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N-acetylcysteine and clotrimazole inhibit sickle erythrocyte dehydration induced by 1-chloro-2,4-dinitrobenzene.
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- Author(s): Shartava A;Shartava A; Shah AK; Goodman SR
- Source:
American journal of hematology [Am J Hematol] 1999 Sep; Vol. 62 (1), pp. 19-24.
- Publication Type:
Journal Article; Research Support, U.S. Gov't, P.H.S.
- Language:
English
- Additional Information
- Source:
Publisher: Wiley-Blackwell Country of Publication: United States NLM ID: 7610369 Publication Model: Print Cited Medium: Print ISSN: 0361-8609 (Print) Linking ISSN: 03618609 NLM ISO Abbreviation: Am J Hematol Subsets: MEDLINE
- Publication Information:
Publication: New York Ny : Wiley-Blackwell
Original Publication: New York, Liss.
- Subject Terms:
- Abstract:
Clotrimazole, a specific inhibitor of the Ca(2+) activated potassium (Gardos) channel, and the antioxidant N-acetylcysteine were found to inhibit the in vitro formation of high-density sickle cells induced by treatment with 1-chloro-2,4-dinitrobenzene (CDNB). The CDNB induced leakage of K(+) can be inhibited by treatment of SS erythrocytes with 20 mM N-acetylcysteine. We conclude that the effect of N-acetylcysteine in preventing K(+) efflux and formation of high-density sickle cells is related to its ability to protect the Gardos channel from oxidative damage caused by diminished levels of reduced glutathione. This effect is due to the ability of N-acetylcysteine to maintain an appropriate level of reduced glutathione and its direct antioxidant activity.
(Copyright 1999 Wiley-Liss, Inc.)
- Grant Information:
3P60HL38639 United States HL NHLBI NIH HHS
- Accession Number:
0 (((dihydroindenyl)oxy)alkanoic acid)
0 (Carboxylic Acids)
0 (Carrier Proteins)
0 (Dinitrochlorobenzene)
0 (Indenes)
0 (Potassium Channels)
0 (Symporters)
G07GZ97H65 (Clotrimazole)
GAN16C9B8O (Glutathione)
RWP5GA015D (Potassium)
WYQ7N0BPYC (Acetylcysteine)
- Publication Date:
Date Created: 19990901 Date Completed: 19990930 Latest Revision: 20231213
- Publication Date:
20231215
- Accession Number:
10.1002/(sici)1096-8652(199909)62:1<19::aid-ajh4>3.0.co;2-c
- Accession Number:
10467272
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