SUMMARY1. The high energy phosphate esters available for the luminescent reaction of the firefly lantern extract correspond, in the dark adapted rods of the frog, to 7 x 10-16 mole of ATP per rod, corresponding to ca. 1'4 mM. 5. The ionophore A23187 decreases the high energy phosphate esters when the extracellular free Ca concentration is greater than 10-7 M, suggesting that ATP is consumed in pumping Ca ions out of the rods, or into the disks contained in the rods, or both.
Nerve cells are very responsive to weak pulsed electromagnetic fields (EMFs). Such non-ionizing radiation, with frequencies of 0-300 Hz and 0.1-100 mT, can affect several cellular activities, with unusual dose-response characteristics. The present study examined the effect of a 2-h exposure of synaptosomes on a system generating a peak magnetic field of 2 mT. We evaluated the changes of the synaptosomal mitochondrial respiration rate and ATP production, membrane potential, intrasynaptosomal Ca2+ concentration, and the release of free iron and F2-isoprostanes. O2 consumption and ATP production remained unchanged in exposed synaptosomes. The intrasynaptosomal Ca2+ concentration decreased slowly and no depolarization of the synaptosomal membrane was detected. Finally, the release of free iron and F2-isoprostanes by synaptosomal suspensions also remained unchanged after EMF exposure. These results indicate that the physiological behavior of cortical synaptosomes was unaffected by weak pulsed EMFs.
Brain ischemia results in neuronal injury and neurological disability. The present study examined the effect of mild (6% O2) and severe (2% O2) hypoxia on mitochondria of rat cortical synaptosomes. During mild and severe hypoxia, JO2 and ATP production significantly decreased and mitochondrial membranes depolarized. Synaptosomal calcium concentration increased slightly, albeit not significantly. After a 1 h re-oxygenation period, JO2, ATP production and mitochondrial membrane potential returned to control levels in synaptosomes incubated in 6% O2. In synaptosomes incubated in 2% O2, however, the ATP production was not restored after re-oxygenation and intrasynaptosomal Ca2+ significantly increased. The results indicate that both mild and severe hypoxia influence the physiology of synaptosomal mitochondria; the modifications are reversible after mild hypoxia and but partly irreversible after severe hypoxia.
The present study examined the effect on rat cortical synaptosomes of a 2 h exposure to 50-Hz electromagnetic fields (EMFs) with a peak magnetic field of 2 mT. We measured modifications of synaptosomal mitochondrial respiration rate, ATP production, membrane potential, intrasynaptosomal Ca(2+) concentration and free iron release. The O(2) consumption remained unvaried in exposed synaptosomes at about 2 nM O(2)/min/mg proteins; ATP production was also unchanged. The intrasynaptosomal Ca(2+) concentration decreased slowly and there was a slight, but non-significant, depolarisation of the synaptosomal membrane. Finally, the free iron release by synaptosomal suspensions, a useful predictor of neuro-developmental outcome, remained unchanged after EMF exposure. On the whole, our results indicate that the physiological behaviour of cortical synaptosomes is not affected by weak pulsed EMFs.
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