Let us make an in-depth study of the cyanide resistant respiration and physiological significance of cyanide resistant respiration.
The flow of electrons in the usual mitochondrial electron transport chain (in both animals and plants) during aerobic respiration is blocked by the presence of cyanides which inhibit the activity of cytochrome oxidase. This type of respiration is therefore, known as cyanide sensitive respiration.
Plant mitochondria, however, differ from the animal mitochondria in having an alternate oxidase system pathway through which terminal oxidation of reduced coenzyme continues even in the presence of cyanides. This type of respiration is known as cyanide resistant (or cyanide insensitive) respiration.
In cyanide resistant respiration, the flow of electrons from reduced coenzymes to Ubiquinone is the same as in usual mitochondrial electron transport chain. But after this point (branch point) the electrons pass from UQ to a flavoprotein FPma (with a mid-range E’0 (= + 0.02 V) and a large absorbance change on redox change), and from there to a cyanide resistant or alternate oxidase (designated as X) and finally to O2 (Fig. 16.17). Usually the reduction of O2 should result in the formation of H2O but present evidences indicate the possibility of H2O2 being formed instead of H2O. The H2O2 can easily be converted into water arid oxygen then by the enzyme catalase.
(The exact nature of alternate terminal oxidase X is not clearly understood. It is probably an iron- containing protein which is neither a hemoprotein nor an iron-sulphur (Fe-S) protein. The activity of alternate oxidase is inhibited by m-CLAM (= m-chlorobenzhydroxamic acid).
P/O ratio (i.e. no. of ADP molecules converted into ATP molecules per O atom) in cyanide resistant respiration is one. As in conventional electron transport chain, the first phosphorylation site is coupled with electron transport chain in cyanide resistant respiration also.
Physiological Significance of Cyanide Resistant Respiration:
The physiological significance of cyanide resistant respiration is not very clear. Following roles are usually attributed to it.
1. Cyanide resistant respiration is believed to be responsible for the climacteric in fruits (i.e., remarkable increase in respiration during and just before ripening). The climacteric is induced by ethylene and the latter may act to implement the cyanide resistant respiration in ripening fruit, (production of H2O2 and superoxide increases the oxidation and breakdown of membrane which are necessary activities in the ripening process).
2. Cyanide resistant respiration is known to generate heat in thermogenic tissues. Thermogenecity is observed in the flowers or inflorescences of some plants such as water lily (Victoria), arum lilies, Arum maculatum, Symplocarpus foetidus (skunk cabbage) etc. The excessive heat produced in the inflorescence of Arum etc. is used to volatilize the odiferous compounds such as amines & indoles which are produced in them and which serve to attract pollinating insects. The amount of heat produced in thermogenic tissues may be as high as 51°C with an atm. temp, of 15°C (e.g., in appendix of Arum italicum).
(In cyanide resistant respiration, most of the energy liberated in the oxidation of respiratory substrate is lost as heat and only little of it is consumed in the production of ATPs. For instance the P/O ratio for 1 NADH molecule is only one in cyanide resistant respiration while in cyanide sensitive or usual respiration it is 3).
3. If ATPs generated in usual respiration in mitochondria are not sufficiently drained off, they may inhibit the Krebs’ cycle (TCA cycle) via the stoppage of electron flow in electron transport chain. Therefore, cyanide resistant respiration may provide continued oxidation of NADH and operation of TCA cycle though the energy demand is lesser. The operation of TCA cycle is important because TCA cycle intermediates are precursors for cellular components.