本文分别采用Cu2+/H2O2、AAPH体系诱导BSA氧化和羰基化损伤、Hemin/nitrite/H2O2诱导BSA硝基化损伤；Fe2+/Vitc、AMVN诱导亚油酸（LA）过氧化及AAPH诱导鲱鱼精DNA氧化损伤的模型，研究了辣椒碱对生物大分子在羟自由基和烷氧自由基攻击下发生氧化损伤的保护作用。结果表明：50 μM~1000 μM的辣椒碱能显著抑制自由基诱导的蛋白质氧化损伤；10 μM~1000 μM的辣椒碱能显著抑制羟自由基诱导的蛋白羰基化、蛋白氧化应激产生的硝基化以及脂质过氧化终产物TBARS的生成，100 μM~1000 μM的辣椒碱能显著抑制烷氧自由基诱导的蛋白羰基化和DNA的氧化损伤。得出结论：辣椒碱对不同自由基诱导的生物大分子氧化损伤有显著的保护作用，且其保护作用在一定浓度范围内与辣椒碱浓度呈正相关。本研究为辣椒碱在食品抗氧化剂以及功能食品中的开发与应用提供了基础依据。

Oxidative damage was induced using several different systems to study the protective effect of capsaicin (CAS) against damage caused by OH? and alkoxy radicals (RO?). Oxidation and carbonylation of bovine serum albumin (BSA) was induced by copper ions/hydrogen peroxide and 2,2'-azobis(2-amidinopropane) hydrochloride (AAPH), respectively. Nitration of BSA was induced by hemin/nitrite/hydrogen peroxide, peroxidation of linoleic acid (LA) was induced by ferrous iron/VitC and 2,2'-azobis(2,4-di-methylvaleronitrile) (AMVN), and oxidative damage to herring sperm DNA was induced by AAPH. The results showed that 50~1000 μM CAS could significantly inhibit the oxidative cleavage of protein induced by reactive oxygen species (ROS); 10~1000 μM CAS could significantly inhibit protein carbonylation induced by OH?, protein nitration, and the formation of thiobarbituric acid reactive substances (TBARS), the final product of LA peroxidation; and 100~1000 μM CAS could significantly inhibit protein carbonylation induced by RO? and DNA oxidative cleavage. It was concluded that CAS had a strong protective effect against oxidative damage to biomolecules caused by various types of free radicals, and the protective effects exhibited a concentration-dependent manner to some degree. This study provides scientific evidence for the development and application of CAS in dietary supplements and functional foods.

中国博士后科学基金面上资助项目（2015M572603）；陕西省自然科学基础研究计划青年人才项目（2015JQ2039）