Disease relevance of L-Buthionine

• Metastasis (number of foci/100 mm(3) of liver) increased in B16MF1 cells pretreated with GSH ester ( approximately 3-fold, P <.01), and decreased in B16MF1/Tet-GGT and B16MF10 cells pretreated with the GSH synthesis inhibitor L-buthionine (S,R)-sulphoximine ( approximately 5-fold and 2-fold, respectively, P <.01) [1].
• The toxicity assay utilized cells that were previously exposed to 100 microM L-buthionine (S,R)-sulfoximine (BSO), an inhibitor of gamma-glutamyl-cysteine synthetase, for 24 h [2].
• Enzyme induction by L-buthionine (S,R)-sulfoximine in cultured mouse hepatoma cells [3].

High impact information on L-Buthionine

• However, ars1 plants produce phytochelatin levels similar to levels produced by the wild type, and the enhanced resistance of ars1 is not abolished by the gamma-glutamylcysteine synthetase inhibitor l-buthionine sulfoxime (BSO) [4].
• An additional gain of DAF-2 fluorescence was obtained when the cells were depleted of glutathione (GSH) with L-buthionine S,R-sulfoximine (BSO) [5].
• L-Buthionine S,R-sulfoximine, an inhibitor of gamma-glutamylcysteine synthetase, prevented DHII-induced increases in wt cell GSH [6].
• Inhibition of complex I by rotenone and depletion of glutathione by L-buthionine sulfoxamine also correlated with an increase in alpha-syn expression, suggesting that oxidative stress may cause an increase in alpha-syn levels in dopaminergic cells [7].
• Coadministration of L-buthionine S,R-sulfoximine and CUR did not affect the anti-apoptotic effect of CUR suggesting a glutathione-independent mechanism of cell protection [8].

Chemical compound and disease context of L-Buthionine

• However, in the presence of the GSH synthesis inhibitor, L-buthionine (S,R)-sulfoximide (BSO), the protective effect of CA toward cadmium toxicity remained [9].

Biological context of L-Buthionine

• Stereoselective pharmacokinetics of L-buthionine SR-sulfoximine in patients with cancer [10].
• In part 2, the effect of glutathione (a major component of NAC hepatoprotection) was examined by measuring ACh-induced vasorelaxation in rings from rats treated with L-buthionine sulfoxamine (BSO, a glutathione synthesis inhibitor) [11].
• In plants treated with 1 mM L-buthionine sulphoximine, a potent inhibitor of GSH/hGSH synthesis, only the oxidative stress symptoms appeared, indicating that the depletion of the GSH/hGSH pool was not sufficient to promote cell death, and that other phytotoxic mechanisms might be involved [12].
• When pre-treated with l-buthionine S,R-sulphoximine (BSO) to deplete GSH, CYP2C9-expressing cells showed also a loss of cell viability as compared to LNCX cells, although to a lesser extent as compared to non-depleted CYP2C9-expressing cells [13].

Anatomical context of L-Buthionine

• When the endogenous GSH content was reduced by pretreatment of the cells with L-buthionine (S,R)-sulfoximine, the cytotoxicity of the herbicides increased strongly in both cell lines [14].

Associations of L-Buthionine with other chemical compounds

• In vitro studies demonstrate that L-buthionine (R)-sulfoximine is a relatively weak inhibitor of rat kidney gamma-glutamylcysteine synthetase; binding is competitive with L-glutamate [15].

Gene context of L-Buthionine

• To elucidate the role of GSH in regulation of AP-1, NF-kappaB, and VCAM-1 expression, we employed l-buthionine (S,R)-sulfoximine (BSO), a specific gamma-glutamylcysteine synthetase (gamma-GCS) inhibitor, to block intracellular GSH synthesis [16].
• Induction of Phase II enzymes of the [Ah] gene battery by L-buthionine (S,R)-sulfoximine (BSO) and other agents was examined in mouse hepatoma Hepa-1c1c7 cells [3].
• L-Buthionine (R)-sulfoximine (0.2 mmol/kg) did not cause significant GSH depletion in liver or pancreas [15].

References