We evaluated 16 Guamanian Chamorros with amyotrophic lateral sclerosis and 33 patients with parkinsonism-dementia for disturbances of calcium and vitamin D metabolism. The serum immunoreactive parathyroid hormone level was mildly elevated in 6 patients with amyotrophic lateral sclerosis and in 5 patients with parkinsonism-dementia. There were significant positive correlations between serum immunoreactive parathyroid levels and duration of illness in male patients with motor neuron disease, but not in female patients or in patients with parkinsonism-dementia. Intestinal absorption of calcium, as assessed by serum and urinary activity of calcium 47 following oral administration, was decreased in 2 patients with amyotrophic lateral sclerosis and in 4 patients with parkinsonism-dementia, all of whom had low levels of serum 1,25-dihydroxyvitamin D. Reductions in cortical bone mass were striking in patients with motor neuron disease. A significant negative correlation was found between the percentage of cortical area of the second metacarpal bone and muscle atrophy and weakness, and significant positive correlations were found between degree of immobility and ratio of urinary hydroxyproline to creatinine in patients with amyotrophic lateral sclerosis and parkinsonism-dementia. In general, abnormalities in calcium metabolism were subtle. Thus, if the demonstrated deposition of metals, particularly calcium and aluminum, in central nervous system tissues of Guamanians with these two conditions is a cause of the diseases and of the early appearance of neurofibrillary tangles in neurons, the accumulation has apparently occurred long before onset of symptoms, and detectable abnormalities of calcium and vitamin D metabolism may already have been corrected.
The effects of parathyroid hormone (PTH) on the transport and distribution of calcium in isolated kidney cells were studied by kinetic analysis of 45Ca desaturation curves. The results show that PTH (15 ng/ml) increases the total cell calcium content, every exchangeable pool, and all exchange rates. The greatest effect is observed in the slowest kinetic phase which reflects a mitochondrial pool. The effects of PTH occur even in the absence of magnesium and of phosphate and the larger effect is again obtained in the mitochondrial pool. These results suggest that PTH stimulates calcium transport in kidney cells by affecting the intracellular distribution of calcium or by stimulating calcium influx.
This paper provides mathematical solutions for calculating calcium fluxes and compartments in isolated kidney cells from calcium-45 desaturation curves. In contrast to other available methods, these solutions allow the calculation of kinetic parameters even if isotopic equilibrium has not been reached at the beginning of the desaturation period. To test the validity of the method, calcium-45 desaturation experiments were performed in isolated kidney cells after labeling periods of 30, 60, 90, or 120 min. Even though the calcium-45 desaturation curves differ with different labeling times, the respective values of the calculated parameters are practically identical. The optical labeling period was found to lie between 60 and 120 min. Since this new method does not require initial isotopic steady state, it allows a formal kinetic analysis of tracer desaturation curves even after short periods of labeling.
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