1970
DOI: 10.1111/j.1365-2141.1970.tb01644.x
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Erythrocyte Glutathione‐Peroxidase Deficiency

Abstract: Summary Glutathione peroxidase deficiency is the most recently described erythrocyte enzyme abnormality. This enzyme occupies a critical position in the pathways leading to the decomposition of peroxides in the erythrocyte. On the basis of our studies of patients with GSH‐P deficiency, it appears that a spectrum of disease quite similar to that found in G‐6‐PD deficiency is present; this includes compensated haemolytic disease, drug‐induced haemolysis and neonatal jaundice.

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Cited by 58 publications
(9 citation statements)
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“…The difference was significant (t = 3.103, p<0.01). The lower value in cord blood GSH-P is in agreement with previous reports [4,6,7,9,10,13].…”
Section: Resultssupporting
confidence: 82%
“…The difference was significant (t = 3.103, p<0.01). The lower value in cord blood GSH-P is in agreement with previous reports [4,6,7,9,10,13].…”
Section: Resultssupporting
confidence: 82%
“…The present data suggest that the sum of genetic and environmental factors may cause an abnormally low RBC GSH-Px activity in some individuals. None of the newborn infants examined showed evidence of haemolysis, although some had a lower RBC GSH-Px activity than the cases with haemolysis described by Necheles et al (1968Necheles et al ( , 1970. This fact does not exclude the possibility that these subjects may haemolyse if exposed to oxidant drugs, but the connection between RBC GSH-Px activity levels and haemolysis in this age group must be regarded with caution.…”
Section: Discussionmentioning
confidence: 79%
“…Clinical interest arises from the critical role played by GSH-Px in preventing biological damage due to peroxide accumulation, and from the possibility that an impairment of this enzyme can cause spontaneous or drug-induced haemolysis. An unexplained 'physiological' GSH-Px deficiency has been observed in normal newborn infants which might explain the increased susceptibility of their RBC to oxidative haemolysis (Gross et all 1967;Bracci et all 1969;Necheles et al, 1970;Boivin et all 1971;Emerson et al, 1972;Luang Eng et al, 1973). Necheles et a1 (1970) reported 11 cases of neonatal jaundice with RBC GSH-Px activity G. Perona et a1 ranging from 28% to 59% of the adult mean normal value.…”
mentioning
confidence: 99%
“…Glutathione peroxidase 1 protects hemoglobin in erythrocytes from oxidative breakdown (24,25) and is down-regulated (mean 2.2-fold) in these anemic patients, suggesting increased destruction of hemoglobin during oxidative injury in acute rejection as another underlying cause of anemia. The erythrocytic carbonic anhydrase I (CA1) is a member of the large family of genes encoding for zinc metalloenzymes; it is a cytosolic protein which reversibly hydrates carbon dioxide and participates in a variety of biologic processes including acid-base balance (26).…”
Section: Gene Profiling Of Anemia In Renal Transplantationmentioning
confidence: 99%