From oxidative phosphorylation

All the ATP comes from oxidative phosphorylation coupled to the metabolism of acetyl-CoA by the TCA cycle. No oxygen, no p oxidation. 

In many instances, substrate phosphorylation is not coupled to oxidation of the electron donor source by the bacteria therefore, growth will result from oxidative phosphorylation with electrons energizing the plasma membrane for ATP production according to the chemiosmotic system. A list of bacteria displaying dissimilatory reduction where growth is coupled to reduction of metaPmetalloid electron acceptors is given in Table 16.4. 

Heart muscle obtains nearly all its ATP from oxidative phosphorylation. 

H.M. Kalckar. 1991. 50 years of biological research From oxidative phosphorylation to energy requiring transport regulationRev. Biochem. 60 1-37. (PubMed)... 

In the cardiac myocyte, the bulk of the ATP necessary to drive the rhythmic beating process is derived from oxidative phosphorylation (Oram et ai, 1973). The acetyl-CoAs necessary for such a process are derived from fatty acid degradation. The trafficking of fatty acids from their site of uptake (plasma membrane) to utilization (mitochondria) is a function presumably filled by the heart FABP. 

The belief that alcoholics are more susceptible to the toxicity of 2,4-DNP during occupational exposure (Perkins 1919) may indicate an interaction with ethanol (and possibly other alcohols) or it may simply be a function of the compromised physiological state of alcoholics. 2,4-DNP appears to markedly increase the rate of ethanol metabolism in rat liver slices by 100-160% (Videla and Israel 1970) and in rats in vivo by 20-30% (Israel et al. 1970). Because 2,4-DNP uncouples mitochondrial electron transport from oxidative phosphorylation, the oxidation of NADH to NAD is accelerated in the mitochondria. Reoxidation of NADH rather than the activity of alcohol dehydrogenase is the rate-limiting step in the metabolism of ethanol, and, therefore, the metabolic effect of 2,4-DNP enhances the clearance of ethanol (Eriksson et al. 1974). Because 2,4-DNP is known to augment the rate of respiration and perspiration, 2.7-8.2% of the initial dose of ethanol was also eliminated by expiration and cutaneous evaporation in the rat (Israel et al. 1970). 

C. The rates of both glucose utilization and ATP generation by glycolysis increase to compensate for the absence of sufficient ATP production from oxidative phosphorylation as a result of oxygen deprivation. Under these circumstances, ATP is used as rapidly as it is made so it is not present in sufficient concentration to inhibit pyruvate kinase. Furthermore, fructose 1,6-bisphosphate tends to stimulate pyruvate kiuase activity. 

The employment of cell organelles has been limited to mitochondrial and microsomal fractions (Table 15). As early as 1976, Guilbault et al. coupled pig heart mitochondrial electron transfer particles (ETP) with an oxygen electrode. This development has been further pursued by Aizawa et al. (1980c). Decoupling of the electron transfer from oxidative phosphorylation makes ETP catalyze the following reactions ... 

DNP is a lipophilic molecule that binds reversibly with protons. It dissipates that proton gradient in mitochondria by transferring protons across the inner membrane. The uncoupling of electron transport from oxidative phosphorylation causes the energy from food to be dissipated as heat. DNP causes liver failure because of insufficient ATP synthesis in a metabolically demanding organ. 

Under ordinary circumstances in mammalian brain, the extracellular Na" " and K" " concentrations are 145 and 3 mM, respectively the intracellular concentrations 12 and 155 mM. However, because the resting membrane potential is a composite of a variety of factors (see earlier section), neither the Na nor the K" " gradient is at equilibrium with the electrical potential spanning the membrane. Hence, even at rest there is a small inward drift of Na+ and a small outward drift of. The Na + -K+ ATPase pump therefo -e maintains this gradient by utilizing energy derived from oxidative phosphorylation of the neuron. 

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