Benzophenone-3 (BP-3) is often used as an ultraviolet (UV) light filter in sunscreen products. Although BP-3 protects the human skin and hair from damage caused by excessive UV radiation, it is reported to exhibit toxic effects in human. However, the cytotoxicity of BP-3 on various cells is still not well understood. In the present study, the cytotoxicity of BP-3 against rat thymocytes was evaluated using a flow cytometric technique with fluorescent probes. Cell mortality increased significantly after 3 h of exposure to 300 μM BP-3, whereas the mean intensity of 5-chloromethylfluorescein diacetate (5-CMF) fluorescence and cellular content of non-protein thiols decreased significantly. However, the membrane potential of thymocytes was not change by BP-3 treatment. Moreover, intracellular Zn²⁺ levels increased significantly in a concentration-dependent manner in response to 30 μM BP-3 or higher. The BP-3-induced changes in intracellular Zn²⁺ levels and non-protein thiol content increased the vulnerability of thymocytes to oxidative stress. We concluded that BP-3-induced cytotoxicity may be caused by oxidative stress associated with an increase in intracellular Zn²⁺ levels.

苯甲酮3（BP-3）通常用作防晒产品中的紫外线（UV）滤光片。尽管BP-3保护人类的皮肤和头发免受过度紫外线辐射造成的损害，但据报道它对人体具有毒性作用。然而，BP-3对各种细胞的细胞毒性仍然没有被很好地理解。在本研究中，使用带有荧光探针的流式细胞仪技术评估了BP-3对大鼠胸腺细胞的细胞毒性。暴露于300μMBP-3 3小时后，细胞死亡率显着增加，而5-氯甲基荧光素二乙酸酯（5-CMF）荧光的平均强度和非蛋白质硫醇的细胞含量显着降低。然而，通过BP-3处理胸腺细胞的膜电位没有改变。此外，细胞内Zn ²⁺响应30μMBP-3或更高水平，血脂水平显着升高，呈浓度依赖性。BP-3-诱导的细胞内Zn ²⁺水平和非蛋白质硫醇含量的变化增加了胸腺细胞对氧化应激的脆弱性。我们得出的结论是BP-3诱导的细胞毒性可能是由氧化应激引起的，该氧化应激与细胞内Zn ²⁺水平的升高有关。