Sina Nikbin, S. B. Jameie, M. Azarbayjani, Nasrin Hosseini
{"title":"毒死蜱对大鼠海马Caspase-3水平及被动回避记忆的影响","authors":"Sina Nikbin, S. B. Jameie, M. Azarbayjani, Nasrin Hosseini","doi":"10.5812/thrita-123356","DOIUrl":null,"url":null,"abstract":"Background: Chlorpyrifos is an organophosphate pesticide that is widely used in the world. Exposure to chlorpyrifos is associated with some problems in cognitive functions, such as learning and memory. Caspase-3 is a cysteine protease that is activated in response to several apoptotic stimuli and triggers some proteolytic events, cell death, and neurodegeneration. Objectives: The aim of the present study was to clear potential mechanisms related to chlorpyrifos neurotoxicity through caspase-3 alteration and passive avoidance memory function. Methods: Male adult rats were randomly divided into the control, sham, and chlorpyrifos groups (eight rats in each group). The chlorpyrifos group received an intraperitoneal injection of chlorpyrifos (3 mg/kg/5 days) dissolved in dimethyl sulfoxide for two consecutive weeks. The caspase-3 levels in the hippocampus were assessed by the western blot technique, and also the passive avoidance task was used for memory evaluation. Results: Our findings showed that chlorpyrifos treatment markedly increased caspase-3 levels in the hippocampus and also increased the time spent in the dark chamber 24 h and one week after receiving foot shock in the chlorpyrifos group. Conclusions: Organophosphate pesticides exposure can impair passive avoidance memory, and high levels of caspase-3 in the hippocampus are proposed as a possible reason for neuronal toxicity and memory impairment.","PeriodicalId":23167,"journal":{"name":"Thrita","volume":"53 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2022-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The Effects of Chlorpyrifos on Hippocampal Caspase-3 Levels and Passive Avoidance Memory in Rats\",\"authors\":\"Sina Nikbin, S. B. Jameie, M. Azarbayjani, Nasrin Hosseini\",\"doi\":\"10.5812/thrita-123356\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Background: Chlorpyrifos is an organophosphate pesticide that is widely used in the world. Exposure to chlorpyrifos is associated with some problems in cognitive functions, such as learning and memory. Caspase-3 is a cysteine protease that is activated in response to several apoptotic stimuli and triggers some proteolytic events, cell death, and neurodegeneration. Objectives: The aim of the present study was to clear potential mechanisms related to chlorpyrifos neurotoxicity through caspase-3 alteration and passive avoidance memory function. Methods: Male adult rats were randomly divided into the control, sham, and chlorpyrifos groups (eight rats in each group). The chlorpyrifos group received an intraperitoneal injection of chlorpyrifos (3 mg/kg/5 days) dissolved in dimethyl sulfoxide for two consecutive weeks. The caspase-3 levels in the hippocampus were assessed by the western blot technique, and also the passive avoidance task was used for memory evaluation. Results: Our findings showed that chlorpyrifos treatment markedly increased caspase-3 levels in the hippocampus and also increased the time spent in the dark chamber 24 h and one week after receiving foot shock in the chlorpyrifos group. Conclusions: Organophosphate pesticides exposure can impair passive avoidance memory, and high levels of caspase-3 in the hippocampus are proposed as a possible reason for neuronal toxicity and memory impairment.\",\"PeriodicalId\":23167,\"journal\":{\"name\":\"Thrita\",\"volume\":\"53 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2022-06-05\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Thrita\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.5812/thrita-123356\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Thrita","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5812/thrita-123356","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The Effects of Chlorpyrifos on Hippocampal Caspase-3 Levels and Passive Avoidance Memory in Rats
Background: Chlorpyrifos is an organophosphate pesticide that is widely used in the world. Exposure to chlorpyrifos is associated with some problems in cognitive functions, such as learning and memory. Caspase-3 is a cysteine protease that is activated in response to several apoptotic stimuli and triggers some proteolytic events, cell death, and neurodegeneration. Objectives: The aim of the present study was to clear potential mechanisms related to chlorpyrifos neurotoxicity through caspase-3 alteration and passive avoidance memory function. Methods: Male adult rats were randomly divided into the control, sham, and chlorpyrifos groups (eight rats in each group). The chlorpyrifos group received an intraperitoneal injection of chlorpyrifos (3 mg/kg/5 days) dissolved in dimethyl sulfoxide for two consecutive weeks. The caspase-3 levels in the hippocampus were assessed by the western blot technique, and also the passive avoidance task was used for memory evaluation. Results: Our findings showed that chlorpyrifos treatment markedly increased caspase-3 levels in the hippocampus and also increased the time spent in the dark chamber 24 h and one week after receiving foot shock in the chlorpyrifos group. Conclusions: Organophosphate pesticides exposure can impair passive avoidance memory, and high levels of caspase-3 in the hippocampus are proposed as a possible reason for neuronal toxicity and memory impairment.