Demonstrates a novel reverse acceptor control phenomenon in rat kidney mitochondria where ADP induces reduction of pyridine nucleotides and slows respiration in specific sodium-containing solutions.
Hypothesis-generating in rat kidney mitochondria; leaves open relevance to human cardiac bioenergetics.
Rat kidney cortex mitochondria incubated in an isotonic solution containing sodium chloride, EDTA, and Pi exhibit a hitherto unreported phenomenon. The addition of substrate induces a rapid respiratory rate, accompanied by a marked oxidation of pyridine nucleotides measured by dual wave length spectroscopy. In contrast to the typical response, subsequent addition of ADP induces a slowing of respiration associated with reduction of pyridine nucleotides (reverse acceptor control). The phenomenon will not occur if Mg++, rutamycin, or uncoupling agents are present. However, if an uncoupling agent is added after substrate, the ADP effects on respiration and pyridine nucleotides are mimicked. The marked susceptibility of kidney mitochondria to uncoupling in sodium-containing solutions appears to be closely related to the mechanism of this phenomenon.
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Weiner et al. (1973) studied this question.
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