“…This by-pass allows intramitochondrial NADH, to be oxidized by the respiratory chain in the presence of rotenone, and it also by-passes the energy conservation process at site 1. Evidence against this pathway operating in the absence of rotenone comes from the observation that the presence of site 1 phosphorylation in isolated mitochondria is correlated with a 25-30% increased growth yield of cells in continuous culture, when compared to that of iron deficient cells that lack site 1 [5] . It seems likely, therefore, that controls normally exist to inhibit the by-pass.…”