Organophosphate flame retardants (OPFRs) have become a growing concern due to their potential environmental and health risk. However, limited studies have described the toxicity, particularly neurotoxicity of alkyl and aromatic OPFRs. This study investigated the neurotoxicity of alkyl tri‐n‐butyl phosphate (TnBP) and aromatic tricresyl phosphate (TCP) to rat adrenal pheochromocytoma (PC12) cells for 24 h. Viability detection showed dose‐response toxicity effect of TCP and TnBP to PC12 cells. The half‐maximal inhibitory concentration of 24 h (24 h‐IC50) of TCP and TnBP were 2415.61 and 338.09 μM, respectively. Both TnBP and TCP significantly changed the acetylcholinesterase (AChE) activity, and TnBP is more likely to cause neurotoxicity to PC12 cells compared to TCP. Also, The results of LDH and caspase‐3 activity detection as well as Hoechst staining suggested that cell apoptosis induced by TCP and TnBP may be the primary pathway. These findings provide a toxicity data of aromatic and alkyl‐substituted OPFRs to PC12 cells, and a new insight into the toxicity of OPFRs on health risk assessment.

中文翻译：

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磷酸三正丁酯烷基酯和磷酸三甲苯酯对 PC12 细胞神经毒性影响的比较评估

由于其潜在的环境和健康风险，有机磷阻燃剂 (OPFR) 已成为日益受到关注的问题。然而，有限的研究描述了烷基和芳香族 OPFR 的毒性，尤其是神经毒性。本研究调查了烷基三正丁基磷酸酯 (TnBP) 和芳香族磷酸三甲苯酯 (TCP) 对大鼠肾上腺嗜铬细胞瘤 (PC12) 细胞 24 小时的神经毒性。活力检测显示 TCP 和 TnBP 对 PC12 细胞的剂量反应毒性效应。TCP 和 TnBP 的 24 小时半数抑制浓度 (24 h-IC50) 分别为 2415.61 和 338.09 μM。TnBP 和 TCP 都显着改变了乙酰胆碱酯酶 (AChE) 活性，与 TCP 相比，TnBP 更可能对 PC12 细胞造成神经毒性。还，LDH和caspase-3活性检测以及Hoechst染色结果提示TCP和TnBP诱导的细胞凋亡可能是主要途径。这些发现提供了芳香族和烷基取代的 OPFRs 对 PC12 细胞的毒性数据，以及对 OPFRs 对健康风险评估毒性的新见解。