Another small addition
There is class of oxidoreductases called oxygenases which incorporate molecular oxygen into the substrates and not just use it as an electron acceptor like in oxidases (note that the terminal enzyme in ETC is an oxidase and there are other such oxidases). In other words, oxygen is not a cofactor but a co-substrate. Oxygenases are further classified into dioxygenases and monooxygenases which incorporate two oxygen atoms and one oxygen atom respectively. Examples:
- Cytochrome P450 family (monooxygenease): involved in detoxification of xenobiotics
- Cyclooxygenase (dioxygenase): involved in production of prostaglandins which are involved in pain and inflammation. Many NSAID painkillers like aspirin, paracetamol and ibuprofen target cyclooxygenase-2 (COX2)
- Lipoxygenase (dioxygenase): Involved in production of leukotrienes which are involved in inflammation.
- Monoamine oxidase (monooxygenase): Involved in catabolism of neurotransmitters such as epinephrine, norepinephrine and dopamine.
Does oxygen deprivation result in death just due to the halting of ATP
production, or is there some other reason as well?
Death predominantly occurs because of halt in ATP production. Some cells such as neurons (and also perhaps cardiac muscles) are highly sensitive to loss of oxygen (for energy requirements) and clinical death because of hypoxia usually occurs because of loss basic brain function.
What percentage of the oxygen we take in through respiration is
expelled later through the breath as carbon dioxide?
As already mentioned, it is said that there is a rough 1:1 ratio of CO2 production and O2 consumption. However, as indicated in a comment by CurtF, O2 does not form CO2; it forms water in the last reaction of ETC. CO2 is produced in other reactions of Krebs cycle.
Glycolysis produces 32 molecules of ATP for 1 molecule of glucose via ETC (see here). There are three complexes in ETC and the third is dependent on oxygen; so you can assume that 1/2 a molecule of O2 consumed for production of 3 ATP molecules. Therefore 32 molecules of ATP would consume 4 molecules of O2. Seems like there is a 1:1 ratio of CO2 production and O2 consumption.
We can see it like this:
FADH2 enters ETC at the second complex whereas NADH enters at the first. We can say that as long as NADH is present FADH2 would not require an extra oxygen.
An NADH or a FADH2 molecule would require 1/2 molecule of O2. There are 8 molecules of NADH and 2 molecules of FADH2 produced during glycolysis+krebs cycle which would require 10/2 = 5 molecules of O2. Glycolysis produces 4 molecules of CO2 during krebs cycle.
However, 2 cytosolic NADH molecules require 2 ATPs (in other words another NADH molecule) to be transported to mitochondria. So the net effect may be actually close to 1:1 O2:CO2.
Another factor to keep in consideration is that the three complexes do not actually produce ATP; they just pump proton to create a chemical potential. The F0F1-ATP synthase would probably work only after a threshold of H+ potential is established. The 1 ATP molecule per complex is most likely the mean value and not exactly what really happens per reaction.