Abstract
The respiration of excised oat (Avena 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-(3,4-dichlorophenyl)-1,1-dimethylurea, diuron, in light, also render part of the respiration KCN-sensitive, 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.
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