scholarly journals Altered heat-lability of a fraction of glutathione reductase in aging human lens

1973 ◽  
Vol 134 (4) ◽  
pp. 995-1000 ◽  
Author(s):  
John J. Harding

An unusually heat-labile fraction of glutathione reductase appears in human lens at about an age of 32 years. No such change was found in glucose 6-phosphate dehydrogenase nor in 3-phosphoglycerate kinase. The change is an intrinsic property of glutathione reductase. A greater proportion of the altered glutathione reductase was found in the core, the older part, of the lens. No evidence of a second band of activity was obtained after electrophoresis. Possible interpretations of the results, including errors of protein synthesis, production of a new isoenzyme and post-synthetic changes, are discussed.

1991 ◽  
Vol 24 (2) ◽  
pp. 111-114 ◽  
Author(s):  
Benedito Barraviera ◽  
Paulo Câmara Marques Pereira ◽  
Jussara Marcondes Machado ◽  
Maria Julia de Souza ◽  
Carlos Roberto G. Lima ◽  
...  

The authors evaluated the isoniazid acetylating phenotype and measured hematocrit, hemoglobin, glucose-6-phosphate dehydrogenase and glutathione reductase activities plus serum sulfadoxin levels in 39 patients with paracoccidioidomycosis (33 males and 6 females) aged 17 to 58 years. Twenty one (53.84%) of the patients presented a slow acetylatingphenotype and 18(46.16%) a fast acetylating phenotype. Glucose-6-phosphate- dehydrogenase (G6PD) acti vity was decreased in 5(23.80%) slow acetylators and in 4(22.22%) fast acetylators. Glutathione reductase activity was decreased in 14 (66.66%) slow acetylators and in 12 (66.66%) fast acetylators. Serum levels of free and total sulfadoxin Were higher in slow acetylator (p < 0.02). Analysis of the resultspermitted us to conclude that serum sulfadoxin levels are related to the acetylatorphenotype. Furthermore, sulfadoxin levels were always above 50 µg/ml, a value considered therapeutic. Glutathione reductase deficiency observed in 66% of patients may be related to the intestinal malabsorption of nutrients, among them riboflavin, a FAD precursor vitamin, inpatients with paracoceidioidomycosis.


1989 ◽  
Vol 9 (6) ◽  
pp. 2322-2331
Author(s):  
A H Beggs ◽  
B R Migeon

Part of the higher-order structure of chromatin is achieved by constraining DNA in loops ranging in size from 30 to 100 kilobase pairs; these loops have been implicated in defining functional domains and replicons and possibly in facilitating transcription. Because the human active and inactive X chromosomes differ in transcriptional activity and replication, we looked for differences in their chromatin loop structures. Since the islands of CpG-rich DNA at the 5' ends of X-linked housekeeping genes are the regions where functional differences in DNA methylation and nuclease sensitivity are found, we looked for scaffold association of these sequences after extraction of histones with lithium diiodosalicylate. Specifically, we examined the 5' CpG islands within the hypoxanthine phosphoribosyltransferase, glucose 6-phosphate dehydrogenase, P3, GdX, phosphoglycerate kinase type 1, and alpha-galactosidase loci in human lymphoblasts obtained from individuals with 1 to 4 X chromosomes. Although we detected no scaffold-associated regions near these genes, we found several such regions at the ornithine transcarbamylase and blood clotting factor IX loci. Our results suggest that the CpG islands are excluded from the nuclear scaffold and that even though transcriptionally active, housekeeping genes are less likely than X-linked tissue-specific genes to be scaffold associated. In all cases, the pattern of scaffold association was the same for loci on active and inactive X chromosomes.


1977 ◽  
Author(s):  
R. McKenna ◽  
T. Ahmad ◽  
H. Frischer

We have previously shown that patients receiving antitumor chemotherapy with 1,3-bis-(2 chloroethyl)-1-nitrosourea (BCNU) rapidly acquire a severe generalized glutathione reductase (GSSG-R) deficiency. We now report that when platelets were exposed in vitro to BCNU (30 minutes, 37°, at 10-3 M, six separate studies), the resulting GSSG-R deficiency was associated with marked impairment of platelet aggregation in response to ADP (1 μM and 3 μM), to epinephrine and to collagen (all p’s< 0. 001). Platelet factor 3 availability was also markedly reduced (p<0.001); prothrombin consumption and glass adhesiveness were unaffected. In additional experiments to evaluate the dose response relationship, epinephrine induced aggregation was abnormal at 5 × 10-6 M BCNU, ADP (1 μM) induced aggregation was abnormal at 10-5 M BCNU, while ADP (3 μM) and collagen aggregation became abnormal at 5 × 10-5 M BCNU. GSSG-R deficiency (less than 11% of control activity), without glucose-6-phosphate dehydrogenase and 6-phosphogluconic dehydrogenase deficiencies, preceded all platelet abnormalities. We have demonstrated that a specific platelet GSSG-R deficiency after BCNU precedes the development of severe platelet dysfunction.


1988 ◽  
Vol 104 (2) ◽  
pp. 87-91
Author(s):  
Benedito Barraviera ◽  
Rinaldo Poncio Mendes ◽  
Paulo Câmara Marques Pereira ◽  
Jussara Marcondes Machado ◽  
Paulo Roberto Curi ◽  
...  

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