Cyanide resistant respiration is an alternative respiratory pathway found in some plant mitochondria that is unaffected by cyanide. It involves an enzyme called alternative oxidase (AOX) that allows electrons to bypass cytochrome c oxidase. This pathway generates heat rather than ATP. It may play roles in fruit ripening, thermogenesis in plants, and continuing cellular respiration under conditions where ATP demand is low. Cyanide poisoning stops aerobic cellular respiration by binding to cytochrome oxidase and inhibiting the electron transport chain, thereby stopping ATP synthesis. It can also affect glycolysis and ion transport by cells.

1. By:Syeda Laraib Zahra

2.  Cyanide resistant respiration discovered at the beginning of
20th century in thermogenic plants during anthesis and was
later found to be typical feature of plant respiration.It is
respiratory pathway,occuring only in mitochondria of some
plants,yeast and bacteria that is unaffected by cyanide.
 Cyanide resistant respiration is not found in plants.
 The phenomenon of respiration resistant to cyanide is
connected with the presence of an additional terminal
oxidase-alternative oxidase(AOX).
 AOX is an approximately 32-kDa homo dimeric integral
mitochondrial inner membrane protein with a non haem di Fe
centre and two membrane spacing protein.

3.  The flow of electron from reduced coenzymes to ubiquinone
is same as in usual mitochondrial ETC.
 The electrons pass from UQ to flavoprotein Fpma and direct
to cyanide resistant alternative oxidase and finally to O2.
 In between UQ and oxygen,a free energy is released as heat.

5.  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).

6. 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

7. 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.

8.  Operation of CRR pathway under phosphorus limiting
conditions prevents over reduction of the mitochondrial ETC
components and formation of ROS during adenylate control
of oxidative phosphorylation.
EFFECT OF CRR ON AEROBIC
RESPIRATION
 The toxicity of cyanide is linked mainly to cessation of
aerobic cell metabolism.Cyanide reversibly binds to the ferric
ions cytochrome oxidase three within mitochondria.This
effectively halts the cellular respiration by blocking the
reduction of oxygen to water.

9.  The cyanide ion,CN,binds to iron atom in cytochrome oxidase
in the mitochondria of the cells and acts as an irreversible
enzyme inhibitor.This prevents cytochrome oxidase from
doing what it needs to do,which is to send electrons to
oxygen in ETC of aerobic cellular respiration.
EFFECT ON ATP SYNTHESIS
 After cyanide poisoning,ETC no longer pump electrons into
intermembrane space.The pH of intermembrane space would
increase,the pH gradient would decrease,and ATP synthesis
would stop.

10.  Cyanide stops the respiration reaction in mitochondria from
happening.This stops active energy,and there is no source of
energy.However,if the cell is provided with energy,active
transport will start up again even though the mitochondria
are still poisoned.
EFFECT ON GLYCOLYSIS
 Cyanide rapidly decreased hepatic oxygen uptake by 70% and
increased rates of glycolysis from less than 10 to over
60g/hr.Rates of glycolysis and mixed function oxidation
subsequently declined in parallel during infusion of KCN.

11.  Cyanide inhibition of oxidative phosphorylation blocked the
Na/K pump to depolarize resting potential and increase
spontaneous firing in most cells,and to raise intracellular
Na(+) level in all cells.