Catapano A L
Institute of Pharmacological Sciences and Centro per lo Studio, la Prevenzione e la Terapia delle Vasculopatie Aterosclerotiche, University of Milano, Italy.
Angiology. 1997 Jan;48(1):39-44. doi: 10.1177/000331979704800107.
Our body generates hydroxyl radicals under a number of conditions. This radical is very unstable and, therefore, very reactive. After attack of radicals on membranes and lipoproteins, lipid peroxidation starts, and may lead to the development of vascular lesions. The human body has developed antioxidant defenses to protect against free radicals such as superoxide dismutases, glutathione peroxidases, plasma iron binding proteins, or alpha tocopherol. Oxidized LDL are believed to play a key role in vascular damage and can modulate several endothelial properties including NO production and expression of adhesion molecules. Antioxidants, such as flavonoids, inhibit "in vitro" oxidation of LDL and their cytotoxicity; in humans consumption of flavonoids appears to be related to a reduction of the risk of cardiovascular diseases. The biochemical mechanisms responsible for this effect remain to be addressed.
在多种情况下,我们的身体会产生羟基自由基。这种自由基非常不稳定,因此具有很强的反应活性。自由基攻击细胞膜和脂蛋白后,脂质过氧化反应开始,可能导致血管病变的发展。人体已经发展出抗氧化防御机制来抵御自由基,如超氧化物歧化酶、谷胱甘肽过氧化物酶、血浆铁结合蛋白或α-生育酚。氧化型低密度脂蛋白被认为在血管损伤中起关键作用,并可调节多种内皮特性,包括一氧化氮的产生和黏附分子的表达。抗氧化剂,如类黄酮,可抑制低密度脂蛋白的“体外”氧化及其细胞毒性;在人类中,食用类黄酮似乎与心血管疾病风险的降低有关。造成这种效应的生化机制仍有待探讨。