Increase of intracellular glutathione by low-level NO mediated by transcription factor NF-kappaB in RAW 264.7 cells.

The mechanism underlying the elevation of intracellular glutathione (GSH) in RAW 264.7 cells exposed to low concentrations of sodium nitroprusside (SNP), a well-known nitric oxide (NO) donor, was investigated. The peak of intracellular GSH was reached at 6 h after exposure of the cells to SNP (0.

Involvement of mitochondrial peroxynitrite in nitric oxide-induced glutathione synthesis.

Cells respond to oxidative stress including nitric oxide (NO) by increasing cellular glutathione concentration, as a part of adaptive response against oxidative injury. To elucidate the mechanism by which NO induces glutathione we investigated the reactive oxygen species (ROS) generated in the cell. Treatment of RAW264.

Does peroxynitrite involve in the elevation of cellular glutathione induced by sodium nitroprusside (SNP) in RAW 264.7 cells?

The mechanism underlying the elevation of intracellular glutathione (GSH) in RAW 264.7 cells exposed to low-level sodium nitroprusside (SNP) was investigated by measuring the expression of mRNA for gamma-glutamylcysteine synthetase (gamma-GCS), the rate-limiting enzyme of de novo GSH synthesis, and the GSH content. A significant elevation of expression of mRNA for gamma-GCS was observed at 3 h after exposure of the cells to SNP at a concentration of 0.

Increase of intracellular glutathione by low-dose gamma-ray irradiation is mediated by transcription factor AP-1 in RAW 264.7 cells.

The mechanism of the elevation of intracellular glutathione induced by low-dose gamma-rays was examined in RAW 264.7 cells. The expression of mRNA for gamma-glutamylcysteine synthetase (gamma-GCS) increased soon after gamma-ray (0.