A novel biologically active selenoorganic compound—IV

Müller, A.; Gabriel, Holger; Sies, Helmut

doi:10.1016/0006-2952(85)90493-9

Cited by 132 publications

(14 citation statements)

References 18 publications

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“…It is therefore not surprising that dithiols like DTT or dihydrolipoate are better cofactors of ebselen than glutathione as observed (41,42 (33), the efficiency of ebselen diselenide reduction is 100 times slower. The mechanism of mammalian TrxR acting on ebselen diselenide can be illustrated in Scheme 2.…”

Section: Discussionmentioning

confidence: 97%

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A Novel Antioxidant Mechanism of Ebselen Involving Ebselen Diselenide, a Substrate of Mammalian Thioredoxin and Thioredoxin Reductase

Zhao

Holmgren

2002

Journal of Biological Chemistry

177

103

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Section: Discussionmentioning

confidence: 97%

“…A number of other thiols, e.g. N-acetyl-L-cysteine (40), dithiothreitol (41), and dihydrolipoate (42) were also used. The endogenous dihydrolipoate was found to be a better cofactor than glutathione for the peroxidase activity of ebselen (42).…”

Section: Ebselen Is a Trx And Trxr Peroxidase Mimic Rather Than A Glumentioning

confidence: 99%

A Novel Antioxidant Mechanism of Ebselen Involving Ebselen Diselenide, a Substrate of Mammalian Thioredoxin and Thioredoxin Reductase

Zhao

Holmgren

2002

Journal of Biological Chemistry

177

103

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“…Some reports have also suggested that Se deficiency affects inflammation [7] and immunity [8], *To whom correspondence should be addressed . but the relationship between Se level and these diseases remains to be clarified.…”

Section: Discussionmentioning

confidence: 99%

Clinical Significance of Selenium Level in Chronic Pancreatitis

Uehara

Honjo

Hirano

et al. 1988

J. Clin. Biochem. Nutr.

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“…Ebselen exhibits glutathione (GSH) peroxidelike activity, reducing hydrogen peroxide with thiol cosubstrates such as GSH and N-acetylcysteine [Mü ller et al, 1985;Cotgreave et al, 1987]. In addition, ebselen has been reported to inhibit both NADPH oxidase [Cotgreave et al, 1989] and iNOS [Hattori et al, 1994].…”

mentioning

confidence: 99%

Selenoorganic compound, ebselen, inhibits nitric oxide and tumor necrosis factor-? production by the modulation of Jun-N-terminal kinase and the NF-?b signaling pathway in rat Kupffer cells

et al. 2000

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In response to the bacterial endotoxin, LPS, Kupffer cells are induced to express NO and TNF-alpha. These compounds are involved in hepatic inflammation/injury, especially that associated with endotoxic shock. In this study, we demonstrate that ebselen (2-phenyl-1,2-benzisoselenazol-3[2H]one), a selenoorganic compound, blocks LPS-induced NO and TNF-alpha production by cultured rat liver Kupffer cells. LPS can activate both the NF-kappaB signaling pathway and MAPK signal transduction pathways such as JNK and p38 MAPK. We find that ebselen inhibits LPS-induced NF-kappaB nuclear translocalization, and also suppresses the LPS-induced phosphorylation of JNK, but not the phosphorylation of p38 MAPK. This inhibition of signal transduction leads to a decrease in the transcription of TNF-alpha and the inducible isoform of NO. Furthermore, ebselen inhibits LPS-induced COX-2 expression, which is responsible for proinflammatory prostaglandin production, without affecting constitutive COX-1 expression. These data suggest the mechanism by which ebselen acts as an antiinflammatory agent, and also suggest that ebselen may be potent in preventing hepatic injury such as endotoxic shock, in which Kupffer cell activation has been implicated.

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A novel biologically active selenoorganic compound—IV

Cited by 132 publications

References 18 publications

A Novel Antioxidant Mechanism of Ebselen Involving Ebselen Diselenide, a Substrate of Mammalian Thioredoxin and Thioredoxin Reductase

A Novel Antioxidant Mechanism of Ebselen Involving Ebselen Diselenide, a Substrate of Mammalian Thioredoxin and Thioredoxin Reductase

Clinical Significance of Selenium Level in Chronic Pancreatitis

Selenoorganic compound, ebselen, inhibits nitric oxide and tumor necrosis factor-? production by the modulation of Jun-N-terminal kinase and the NF-?b signaling pathway in rat Kupffer cells

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