Gill Kiran, Bindal Eshika, Garg Parul, Kumar Deepak, Bhattacharyya Rajasri, Banerjee Dibyajyoti
Experimental Medicine and Biotechnology Department, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Cell Biol Int. 2025 Jun;49(6):709-722. doi: 10.1002/cbin.70017. Epub 2025 Mar 18.
Nonalcoholic fatty liver disease poses a significant public health concern, as do the issues surrounding plastic usage. The bisphenols are reported to cause fat accumulation in the liver. However, literature is scanty about the effect of bisphenols on lysosomes or lysosomal functions. We predicted the interaction of bisphenols with lysosomal proteins available in the online databases using in silico tools. Molecular docking revealed that chosen Bisphenols interact with critical lysosomal proteins including lipid hydrolyzing enzymes. Following exposure of BPA, BPB and BPC to HepG2 cells fat accumulation and lysosomal functions were evaluated. Exposure to BPB and BPC results intracellular fat accumulation under experimental conditions like BPA. All three Bisphenols disturb lysosomal homeostasis perhaps by different mechanisms. Overall our results suggest that Bisphenols can also cause fat accumulation in liver by disturbing lysosomal homeostasis.
非酒精性脂肪性肝病对公众健康构成重大威胁，塑料使用相关问题亦是如此。据报道，双酚会导致肝脏脂肪堆积。然而，关于双酚对溶酶体或溶酶体功能影响的文献却很少。我们使用计算机工具预测了双酚与在线数据库中可用的溶酶体蛋白之间的相互作用。分子对接显示，所选双酚与包括脂质水解酶在内的关键溶酶体蛋白相互作用。将双酚A、双酚B和双酚C暴露于HepG2细胞后，评估了脂肪堆积和溶酶体功能。在与双酚A相同的实验条件下，暴露于双酚B和双酚C会导致细胞内脂肪堆积。所有三种双酚可能通过不同机制扰乱溶酶体稳态。总体而言，我们的结果表明，双酚也可通过扰乱溶酶体稳态导致肝脏脂肪堆积。
