Selected diet-derived lipids may influence cytokine-mediated endothelial cell dysfunction, including TNF-induced apoptosis. To test this hypothesis, oxidative stress, intracellular calcium levels, barrier function, mitochondrial function, as well as chromatin condensation and DNA fragmentation were measured in endothelial cells treated with linolelc acid (18:2; 90 μM) and/or TNF (100 U/mL). In cells exposed to 18:2 plus TNF, pretreatment with 18:2 began 4.5 hours before exposure to TNF. The combined exposure to 18:2 plus TNF was then continued for up to 19.5 hours. After treatment exposure, endothelial cultures were washed and incubated with maintenance medium for up to 7 days. Although initial treatment with TNF or 18:2 significantly increased oxidative stress and intracellular calcium levels, only exposure to TNF induced apoptotic processes in cultured endothelial cells. Furthermore, the combined exposure to 18:2 plus TNF amplified TNF-induced apoptosis. Vitamin E did not protect against TNF-induced apoptosis. However, vitamin E reversed the 18:2-mediated potentiation of apoptosis in endothelial cells exposed to 18:2 plus TNF. These studies provide evidence that the lipid environment may be crucial during local TNF-induced events in the vascular endothelium.
|Original language||English (US)|
|State||Published - Dec 1 1996|
ASJC Scopus subject areas
- Molecular Biology