Tian Luwei, Wu Yanan, Jia Yankun, Guo Ming
College of Chemistry and Materials Engineering, Zhejiang Agriculture & Forestry University, Hangzhou 311300, China.
Int J Mol Sci. 2025 Mar 25;26(7):2990. doi: 10.3390/ijms26072990.
Benzophenone UV absorbers (BPs), a widely used family of organic UV absorbers (UVAs), have attracted considerable attention for their effects on organisms in recent years. Previous research has been unable to illuminate the intricate situation of BP pollution. To address this knowledge gap, we devised a BAPG-chain model that surpasses existing approaches based on biochemical detection, antioxidant defense systems, proteins, and genes to investigate the biological mechanisms of benzophenone-1 (BP-1) and benzophenone-3 (BP-3) within human hepatoma SMMC-7721 cells as model organisms. The BAPG-chain model links the cellular model, molecular level, macroscopic scale, and microscopic phenomena by adopting a global assessment mindset. Our findings indicate that BPs induce apoptosis via the excessive production of reactive oxygen species (ROS), mitochondrial and nuclear damage, and disruption of the antioxidant stress system. Notably, BPs induce apoptosis via alterations in the expression of genes and proteins associated with apoptosis in the mitochondria. Our experimental evidence sheds light on the biological effects of BPs and highlights the need for further research in this area.
二苯甲酮紫外线吸收剂（BPs）是一类广泛使用的有机紫外线吸收剂（UVAs），近年来其对生物体的影响已引起相当大的关注。以往的研究未能阐明BP污染的复杂情况。为了填补这一知识空白，我们设计了一种BAPG链模型，该模型超越了基于生化检测、抗氧化防御系统、蛋白质和基因的现有方法，以人类肝癌SMMC - 7721细胞作为模式生物来研究二苯甲酮 - 1（BP - 1）和二苯甲酮 - 3（BP - 3）的生物学机制。BAPG链模型通过采用全局评估思维方式，将细胞模型、分子水平、宏观尺度和微观现象联系起来。我们的研究结果表明，BPs通过活性氧（ROS）的过量产生、线粒体和细胞核损伤以及抗氧化应激系统的破坏诱导细胞凋亡。值得注意的是，BPs通过线粒体中与细胞凋亡相关的基因和蛋白质表达的改变诱导细胞凋亡。我们的实验证据揭示了BPs的生物学效应，并强调了该领域进一步研究的必要性。
