The respiration of excised oat (A vena sativa cv Victory) leaves and their sensitivity to inhibitors was followed during senescence under varied conditions. The respiration rate, which in controls reaches its peak on the third day in darkness, is lowered at the time of fastest loss of chlorophyll (as reported earlier) by seven unrelated reagents that all delay dark senescence. When senescence is delayed by white light or by cytokinins, the respiratory rise is correspondingly delayed. Kinetin and L-serine, which act as antagonists on senescence, also act as antagonists on the respiratory rate. However, an exception to this close correspondence between senescence and the respiratory rise is offered by the lower aliphatic alcohols, which delay dark senescence and yet accelerate the onset of the respiratory rise.The respiration of freshly cut leaves is insensitive to KCN up to 8 millimolar, but sensitive to benzhydroxamate (BAM), 1 to 2 millimolar BAM causing 25% promotion and higher concentrations inhibiting. At the respiratory peak, however, part of the respiration becomes KCN-sensitive. Low concentrations of alcohols in darkness, or 3-(3,4dichlorophenyl)-1,1-dimethylurea, diuron, in light, also render part of the respiration KCNsensitive, but this sensitivity soon disappears again. Some 10 to 15% of the respiration is insensitive to both inhibitors. Thus, cyanide sensitivity comes and goes, while BAM sensitivity is always present. The current concept of the cyanide-resistant pathway as an overflow, therefore, does not fit well with behavior of these leaves. The respiratory rise in leaf senescence is similar to, but not identical with, the climacteric in ripening fruits and the aging phenomenon in tuber slices.During senescence in the dark, detached leaves of seedling oats (A vena sativa cv Victory) undergo a marked increase in respiratory rate, which reaches a peak at about 250%o of the initial rate on the 3rd d (23). By that day, the Chl loss and proteolysis are well advanced, and by the 4th d, when the respiratory rate falls, more than 65% of both Chi and protein have been lost. Cytokinins, at concentrations that inhibit or delay senescence, correspondingly delay this respiratory rise (23). It was therefore concluded that the respiratory rise was either itself the cause or perhaps the direct result of the senescence process. A first suggestion was that both are due to respiratory uncoupling and the consequent loss of phosphorylative energy, but direct determination of the ATP content of the leaves showed that this was not the case (13 (1, 2, 6-8, 16, 24, 29). It has also been established that opening of the stomata invariably accompanies, and indeed seems to cause, the delay of senescence in darkness, while closure of the stomata causes accelerated senescence in light (29). White light is itself an important factor in delaying senescence and causes immediate stomatal opening which is followed by very gradual closure (29). Its influence reaches saturation at irradiances well below those that saturate ph...