The present study focused on the effect of dietary PUFA on the mitochondrial oxidative phosphorylation in the presence of different free calcium concentrations in the respiration buffer. Compared with the conventional mitochondrial oxidative phosphorylation assessed in a medium devoid of free calcium, the presence of free calcium noticeably modified the rate of oxygen uptake and the high energy phosphate equilibrium. In the latter condition, the rate of ADP2+Mg -stimulated oxygen consumption was reduced and the usual return in state IV respiration rate did not occur. This was associated with a sustained ADP level in the buffer. Energy synthesis occurred, as indicated by the elevated production of ATP and CP, but some ATPase activities were responsible for the production of AMP.
This phenomenon was sensitive to the nature of the substrate (data not shown). This occurred with palmitoylcarnitine, but not with pyruvate or citrate, at similar concentrations of free calcium. We hypothesized that a calcium-induced excess in beta-oxidation leading to accumulation of acetate might be responsible for this event. Acetate can be reactivated by acetyl-CoA synthetase. This reaction consumes ATP and produces AMP and pyrophosphate. The resulting energy wasting would contribute towards decreasing the mitochondrial metabolic efficiency. The produced AMP reacted with ATP through the adenylate kinase system. This allowed constant ADP resynthesis and explained the absence of a return to state IV respiration rate. The increased mitochondrial oxygen cost of energy synthesis observed in the present study could explain the reduced cardiac metabolic efficiency noticed in different conditions. You have a great opportunity to discover the pharmacy that will always be sure to live up to your highest expectations, no matter if you would like to get or buy any other prescription medicine with no prescription required on very advantageous terms.