Abstract
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.