Abstract
1. Trialkyltin compounds inhibited the mitochondrial respiration stimulated by ADP and the synthesis of ATP but affected little the state 4 respiration.
2. Tri-n-butyltin chloride inhibited Pi32-ATP exchange reaction and DNP-induced ATPase activity to the same extent as the inhibition to oxidative phosphorylation.
3. Inhibitory potency of trialkyltin de-rivatives to the phosphorylating respiration was compared.
4. A stoichiometric inhibitory pattern between TBTC and mitochondria was de-monstrated.
5. TBTC did not inhibit the DNP-stimulated respiration at the concentration which was sufficient to the inhibition to the phosphorylating respiration.
6. From the above results, the mecha-nisms of action of trialkyltins were discussed.
