Butyric acid induces apoptosis via oxidative stress in jurkat T-cells

Reactive oxygen species (ros) are essential for the induction of t-cell apoptosis by butyric acid,an extracellular metabolite of periodontopathic bacteria. to determine the involvement of oxidative stress in apoptosis pathways,we investigated the contribution of ros in mitochondrial signaling pathways,death-receptor-initiated signaling pathway,and endoplasmic reticulum stress in butyric-acid-induced t-cell apoptosis. n-acetyl-l-cysteine (nac) abrogated mitochondrial injury,cytochrome c,aif,and smac release,and bcl-2 and bcl-xl suppression and bax and bad activation induced by butyric acid. however,the decrease in cflip expression by butyric acid was not restored by treatment with nac; increases in caspase-4 and -10 activities by butyric acid were completely abrogated by nac. nac also affected the elevation of grp78 and chop/gadd153 expression by butyric acid. these results suggest that butyric acid is involved in mitochondrial-dysfunction- and endoplasmic reticulum stress-mediated apoptosis in human jurkat t-cells via a ros-dependent mechanism.