Abstract
Furazolidone is a nitrofuran drug which causes dilated cardiomyopathy in turkeys and serves as an important model of human dilated cardiomyopathy. Although extensively investigated, the chemical mechanism by which furazolidone produces injury remains unknown. In this work we used electron paramagnetic resonance (EPR) spectroscopy to show that furazolidone was reduced to its corresponding nitro anion radical by ascorbate and hypoxanthine. Glutathione prevented the generation of this anion radical. These results document directly, with EPR spectroscopy, the presence of furazolidone anion radical during biochemical reduction and suggest a protective role of glutathione in furazolidone-induced injury. These data enhance our understanding of furazolidone metabolism and may be useful in defining its role in furazolidone-induced dilated cardiomyopathy.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 56-63 |
| Number of pages | 8 |
| Journal | Biochemical Medicine and Metabolic Biology |
| Volume | 48 |
| Issue number | 1 |
| DOIs | |
| State | Published - 1992 |
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ASJC Scopus subject areas
- Biochemistry
- Endocrinology, Diabetes and Metabolism
Cite this
Generation of furazolidone radical anion and its inhibition by glutathione. / Lax, Daniela; Kukolich, Stephen G.
In: Biochemical Medicine and Metabolic Biology, Vol. 48, No. 1, 1992, p. 56-63.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Generation of furazolidone radical anion and its inhibition by glutathione
AU - Lax, Daniela
AU - Kukolich, Stephen G
PY - 1992
Y1 - 1992
N2 - Furazolidone is a nitrofuran drug which causes dilated cardiomyopathy in turkeys and serves as an important model of human dilated cardiomyopathy. Although extensively investigated, the chemical mechanism by which furazolidone produces injury remains unknown. In this work we used electron paramagnetic resonance (EPR) spectroscopy to show that furazolidone was reduced to its corresponding nitro anion radical by ascorbate and hypoxanthine. Glutathione prevented the generation of this anion radical. These results document directly, with EPR spectroscopy, the presence of furazolidone anion radical during biochemical reduction and suggest a protective role of glutathione in furazolidone-induced injury. These data enhance our understanding of furazolidone metabolism and may be useful in defining its role in furazolidone-induced dilated cardiomyopathy.
AB - Furazolidone is a nitrofuran drug which causes dilated cardiomyopathy in turkeys and serves as an important model of human dilated cardiomyopathy. Although extensively investigated, the chemical mechanism by which furazolidone produces injury remains unknown. In this work we used electron paramagnetic resonance (EPR) spectroscopy to show that furazolidone was reduced to its corresponding nitro anion radical by ascorbate and hypoxanthine. Glutathione prevented the generation of this anion radical. These results document directly, with EPR spectroscopy, the presence of furazolidone anion radical during biochemical reduction and suggest a protective role of glutathione in furazolidone-induced injury. These data enhance our understanding of furazolidone metabolism and may be useful in defining its role in furazolidone-induced dilated cardiomyopathy.
UR - http://www.scopus.com/inward/record.url?scp=0026783760&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0026783760&partnerID=8YFLogxK
U2 - 10.1016/0885-4505(92)90048-4
DO - 10.1016/0885-4505(92)90048-4
M3 - Article
C2 - 1326300
AN - SCOPUS:0026783760
VL - 48
SP - 56
EP - 63
JO - Molecular Genetics and Metabolism
JF - Molecular Genetics and Metabolism
SN - 1096-7192
IS - 1
ER -