Developmental changes in erythrocyte Na+,K+-ATPase subunit abundance and enzyme activity in neonates

Vásárhelyi, Barna

doi:10.1136/fn.83.2.f135

Cited by 16 publications

(9 citation statements)

References 18 publications

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“…Therefore, it behaves differently from Na + /K + -ATPase. However, similarly to Na + /K + -ATPase [9], the abundance of PMCA molecules is somehow influenced by the gestational age, since we detected a 30% higher molecule expression in pre-term compared to full-term neonates.…”

Section: Discussionmentioning

confidence: 78%

“…Erythrocyte PMCA differs from the erythrocyte Na + /K + -ATPase: the relative abundance and isoform composition of Na + /K + pump molecules alter with gestational age [9]. However, the lack of such a process in erythrocytes does not necessarily mean that the isoform shift of PMCA is absent in other human cells.…”

Section: Discussionmentioning

confidence: 98%

“…Recently it has been reported that the expression and activity of Na + /K + -ATPase changes during perinatal and postnatal development [9][10][11]. The activity of the Na + /H + countertransport system also changes postnatally [12].…”

Section: Introductionmentioning

confidence: 99%

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Expression and Activity of the Ca<sup>2+</sup>-ATPase Enzyme in Human Neonatal Erythrocytes

et al. 2001

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The plasma membrane Ca²⁺-ATPase (PMCA) is one of the main regulators of Ca²⁺ homeostasis. We studied the perinatal alteration of the abundance and the activity of PMCA molecules in human erythrocytes in pre-term and full-term neonates and children at the age of 1–4 years. The lower abundance of the 4b isoform was associated with lower enzyme activity in full-term neonates compared to children. Although the number of PMCA molecules was higher in pre-term neonates, their total PMCA activities were identical to those of full-term neonates. Our findings suggest that the abundance of PMCA molecules changes during the perinatal development. The same activity at higher enzyme molecule numbers might indicate a potential immaturity of the enzyme in the pre-term infant.

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Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 98%

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Expression and Activity of the Ca<sup>2+</sup>-ATPase Enzyme in Human Neonatal Erythrocytes

et al. 2001

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“…Acute hyperkalemia is a rare condition in full-term neonates, but common in very low birth weight infants during the first days of life, and is caused by a Na-K ATPase immaturity [9,10,11]. If parenteral K overload and pseudohyperkalemia due to hemolysis of blood samples are excluded, the differential diagnosis includes several clinical conditions (Fig.…”

Section: Discussionmentioning

confidence: 99%

Rare causes of acute hyperkalemia in the 1st week of life

et al. 2004

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We describe three neonates with hyperkalemia and renal salt wasting during the 1st week of life. Endocrinological evaluation led to the diagnosis of selective hypoaldosteronism (HA) in two neonates and secondary pseudohypoaldosteronism (PHA) in one. The infant with PHA developed a urinary tract infection, and radiological investigation demonstrated a small dysplastic left kidney with vesicoureteral reflux. The electrolyte and hormonal disturbances in this infant persisted throughout the first months of life. The two infants with selective HA improved rapidly after administration of fludrocortisone orally and the electrolytes and renin values returned to normal. Secondary PHA and selective HA should be considered in the differential diagnosis in salt-losing neonates during the first days of life. Renal ultrasonography, urine culture, and assays of aldosterone and plasma renin activity should be performed in any infant presenting with hyperkalemia and salt wasting after the exclusion of congenital adrenal hyperplasia.

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“…Membrane composition has a high ratio of ACTA PAEDIATR SUPPL 438 (2002) polyunsaturated fatty acids to total lipids, indicating susceptibility to lipid peroxidation (38). These predisposing conditions in newborns seem somehow compensated by more active GSH recycling than in adult red cells, and by a higher activity of Na ‡ /K ‡ -ATPase (39,40). However, hypoxia severely depresses Ca 2 ‡ -ATPase, inducing oxidative injury (41).…”

Section: Oxidative Injury Of the Neonatal Red Cellmentioning

confidence: 99%

Oxidant injury in neonatal erythrocytes during the perinatal period

2002

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It has been known for many decades that oxidative stress leads to oxidation of hemoglobin and damage to the erythrocyte membrane. More recently, the factors involved in denaturating of membrane proteins and lipid peroxidation have been investigated in detail, as well as the mechanism of reactive oxygen species formation in red cells. Oxidative stress depletes adenosine triphosphate (ATP) and adenine nucleotides, whereas adenosine monophosphate (AMP) deaminase seems to depress energy metabolism by blocking the salvage pathway of purine nucleotides. Depletion of ATP and activation of AMP deaminase are related to calcium ion concentrations. Denaturating of membrane proteins generally precedes lipid peroxidation and consequent phagocytosis due to caspase activation. Extensive investigations demonstrated the key role of oxidative stress and iron release in a reactive form causing membrane protein damage via the Fenton reaction and hydroxyl radical production. In the absence of efficient protection by antioxidant factors and other molecules such as flavonoids, oxidative stress is responsible for the release of iron in reactive form, predisposing red cells to hemolysis through the formation of senescence antigen. Other well‐known sources of oxidative stress in red cells are free radical production outside the red cell by activated phagocytes, endothelial metabolism, hyperoxia, ischemia‐reperfusion and the arachidonic acid cascade. Conclusion: The recent insight into the mechanism of oxidative injury of red cells and evidence of relationships between erythrocyte oxidative stress and hypoxia suggest that increased hemolysis is induced by severe hypoxia and acidosis in the fetus as well as the newborn.

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Developmental changes in erythrocyte Na+,K+-ATPase subunit abundance and enzyme activity in neonates

Abstract: (Arch Dis Child Fetal Neonatal Ed 2000;83:F135-F138)

Cited by 16 publications

References 18 publications

Expression and Activity of the Ca<sup>2+</sup>-ATPase Enzyme in Human Neonatal Erythrocytes

Expression and Activity of the Ca<sup>2+</sup>-ATPase Enzyme in Human Neonatal Erythrocytes

Rare causes of acute hyperkalemia in the 1st week of life

Oxidant injury in neonatal erythrocytes during the perinatal period

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