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In vitro, LMPs considerably diminished human umbilical vein endothelial cell survival and proliferation in a concentration-dependent manner. Mechanistically, the antioxidants U-74389G and U-83836E were partially protective against the antiproliferative effects of LMPs, whereas the NADPH oxidase (NOX) inhibitors apocynin and diphenyleneiodonium significantly abrogated these effects. Moreover, LMPs increased not only the expression of the NOX subunits gp91<jats:sup>phox<\/jats:sup>, p22<jats:sup>phox<\/jats:sup>, and p47<jats:sup>phox<\/jats:sup>, but also the production of ROS and NOX-derived superoxide (O<jats:sub>2<\/jats:sub><jats:sup>\u2212<\/jats:sup>). Importantly, LMPs caused a pronounced augmentation in the protein expression of the CD36 antiangiogenic receptor while significantly downregulating the protein levels of VEGF receptor type 2 and its downstream signaling mediator, phosphorylated ERK1\/2. 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