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Oxidative stress mediates homocysteine proatherosclerotic effects on human endothelial cells through a MAP kinase pathway

Homocysteine (Hcy) is implicated in inducing cellular oxidative stress (OXS) which mediates endothelial cell (EC) damage via unknown mechanisms. We have previously shown Hcy induces activation of MAPK JNK and increases EC:leukocyte interactions. However, the JNK activator has yet to be identified. OXS is known to cause activation of the JNK MAP kinase pathway. Objective: to study the effects of antioxidants on Hcy EC damage.