Affiliation:
1. Department of Neurosurgery Kaohsiung Veterans General Hospital Kaohsiung Taiwan
2. Department of Neurosurgery National Defense Medical Center Taipei Taiwan
3. College of Health and Nursing Meiho University Pingtung Taiwan
4. Department of Neurosurgery Pingtung Veterans General Hospital Pingtung Taiwan
5. Department of Pathology and Laboratory Medicine Kaohsiung Veterans General Hospital Kaohsiung Taiwan
6. Department of Pharmacy and Master Program, College of Pharmacy and Health Care Tajen University Pingtung Taiwan
7. Department of Medical Education and Research Kaohsiung Veterans General Hospital Kaohsiung Taiwan
Abstract
AbstractOrganophosphate pesticides (OPs), which are among the most widely used synthetic chemicals for the control of a wide variety of pests, are however associated with various adverse reactions in animals and humans. Chlorpyrifos, an OP, has been shown to cause various health complications due to ingestion, inhalation, or skin absorption. The mechanisms underlying the adverse effect of chlorpyrifos on neurotoxicity have not been elucidated. Therefore, we aimed to determine the mechanism of chlorpyrifos‐induced cytotoxicity and to examine whether the antioxidant vitamin E (VE) ameliorated these cytotoxic effects using DBTRG‐05MG, a human glioblastoma cell line. The DBTRG‐05MG cells were treated with chlorpyrifos, VE, or chlorpyrifos plus VE and compared with the untreated control cells. Chlorpyrifos induced a significant decrease in cell viability and caused morphological changes in treated cultures. Furthermore, chlorpyrifos led to the increased production of reactive oxygen species (ROS) accompanied by a decrease in the level of reduced glutathione. Additionally, chlorpyrifos induced apoptosis by upregulating the protein levels of Bax and cleaved caspase‐9/caspase‐3 and by downregulating the protein levels of Bcl‐2. Moreover, chlorpyrifos modulated the antioxidant response by increasing the protein levels of Nrf2, HO‐1, and NQO1. However, VE reversed the cytotoxicity and oxidative stress induced by chlorpyrifos treatment in DBTRG‐05MG cells. Overall, these findings suggest that chlorpyrifos causes cytotoxicity through oxidative stress, a process that may play an important role in the development of chlorpyrifos‐associated glioblastoma.
Funder
Kaohsiung Veterans General Hospital
Subject
Health, Toxicology and Mutagenesis,Management, Monitoring, Policy and Law,Toxicology,General Medicine
Cited by
3 articles.
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