phenylethyl isothiocyanate/necrosis

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beta-Phenylethyl isothiocyanate-mediated apoptosis in hepatoma HepG2 cells.

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beta-Phenylethyl isothiocyanate (PEITC) is a promising chemoprotective compound that is routinely consumed in the diet as its glucosinolate precursor. Previous studies have shown that PEITC can inhibit phase I enzymes and induce phase II detoxification enzymes along with apoptosis in vitro. The

Suppression of inflammatory mediators by cruciferous vegetable-derived indole-3-carbinol and phenylethyl isothiocyanate in lipopolysaccharide-activated macrophages.

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This study was aimed to examine the effects of indole-3-carbinol (I3C) and beta-phenylethyl isothiocyanate (PEITC), bioactive components present in cruciferous vegetable, on the production of inflammatory mediators, including nitric oxide (NO), tumor necrosis factor-alpha (TNF-alpha) and

Induction of apoptosis in a non-small cell human lung cancer cell line by isothiocyanates is associated with P53 and P21.

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This study was aimed at examining the effects of glucosinolate derivatives including phenylethyl isothiocyanate (PEITC), benzyl isothiocyanate (BITC), and indole-3-carbinol (I3C), on the induction of apoptosis in human non-small cell lung carcinoma A549 cells. The results indicated that all tested

Differential activation of MAPK and ICE/Ced-3 protease in chemical-induced apoptosis. The role of oxidative stress in the regulation of mitogen-activated protein kinases (MAPKs) leading to gene expression and survival or activation of caspases leading to apoptosis.

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Chemical-induced oxidative stress to a cell can signal many cellular responses which include proliferation, differentiation, hemeostasis, apoptosis or necrosis. To better understand the underlying molecular mechanisms after exposure to chemicals, we investigated the signal transduction pathways, in

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