Abstract

1. 1. The oxidation of 2,3-dimercaptopropanol (BAL) by oxygen in the presence of the Keilin and Hartree heart-muscle preparation is coupled with the peroxidation of unsaturated fatty acids. This process is probably catalysed by traces of Fe 2+ present in the preparation. 2. 2. A number of substances, particularly Fe 2+, haemoglobin and cytochrome c, increased the peroxidation when added together with BAL but protected the succinic oxidase system against BAL. 3. 3. On the other hand, treatment of the heart-muscle preparation with an ion-exchange resin decreased the peroxidation but made the succinic oxidase more sensitive to BAL. 4. 4. Serotonin almost completely inhibited peroxidation in the presence of BAL but did not protect the succinic oxidase system. 5. 5. It is concluded that peroxidation of lipid in the presence of BAL is not an important cause of the inactivation of the respiratory chain by BAL. 6. 6. On the other hand, lipid peroxidation probably makes a major contribution to the “excess oxygen uptake” (oxygen in excess of that required to oxidize BAL to the disulphide). 7. 7. A part of the BAL is oxidized through the cytochrome c-cytochrome c oxidase system. This does not lead to excess oxygen uptake, lipid peroxidation, or inactivation of the respiratory chain. 8. 8. It is concluded that a third pathway for the oxidation of BAL leads to the inactivation of the succinic oxidase, probably by causing the oxidation of an unidentified component of the preparation. The inactivation is inhibited by cyanide and ethylenediaminetetraacetate.

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