The finding of electron leakage during the electron transport within the mitochondrial membrane (in eukaryotes) or in the cell membrane is an important issue for the accumulation of the reactive oxygen species (ROS) in the cytosol. Mitochondria is known to be the major site of the ROS generation in different pathological processes which in turn may cause cell damages as evident through the ischemia-reperfusion (I/R) injury, respiratory diseases, cell apoptosis, and even the onset of cancer. Hence the leaky mitochondrion and the physiological roles of leaked protons and electrons grow up with further interest to in course of energy metabolism.
I think that proton leak and ROS generation are separate processes...at least from a metabolically point of view.
Okay. If really so, then I shall have to think in different way. Thanks a lot for your kind response.
Dear Rashed Noor and Tomas Koltai,
As it happens far too often, researchers for many reasons do not know much what is happening in adjacent areas. It is long to explain, therefore I have attached a few of my recent articles which, probably, will answer some your questions. One of the new statements is that when you use physiological mixture of substrates, say, for the heart, that means that one of the substrates MUST be acyl-carnitine/ Fatty acids are very well oxidized in the presence of other metabolites, and this increases respiration in all metabolic states, but especially in MS-4. This increase is caused by the leak of electrons to production of superoxide radicals, which serves as a sink for electrons. This is not uncoupling, it the sign of the high degree of energization.
Any metabolis studies MUST include fatty acids.
Because dueing aging people finally enter the last stage of ontogenesis, their metabolism reminds the metabolism of their predecessors, who lived long-long time ago ant did not ate sugar, pasta etc. Their ate meat and fat. Increased oxidation of fatty acids is the reason of the increased oxidative stress and accelerated aging. But no currently widely discussed radicals are responsible for this. The exception is the protonated form of superoxide radical.
I would highly recommend you to read the following papers:
Murphy M.P. (2009) How mitochondria produce reactive oxygen species. Biochem. J. 417, 1-13.
Perevoshchikova I.V., C.L. Quinlan, A.L. Orr, A.A. Gerencser, M.D. Brand. (2013) Sites of superoxide and hydrogen peroxide production during fatty acid oxidation in rat skeletal muscle mitochondria. Free Radic. Biol. Med. 61, 298-309.
Quinlan C.L., Orr A.L., Perevoshchikova I.V., et al. (2012) Mitochondrial Complex II Can Generate Reactive Oxygen Species at High Rates in Both the Forward and Reverse Reactions. J. Biol. Chem. 287, 27255–2726.
Quinlan C. L., I. V. Perevoshchikova, R. L. Goncalves, M. Hey-Mogensen, M. D. Brand (2013) The determination and analysis of site-specific rates of mitochondrial reactive oxygen species production. Methods Enzymol. 526, 189-217.
Brand M.D. (2016) Mitochondrial generation of superoxide and hydrogen peroxide as the source of mitochondrial redox signaling. Free Rad. Biol.Med. 100, 14-31.
Dear Dr. Panov, thanks for sending your articles. I’ll go through those.
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