AlKahtane Abdullah A, Alarifi Saud, Al-Qahtani Ahmed A, Ali Daoud, Alomar Suliman Y, Aleissia Mohammed S, Alkahtani Saad
Department of Zoology, Science College, King Saud University, Riyadh, Saudi Arabia.
Department of Infection and Immunity, Research Center, King Faisal Specialist Hospital & Research Center, Riyadh, Saudi Arabia.
Dose Response. 2018 Apr 15;16(2):1559325818760880. doi: 10.1177/1559325818760880. eCollection 2018 Apr-Jun.
Most of the agricultural workers are potentially exposed to pesticides through different routes. Inhalation exposures may result in numerous diseases that can adversely affect an individual's health and capacity to perform at work. The aim of this study was to determine the cytotoxic potential of cypermethrin pesticide on cultured human hepatocarcinoma (HepG2) cells. The HepG2 cells were exposed to cypermethrin (0, 5, 15, 40 ng/mL) for 24 and 48 hours. We observed that cypermethrin caused cell death of HepG2 cells using 3-(4, 5-dimethylthiozolyl-2)-2,5-diphenyl tetrazolium bromide (MTT) and lactate dehydrogenase tests. Furthermore, cypermethrin reduced HepG2 cells viability in a time and dose dependent basis, that was probably mediated through the induction of reactive oxygen species (ROS) and apoptosis. An increase in ROS generation with a concomitant increase in expression of the proapoptotic protein Bcl-2 and cytochrome c and decrease in the antiapoptosis protein Bax suggested that a mitochondria-mediated pathway was involved in cypermethrin-induced apoptosis. These findings provide insights into the underlying mechanisms involved in cytotoxicity of cypermethrin in HepG2 cells.
大多数农业工人都有可能通过不同途径接触到农药。吸入接触可能导致多种疾病，这些疾病会对个人健康和工作能力产生不利影响。本研究的目的是确定氯氰菊酯农药对培养的人肝癌（HepG2）细胞的细胞毒性潜力。将HepG2细胞暴露于氯氰菊酯（0、5、15、40 ng/mL）中24小时和48小时。我们使用3-（4,5-二甲基噻唑-2）-2,5-二苯基溴化四氮唑（MTT）和乳酸脱氢酶试验观察到氯氰菊酯导致HepG2细胞死亡。此外，氯氰菊酯在时间和剂量依赖性基础上降低了HepG2细胞的活力，这可能是通过诱导活性氧（ROS）和凋亡介导的。ROS生成增加，同时促凋亡蛋白Bcl-2和细胞色素c的表达增加，抗凋亡蛋白Bax减少，表明线粒体介导的途径参与了氯氰菊酯诱导的凋亡。这些发现为氯氰菊酯在HepG2细胞中细胞毒性的潜在机制提供了见解。
