结论晚期氧化蛋白产物能通过氧化应激引起血管内皮细胞损伤。
Conclusion AOPP decreased endothelial cell viability via induction of oxidative stress.
氧化低密度脂蛋白诱导通过细胞内活性氧簇和脂质过氧化反应产物水平测量的氧化应激。
OxLDL induced oxidative stress, measured by the intracellular levels of reactive oxygen species (ROS) and lipid peroxidation products.
铁，作为血红蛋白的降解产物，在许多疾病的神经损害中起着关键作用，脑内铁含量的增加可导致脂质过氧化和自由基产生。
Iron, a hemoglobin degradation product, plays a key role in neurodegeneration in many disease states, and an increase in brain iron can result in lipid peroxidation and free radical formation.
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