Glycerol phosphate dehydrogenase derivatives

EDRF endothelium-derived relaxing factor GPDH glycerol phosphate dehydrogenase... 

Electrons from succinate are transferred to FAD in complex n and several Fe-S centers and then to UQ. Electrons from cytoplasmic NADH are transferred to UQ via a pathway involving glycerol-3-phosphate and the flavoprotein glycerol-3-phosphate dehydrogenase (see p. 316). Fatty acids are oxidized as coenzyme A derivatives. Acyl-CoA dehydrogenase, one of several enzymes in fatty acid oxidation, transfers 2 electrons to FAD. They are then donated to UQ. 

Of the (13 0), (15 1), (17 1), and (17 2)-anacardic acids, the (17 2) is the most active inhibitor [280] of glycerol 3-phosphate dehydrogenase (GPDH) and nearly comparable in action to the adipostatins [201,281 ][72], (15 0)-cardol derivatives, potentially of interest in human obesity studies. Inhibition of lipid biosynthesis in bacteria, yeast and animal cells by anacardic acids from Ginkgo biloba has also been reported by the same authors [282]. 

Figure 7-4. The electron transport chain. Electrons enter from NADH to complex I or succinate dehydrogenase, which is complex II. Electrons derived from glycolysis through the glycerol-3-phosphate shuttle, complex I, and complex II join at coenzyme Q and are transferred to oxygen as shown. As electrons pass through complexes I, III, and IV, protons are transported across the membrane, creating a pH gradient.

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