[Calcium and phosphorus metabolism and alkaline phosphatase].
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Serum immunoreactive parathyroid hormone (iPTH) and plasma total calcium, ionized calcium, magnesium, and phosphorus levels were determined during the first 9 days of life in 137 normal term infants, 55 "sick" infants, and 43 hypocalcemic (Ca <7.5 mg/100 ml; Ca(++)<4.0 mg/100 ml) infants. In the cord blood, elevated levels of plasma Ca(++) and Ca were observed, while levels of serum iPTH were either undetectable or low. In normal newborns during the first 48 h of life there was a decrease in plasma Ca and Ca(++), while the serum iPTH level in most samples remained undetectable or low; after 48 h there were parallel increases in plasma Ca and Ca(++) and serum iPTH levels. Plasma Mg and P levels increased progressively after birth in normal infants. In the sick infants, plasma Ca, Ca(++) and P levels were significantly lower than in the normal newborns, while no significant differences were found in the plasma Mg levels. The general pattern of serum iPTH levels in the sick infants was similar to that observed in the normal group, though there was a tendency for the increase in serum iPTH to occur earlier and for the iPTH levels to be higher in the sick infants. In the hypocalcemic infants, plasma Mg levels were consistently lower than in the normal infants after 24 h of age, while no significant differences were found in the plasma P levels. Hyperphosphatemia was uncommon and did not appear to be a contributing factor in the pathogenesis of hypocalcemia in most infants. Most of the hypocalcemic infants, including those older than 48 h, had inappropriately low serum iPTH levels. Evidence obtained from these studies indicates that parathyroid secretion is normally low in the early new born period and impaired parathyroid function, characterized by undetectable or low serum iPTH, is present in most infants with neonatal hypocalcemia. Additional unknown factors appear to contribute to the lowering of plasma Ca in the neonatal period. The net effect of unknown plasma hypocalcemic factor(s) on the one hand and parathyroid activity on the other may account for differences in plasma Ca levels observed between normal, sick, and hypocalcemic infants. Depressed plasma Mg is frequently present in hypocalcemic infants. To what degree the hypomagnesemia reflects parathyroid insufficiency or the converse, to what degree parathyroid insufficiency and hypocalcemia are secondary to hypomagnesemia, is uncertain.
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This 6-week study was designed to determine the effects of graded doses of caffeine intake (3, 25 or 100 mg/kg per day) on the metabolic balance and tissue concentrations of fluoride, calcium and phosphorus in Sprague-Dawley rats. Caffeine intake did not affect the absorption, urinary excretion or balance of fluoride, the plasma, bone or enamel concentrations of fluoride, nor the occurrence of incisor enamel fluorosis. Neither did it affect the metabolism of calcium or phosphorus except that the urinary excretion of calcium was increased. This effect, however, was not sufficient to influence significantly calcium balance. The ash content of the femur epiphysis and bone mineral content of the tibia were significantly reduced only in the group exposed to the highest dose of caffeine. These effects on bone were not significantly related to the balance of calcium or phosphorus. It was concluded that caffeine, even at an extremely high level of intake, has no detectable effect on the balance or tissue concentrations of fluoride, calcium or phosphorus in the rat.
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Plant viruses affect production through symptom induction in host plants. These symptoms could partially arise from nutrient deprivation: The resource competition hypothesis posits that massive viral replication deprives hosts of essential nutrients, yet direct evidence for phosphorus (P) competition is lacking. Moreover, it is reported that biotic stresses can lead to alterations on P metabolism. Using a hydroponic system enabling separate analysis of shoots and roots in adult Arabidopsis thaliana plants, we investigated whether Turnip mosaic virus (TuMV) drawed significant P internal pools leading to P competition or altered P metabolism. TuMV genomic RNA represented < 0.3% of the P pool allocated to 18S rRNA, refuting the resource competition hypothesis. Instead, TuMV induced a marked shoot-to-root P redistribution: Shoot/Root Pi and Porg changed from 1.7 to 1.04 to 0.71 and 0.68, respectively. This altered partitioning correlated with organ-specific gene expression changes: high-affinity transporters PHT1; 4 and PHT1; 5 were co-induced in shoots, whereas immunity-related PHT1; 4 was uniquely repressed in roots. The senescence-associated gene SEN1 showed opposite regulation between organs (repressed in shoots, induced in roots), distinguishing virus-induced responses from canonical senescence. Multivariate analysis revealed that shoots and roots only partially share physiological and molecular responses to TuMV. The virus reprograms phosphorus metabolism through organ-specific changes, not through resource depletion, and roots act as a distinct hub integrating infection response, senescence, and nutrient dynamics. This study advances the understanding of growth-defense trade-offs in plant mineral nutrition and identifies new targets for maintaining crop productivity under biotic stress.
Hemodialysis induced changes in calcium (Ca) and phosphorous (P) metabolism are studied in a group of ten (10) patients with chronic renal failure. There was a significant rise in total serum calcium (Ca), that was closely related to changes in serum proteins level, and a very significant decrease in serum phosphorous (P). Calcium levels of 7 to 8 mgs/100 cc in the dialyzer fluid were considered ideale.
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