Please use this identifier to cite or link to this item:
Title: Enhancement of glutathione-dependent haemin degradation by ascorbic acid
Contributor(s): Zou, C (author); Agar, NS (author); Jones, GL  (author)orcid 
Publication Date: 2002
DOI: 10.1016/S0006-2952(02)01214-5
Handle Link:
Abstract: In the current work, we investigated the effect of ascorbic acid on GSH-mediated haemin degradation. GSH-mediated haemin degradation in the presence of ascorbic acid in phosphate-buffered saline and in erythrocyte ghosts was determined by recording absorbance at 365 and 399nm, respectively. Generation of intracellular H(2)O(2) was measured indirectly in terms of the inactivation of endogenous catalase in erythrocytes in the presence of 3-amino-1,2,4-triazole. Although ascorbic acid itself did not induce haemin degradation, it enhanced GSH-mediated haemin degradation. Experiments with catalase showed that H(2)O(2) was essential in this process. The oxidation of ascorbic acid in the presence of haemin was stimulated by GSH, suggesting that ascorbic acid can alter the mechanism of H(2)O(2) generation observed with GSH and haemin alone. These results suggest that enhancement of GSH-mediated haemin degradation by ascorbic acid may be due to an increase in the production of H(2)O(2) generated by GSH and haemin in the absence of ascorbic acid.
Publication Type: Journal Article
Source of Publication: Biochemical Pharmacology, 64(4), p. 565-572
Publisher: Pergamon-Elsevier Science Ltd
Place of Publication: Oxford, England
ISSN: 0006-2952
Field of Research (FOR): 060104 Cell Metabolism
Peer Reviewed: Yes
HERDC Category Description: C1 Refereed Article in a Scholarly Journal
Statistics to Oct 2018: Visitors: 725
Views: 734
Downloads: 0
Appears in Collections:Journal Article

Files in This Item:
3 files
File Description SizeFormat 
Show full item record


checked on Nov 26, 2018

Page view(s)

checked on Dec 29, 2018
Google Media

Google ScholarTM



Items in Research UNE are protected by copyright, with all rights reserved, unless otherwise indicated.