Uncoupling phenomenon

However, as outlined above, the alterations occurring in the course of ischemia, especially in the in vivo situation, are so complex that it may be difficult to ascribe a phenomenon such as cellular uncoupling to only a single factor. Since other factors occurring in ischemia can also contribute to uncoupling this phenomenon may be a multicausal rather than monocausal process including a rise in intracellular calcium [De Mello, 1975 Maurer and Weingart, 1987 Noma and Tsuboi, 1985], intracellular protons [Noma and Tsuboi,... 

This interpretation of the dynamic phenomenon is based on the changes of the frequency of the macroscopic magnetisation vector hence in this form it can be applied to uncoupled spins only. 

Fig. 10.6. The effect of respiration and membrane potential (Ai )) on Cl permeation in brown adipose tissue mitochondria. When brown fat mitochondria were incubated in KCl in the presence of the ionophore, nigericin, they swelled (A, B). If a respiratory substrate (here G-3-P glycerol-3-phosphate) was added to the expanded mitochondria, they contracted, and this contraction ceased immediately and swelling was reintroduced if azide (NaNj) and an uncoupler (FCCP) were added (Fig. A). The passive halide ion permeability can be inhibited by GDP (cf.. Fig. 10.5), but respiration-driven contraction in KCl-expanded mitochondria was only partially inhibited by the presence of GDP (Fig. B) if again azide and uncoupler were added during the contraction, the mitochondria did not swell, indicating that the thermogenin channel was closed by GDP. This behaviour can partly be explained by the fact that the Cl permeation is driven by the membrane potential. Indeed, when, under similar conditions, the rate of contraction was plotted as a function of the membrane potential, it was seen that the rate was membrane potential dependent. It should, however, he noted that at low membrane potentials GDP nearly totally abolished the Cl permeation but when the membrane potential was increased above 30 mV, the inhibitory effect of GDP was apparently partially lost. The basis for this phenomenon is not understood it is not even known if there is a lower affinity of thermogenin for GDP in the energized membrane, as measurements of GDP affinities always refer to the non-energized situation. (Adapted from Nicholls et al. [27] (A, B) and Nicholls [94] (C).)...

Because 2,4-DNP uncouples oxidative phosphorylation but does not interfere with glycolysis in most tissues, one would not expect 2,4-DNP to affect lens metabolism. However, oxidative phosphorylation may be more important in the lens epithelial cells of humans, rabbits, and domestic birds (e.g., chicks and ducklings), as these species appear to be more susceptible to cataract formation after 2,4-DNP exposure (Kuck 1970). In domestic birds, cataracts occur almost immediately after exposure to 2,4-DNP and are reversible (Buschke 1947). However, in humans, cataracts can occur some time after treatment is terminated and may not be reversible. This phenomenon has not been fully explained. 

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