c reduction (ICs,, -2-3 pM) when 0,-was produced from xanthine oxidase. In contrast, Hg(1) did not react with 0, in either system, suggesting little involvement of Hg(1) in the apparent dismutation of 0,-by Hg(I1). Hg(I1) also inhibited the reactions of KO, (i.e., 0,) with hemin or horseradish peroxidase dissolved in dimethyl sulfoxide (DMSO). Finally, a combination of Hg(I1) and KO, in DMSO resulted in a stable UV absorbance spectrum [currently assigned Hg(I1)-peroxide1 distinct from either Hg(I1) or KO,. These results suggest that Hg(II), despite possessing little redox activity, enhances the rate of 0% dismutation, leading to increased production of H,O, by renal mitochondria. This property of Hg(I1) may contribute to the oxidative tissue-damaging properties of mercury compounds.