Why do cells need oxygen? Insights from mitochondrial composition and function

Mitochondrial membrane-embedded redox proteins are classically perceived as deterministic ‘electron transport chain’ (ETC) arrays cum proton pumps; and oxygen is seen as an ‘immobile terminal electron acceptor’. This is untenable because: (1) there are little free protons to be pumped out of the matrix; (2) proton pumping would be highly endergonic; (3) ETC-chemiosmosis-rotary ATP synthesis proposal is ‘irreducibly complex’/‘non-evolvable’ and does not fit with mitochondrial architecture or structural/distribution data of the concerned proteins/components; (4) a plethora of experimental observations do not conform to the postulates/requisites; e.g. there is little evidence for viable proton-pumps/pH-gradient in mitochondria, trans-membrane potential (TMP) is non-fluctuating/non-trappable, oxygen is seen to give copious ‘diffusible reactive (oxygen) species’ (DRS/DROS) in milieu, etc. Quite contrarily, the newly proposed murburn model’s tenets agree with known principles of energetics/kinetics, and build on established structural data and reported observations. In this purview, oxygen is needed to make DRS, the principal component of mitochondrial function. Complex V and porins respectively serve as proton-inlet and turgor-based water-exodus portals, thereby achieving organellar homeostasis. Complexes I to IV possess ADP-binding sites and their redox-centres react/interact with O2/DRS. At/around these complexes, DRS cross-react or activate/oxidize ADP/Pi via fast thermogenic one-electron reaction(s), condensing to form two-electron stabilized products (H2O2/H2O/ATP). The varied architecture and distribution of components in mitochondria validate DRS as the- (i) the coupling agent of oxidative reactions and phosphorylations, and (ii) the primary reason for manifestation of TMP in steady-state. Explorations along the new precepts stand to provide greater insights on mitochondrial function and pathophysiology.

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