Persistent diazinon induced neurotoxicity: The effect on inhibitory avoidance memory performance, amyloid precursor proteins, and TNF-α levels in the prefrontal cortex of rats.
Autor: | Afshari S; Students Research Committee, Pharmacy School, Ardabil University of Medical Sciences, Ardabil, Iran., Sarailoo M; Students Research Committee, School of Public Health, Ardabil University of Medical Sciences, Ardabil, Iran., Asghariazar V; Cancer Immunology and Immunotherapy Research Center, Ardabil University of Medical Sciences, Ardabil, Iran.; Deputy of Research & Technology, Ardabil University of Medical Sciences, Ardabil, Iran., Safarzadeh E; Cancer Immunology and Immunotherapy Research Center, Ardabil University of Medical Sciences, Ardabil, Iran.; Department of Microbiology, Parasitology, and Immunology, Ardabil University of Medical Sciences, Ardabil, Iran., Dadkhah M; Pharmaceutical Sciences Research Center, Ardabil University of Medical Sciences, Ardabil, Iran.; School of Pharmacy, Ardabil University of Medical Sciences, Ardabil, Iran. |
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Jazyk: | angličtina |
Zdroj: | Human & experimental toxicology [Hum Exp Toxicol] 2024 Jan-Dec; Vol. 43, pp. 9603271241235408. |
DOI: | 10.1177/09603271241235408 |
Abstrakt: | Introduction: Organophosphate pesticides (Ops) like diazinon (DZN) have well-known neurotoxic effects and low-level chronic exposure has been linked to detrimental neurobehavioral impairments and memory deficits. However, it's not entirely clear how DZN-induced biological changes, particularly in the prefrontal cortex (PFC) contribute to these effects. The purpose of this study is to investigate the impact of DZN exposure on inhibitory avoidance (IA) memory function, amyloid precursor expression (APP), and proinflammatory tumor necrosis factor-α (TNF-α) levels in the rat cortex. Materials and Methods: Rats were divided into 4 groups and recived 2 mg/kg DZN for 5-days or 12-weeks and two control groups recived the same volume of vehicle. IA memory was assesed using the shuttle box apparatus. Rats were sacrificed and the prefrontal cortex PFC were removed. Real-time PCR and Western blotting were used to messure TNF-α, and amyloid protein precursors gene expression and protein levels. Results: Our findings indicated that DZN caused body weight loss and a notable decline in performance on the IA memory. Additionally, 5-days exposure increased APP and APLP2 protein levels in the PFC, while 12-weeks exposure decreased these levels. Furthermore, expression of APP and APLP2 gens were decreased in PFC. TNF-α levels increased as a result of 5-days exposure to DZN, but these levels dropped to normal after 12-weeks administration, and this observation was significant. Conclusion: Taken together, exposure to low doses of DZN leads to disturbances in IA memory performance and also alternations in amyloid beta precursors that can be related to increased risk of Alzheimer's disease. Competing Interests: Declaration of Conflicting InterestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. |
Databáze: | MEDLINE |
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