Conclusion
Lipids from the atherosclerotic plaque may contribute to the progression of atherogenic conditions in adjacent regions by weakening the cellular antioxidant system and promoting oxidative stress, mainly through H(2)O(2) production.
Objective
In this study, we challenged this idea by investigating the effect of carotid plaque lipid extract on the human monocyte antioxidant system.
Results
Exposure of monocytes to carotid plaque lipid extract (LE) for up to 72 h resulted in a significant increase in the ROS level (170%), with a simultaneous rise of 177% in glutathione oxidation. Experiments revealed a significant decrease, in the intracellular antioxidant enzyme activity of CAT, GPx and TRxR, (by 17, 33 and 43%, respectively). Although the activity of these enzymes subsequently returned to those of the controls, the levels of ROS did not decrease but rather continued increasing with extended LE exposure. Intriguingly, intracellular SOD activity rose significantly and remained high (176%), implying that endogenously produced H(2)O(2), and not O(2)·¯ < is the factor that promotes the oxidative stress resulting from the presence of LE.