N-acetylcysteine and clotrimazole inhibit sickle erythrocyte dehydration induced by 1-chloro-2,4-dinitrobenzene

Archil Shartava, Arvind K. Shah, Steven Goodman

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Clotrimazole, a specific inhibitor of the Ca2+ 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.

Original languageEnglish (US)
Pages (from-to)19-24
Number of pages6
JournalAmerican Journal of Hematology
Volume62
Issue number1
DOIs
StatePublished - Sep 13 1999
Externally publishedYes

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Clotrimazole
Dinitrochlorobenzene
Acetylcysteine
Dehydration
Erythrocytes
Glutathione
Cell Count
Antioxidants
Potassium Channels

All Science Journal Classification (ASJC) codes

  • Hematology

Cite this

N-acetylcysteine and clotrimazole inhibit sickle erythrocyte dehydration induced by 1-chloro-2,4-dinitrobenzene. / Shartava, Archil; Shah, Arvind K.; Goodman, Steven.

In: American Journal of Hematology, Vol. 62, No. 1, 13.09.1999, p. 19-24.

Research output: Contribution to journalArticle

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