Abstract
When acetyl ethyl tetramethyl tetralin (AETT), at 10–50 μg/ml, was added to rat liver mitochondria respiring with succinate or with glutamate plus malate as substrate, the rate of mitochondrial respiration increased significantly after an initial lag period, of 2–3 min. AETT also stimulated respiration in the presence of oligomycin, and at higher concentrations of AETT a phase of strongly inhibited respiration followed an initial stimulatory phase. These observations suggest that AETT uncouples oxidative phosphorylation. A diketo derivative (DK) of tetramethyl tetralin also appears to be an uncoupling agent, according to those criteria, and both compounds uncoupled mitochondria from brain as well as liver. DK and many other uncoupling agents, such as hexachlorophene (HCP), produced an immediate burst of respiration, whereas the brief lag after addition of AETT was similar to that seen after addition of triethyltin (TET).
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