Wang Jing, Wang Jiaxi, Zhang Lu, Liu Rutao, Zong Wansong
School of Environmental and Material Engineering, Yantai University , 30 Qingquan Road, Yantai 264005, People's Republic of China.
School of Environmental Science and Engineering, Shandong University, China-America CRC for Environment & Health , 27 Shanda South Road, Jinan, Shandong Province 250100, People's Republic of China.
J Agric Food Chem. 2017 Apr 12;65(14):3039-3047. doi: 10.1021/acs.jafc.7b00291. Epub 2017 Mar 29.
This study investigated the adverse effects of sodium dodecylbenzenesulfonates (SDBS) on mouse primary hepatocytes by conducting cell viability, intracellular oxidative stress level, and catalase (CAT) activity assays. It was shown that SDBS altered CAT activities, triggered oxidative stress, and thus exhibited cytotoxicity to the hepatocytes. Both the stimulation of intracellular CAT production and the inhibition of molecular CAT activity contributed to intracellular CAT activity change. Molecular mechanisms underlying CAT activity inhibition and structural changes were explored by isothermal titration calorimetry, multispectroscopy, and molecular docking studies. SDBS binds to CAT with 8.81 ± 0.751 sites via electrostatic forces, resulting in structural changes with α-helix significantly decreasing to 9.7 ± 1.2%. SDBS could interact with HIS 74, ASN 147, and TYR 357 around the active sites as well as TRP 185, ASP 127, and GLN 167 within the substrate channel and therefore might result in the inhibition of molecular CAT activity.
本研究通过进行细胞活力、细胞内氧化应激水平和过氧化氢酶（CAT）活性测定，研究了十二烷基苯磺酸钠（SDBS）对小鼠原代肝细胞的不良影响。结果表明，SDBS改变了CAT活性，引发了氧化应激，从而对肝细胞表现出细胞毒性。细胞内CAT产生的刺激和分子CAT活性的抑制均导致细胞内CAT活性变化。通过等温滴定量热法、多光谱法和分子对接研究，探索了CAT活性抑制和结构变化的分子机制。SDBS通过静电力与CAT的8.81±0.751个位点结合，导致结构变化，α-螺旋显著减少至9.7±1.2%。SDBS可与活性位点周围的HIS 74、ASN 147和TYR 357以及底物通道内的TRP 185、ASP 127和GLN 167相互作用，因此可能导致分子CAT活性的抑制。
