The experiments referred to in this article point to the fact that relatively low concentrations of Hg2+ (5-10 mM) produce damage to the internal mitochondrial membrane. This damage results in the formation of ionic channels that allow the spontaneous effusion of Ca+2 from the matrix. Together with this, the formation of channels produce the balance of the chemo-osmotic gradient, resulting in the overcoming of the transmembrane potential and the uncoupling of oxidative phosphorylation. The experiments carried out in vivo, point to the fact mercury produces acute tubular necrosis of kidney tissue. These toxic effects produced by Hg2+ in vitro with the addition of 15 microM of the inhibition of the angiotensin converting enzyme, captopril. In vivo experiments show that intraperitoneal infection of captopril (40 mg/kg) completely protects from mitochondrial dysfunction produced by mercurial intoxication.