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Mechanism of acute endosulfan intoxication-induced neurotoxicity in Sprague-Dawley rats

Tae-chang Jang ; Department of Emergency Medicine, School of Medicine, Catholic University of Daegu, Korea
Jung-hee Jang ; Department of Pharmacology, School of Medicine, Keimyung University, Korea
Kyung-won Lee orcid id ; Department of Emergency Medicine, Seoul National University Hospital, Korea

Puni tekst: engleski pdf 531 Kb


str. 9-17

preuzimanja: 603



The purpose of this study was to investigate the molecular mechanism underlying oxidative and inflammatory neuronal cell death induced by endosulfan, a pesticide belonging to the chemical family of organochlorines. The cortical and hippocampal tissues derived from Sprague-Dawley (SD) rats treated with endosulfan exhibited increased intracellular accumulation of reactive oxygen species and oxidative damages to cellular macromolecules such as depletion of glutathione, lipid peroxidation, and protein carbonylation. Conversely, the expression of antioxidant enzymes including γ-glutamylcysteine ligase (GCL), superoxide dismutase (SOD), and heme oxygenase-1 (HO-1) was markedly reduced in the brain tissues exposed to endosulfan. Moreover, during endosulfan-induced neuronal cell death, mRNA expression of pro-inflammatory cytokines such as tumour necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) was elevated, which seemed to be mediated by the activation of nuclear factor-kappa B (NF-κB) by phosphorylation of p65 subunit. These results suggest a new molecular mechanism underlying the endosulfan-induced acute neurotoxicity via induction of oxidative stress and pro-inflammatory responses.

Ključne riječi

endosulfan; inflammation; neurotoxicity; oxidative stress

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