School of Public Health, Health Science Center, Shenzhen University, Shenzhen, Guangdong 518060, People's Republic of China.
Department of Respiratory & Allergy, Third Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong 518020, People's Republic of China.
J Agric Food Chem. 2021 May 26;69(20):5725-5733. doi: 10.1021/acs.jafc.1c00559. Epub 2021 May 11.
This study analyzed the effect of lipid peroxidation using 2,2'-azobis(2-amidinopropane)dihydrochloride (AAPH) and acrolein on the and allergenicity of α-lactalbumin (α-La). The structure of oxidized α-La was evaluated by sodium dodecyl sulfate polyacrylamide gel electrophoresis, fluorescence spectroscopy, and circular dichroism, whereas the changes in the allergenic properties were evaluated. Lipid peroxidation induced changes to the structural properties that might destroy and/or mask α-La epitopes. In comparison to native α-La, oxidation complexes caused a decrease in the immunoglobulin E (IgE) binding capacity, as observed via immunoblotting. Moreover, the capacity to release mediators and cytokines from KU812 cells was also greatly reduced. , oxidation with AAPH and acrolein caused a significant reduction in IgE, IgG, IgG1, mast cell protease 1, and plasma histamine, along with the reduction of mast surface c-Kit and FcεRI expression. Therefore, these results indicate that oxidation via AAPH and acrolein can potentially reduce the allergenicity of α-La, which can help with the better understanding of the changes in allergenicity of milk allergen by lipid peroxidation.
本研究分析了脂质过氧化作用对α-乳白蛋白（α-La）的 和变应原性的影响，使用 2,2'-偶氮双（2-脒基丙烷）二盐酸盐（AAPH）和丙烯醛。通过十二烷基硫酸钠聚丙烯酰胺凝胶电泳、荧光光谱和圆二色性评估氧化α-La 的结构，同时评估变应原性质的变化。脂质过氧化诱导的结构性质变化可能破坏和/或掩盖α-La 表位。与天然α-La 相比，氧化复合物导致免疫球蛋白 E（IgE）结合能力下降，如免疫印迹所示。此外，从 KU812 细胞释放介质和细胞因子的能力也大大降低。 ，AAPH 和丙烯醛的氧化导致 IgE、IgG、IgG1、肥大细胞蛋白酶 1 和血浆组胺显著减少，同时降低肥大细胞表面 c-Kit 和 FcεRI 表达。因此，这些结果表明，AAPH 和丙烯醛的氧化可能降低α-La 的变应原性，有助于更好地理解脂质过氧化作用对牛奶过敏原变应原性的变化。
