To proceed at a high rate, phosphorylating respiration requires ADP to be available. In the resting state, when the energy consumption is low, the ADP concentration decreases so that phosphorylating respiration ceases. This may result in an increase in the intracellular concentrations of O-2 as well as of one-electron O-2 reductants such as Q(2)(radical anion). These two events should dramatically enhance non-enzymatic formation of reactive oxygen species, i.e. of O-2(radical anion), H2O, and OH., and, hence, the probability of oxidative damage to cellular components. In this paper, a concept is put forward proposing that non-phosphorylating (uncoupled or non-coupled) respiration takes part in maintenance of low levels of both O-2 and the O-2 reductants when phosphorylating respiration fails to do this job due to lack of ADP. In particular, it is proposed that some increase in the H+ leak of mitochondrial membrane in State 4 lowers Delta(<(mu)over bar>H+), stimulates O-2 consumption and decreases the level of CoQ(radical anion) which otherwise accumulates and serves as one-electron O-2 reductant. In this connection, the role of natural uncouplers (thyroid hormones), recouplers (male sex hormones and progesterone), non-specific pore in the inner mitochondrial membrane, and apoptosis, as well as of non-coupled electron transfer chains in plants and bacteria will be considered.