Key Laboratory of Environmental Medicine Engineering of Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, Jiangsu, China; Jiangsu Provincial Center for Disease Prevention and Control, Nanjing 210000, Jiangsu, China.
Key Laboratory of Environmental Medicine Engineering of Ministry of Education, School of Public Health, Southeast University, Nanjing 210009, Jiangsu, China.
Ecotoxicol Environ Saf. 2022 Nov;246:114142. doi: 10.1016/j.ecoenv.2022.114142. Epub 2022 Sep 30.
Benzene is a common industrial chemical and environmental pollutant. However, the mechanism of hematotoxicity caused by exposure to low doses of benzene is unknown. Let-7e-5p pathway regulatory networks were constructed by bioinformatics analysis using a benzene-induced aplastic anemia (BIAA) mouse model. The MTT assay, EdU staining, flow cytometric analysis, dual luciferase reporter gene assay, and RIP assay were utilized to evaluate the effects of benzoquinone (1,4-BQ) on let-7e-5p pathway. This study consisted of 159 workers with a history of low-level benzene exposure and 159 workers with no history of benzene exposure. After the confounding factors were identified, the associations between let-7e-5p expression and hematotoxicity were assessed by multiple linear regression. Furthermore, we used four machine learning algorithms (decision trees, neural network, Bayesian network, and support vector machines) to construct a predictive model for detecting benzene-causing hematotoxicity in workers. In this study, compared with respective controls, let-7e-5p expression was decreased in BIAA mice and benzene-exposed workers. After 1,4-BQ exposure, let-7e-5p overexpression negatively regulated caspase-3 and p21 expression, protected cells from apoptosis, and facilitated cell proliferation. RIP assays, and dual luciferase reporter gene assays confirmed that let-7e-5p could target p21 and caspase-3 and regulate the cell cycle and apoptosis. The support vector machines classifier achieved the best prediction of benzene-induced hematotoxicity (prediction accuracy = 88.27, AUC = 0.83) by statistically characterizing the internal dose of benzene exposure and the oxidative stress index, as well as the expression levels of let-7e-5p pathway-related genes in benzene-exposed workers. Let-7e-5p may be a potential therapeutic target of benzene-induced hematotoxicity, provide a basis for evaluating the health hazards of long-term and low-dose benzene exposure in workers, and supply a reference for revising occupational health standards.
苯是一种常见的工业化学物质和环境污染物。然而,暴露于低剂量苯引起血液毒性的机制尚不清楚。本研究采用生物信息学分析方法,构建了苯致再生障碍性贫血(BIAA)小鼠模型的 Let-7e-5p 通路调控网络。通过 MTT 检测、EdU 染色、流式细胞术分析、双荧光素酶报告基因检测和 RIP 实验评估了对苯醌(1,4-BQ)对 Let-7e-5p 通路的影响。本研究纳入了 159 名有低水平苯暴露史的工人和 159 名无苯暴露史的工人。在确定混杂因素后,采用多元线性回归评估 Let-7e-5p 表达与血液毒性的关系。此外,我们使用四种机器学习算法(决策树、神经网络、贝叶斯网络和支持向量机)构建了用于检测工人苯致血液毒性的预测模型。与各自的对照组相比,BIAA 小鼠和苯暴露工人的 Let-7e-5p 表达均降低。经 1,4-BQ 处理后,Let-7e-5p 过表达负调控 caspase-3 和 p21 的表达,保护细胞免于凋亡并促进细胞增殖。RIP 实验和双荧光素酶报告基因实验证实,Let-7e-5p 可靶向 p21 和 caspase-3 并调节细胞周期和凋亡。支持向量机分类器通过统计苯暴露的内剂量和氧化应激指标以及苯暴露工人 Let-7e-5p 通路相关基因的表达水平,对苯引起的血液毒性进行了最佳预测(预测准确率=88.27%,AUC=0.83)。Let-7e-5p 可能是苯致血液毒性的潜在治疗靶点,为评估工人长期低剂量苯暴露的健康危害提供了依据,并为修订职业健康标准提供了参考。