The effect of calcium on the oxidation of acetaldehyde by rat liver mitochondria.

Isolated liver mitochondria oxidized acetaldehyde in the following order: State 4< state 3< valinomycin. Ca²⁺, in concentrations greater than 0.10 mM, inhibited the oxidation of acetaldehyde by isolated liver mitochondria under all conditions. Valinomycin-stimulated oxidation of acetaldehyde was more sensitive to inhibition by Ca²⁺ than were the state 3 or 4 rates of acetaldehyde oxidation. Acetaldehyde could support an energy-dependent uptake of Ca²⁺ at rates about 20 percent that found with succinate. Ruthenium red, an inhibitor of Ca²⁺ translocation, almost completely prevented the inhibition by Ca²⁺, under all conditions. The addition of externally added NAD⁺ or NADH provided complete relief against the inhibitions by Ca²⁺ of the state 4 and 3 rates of acetaldehyde oxidation. Although some relief was also observed with the valinomycin-stimulated system, significant inhibition persisted. Cations such as Zn²⁺, Cu²⁺, or Hg²⁺ also inhibited acetaldehyde oxidation, whereas Mg²⁺ and Mn²⁺ were without effect. These cations also blocked glutamate oxidation and presumably inhibit acetaldehyde oxidation by preventing reoxidation of NADH. The greater sensitivity of the ionophore-stimulated oxidation of acetaldehyde to inhibition by Ca²⁺ may reflect release of intramitochondria K⁺, which is known to occur in the presence of Ca²⁺, suggesting that acetaldehyde oxidation is influenced by the cation environment within the mitochondria.