{"title":"In-feed antiparasitic veterinary drug emamectin benzoate impairs acetylcholinesterase activity and brain tissue histoarchitecture of Oreochromis niloticus fry","authors":"Thangapalam Jawahar Abraham , Jasmine Singha , Avishek Bardhan , Sutanu Karmakar , Ravindran Rajisha , Satyen Kumar Panda , Prasanna Kumar Patil","doi":"10.1016/j.eas.2024.100042","DOIUrl":null,"url":null,"abstract":"<div><p>Emamectin benzoate (EB) is an antiparasitic veterinary drug in temperate aquaculture to control ectoparasites. Research on its safety, tolerability and toxicity in tropical aquaculture is growing recently. This study examined the neurological and brain histopathological effects and the accumulation of tissue residues in all-male <em>Oreochromis niloticus</em> fry when fed top-coated EB feeds containing doses ranging from 50 to 500 µg/kg biomass/day for 14 days. A dose-dependent increase in mortalities (3.33–13.75 %) and inhibition in acetylcholinesterase activity (43.80–83.52 %) were documented. In the<!--> <!-->50-µg group, the muscle EB-residues peaked at 2.77 ng/g and then dropped after dose<!--> <!-->termination. Yet, traces of residues were demonstrable in the treated groups even after 21 days of cessation of EB feeding. Histologically, dose-dependent alterations like granular layer degeneration, spongiosis, necrotized areas in the stratum album centrale, stratum griserum centrale stratum griseum superficiale, and stratum marginale and stratum opticum degeneration in the brain tissues were documented. The neuron cells were scattered or degenerated and stretched with a shrunken nucleus in the treated groups. The revocable alterations in acetylcholinesterase and brain histoarchitecture upon the termination of dosing indicated that the fry can able to tolerate and mount adaptive responses to overcome the EB toxicity.</p></div>","PeriodicalId":100464,"journal":{"name":"Emerging Animal Species","volume":"10 ","pages":"Article 100042"},"PeriodicalIF":0.0000,"publicationDate":"2024-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2772813724000027/pdfft?md5=5782446c698f877811d525ae5bd0337e&pid=1-s2.0-S2772813724000027-main.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Emerging Animal Species","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S2772813724000027","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Emamectin benzoate (EB) is an antiparasitic veterinary drug in temperate aquaculture to control ectoparasites. Research on its safety, tolerability and toxicity in tropical aquaculture is growing recently. This study examined the neurological and brain histopathological effects and the accumulation of tissue residues in all-male Oreochromis niloticus fry when fed top-coated EB feeds containing doses ranging from 50 to 500 µg/kg biomass/day for 14 days. A dose-dependent increase in mortalities (3.33–13.75 %) and inhibition in acetylcholinesterase activity (43.80–83.52 %) were documented. In the 50-µg group, the muscle EB-residues peaked at 2.77 ng/g and then dropped after dose termination. Yet, traces of residues were demonstrable in the treated groups even after 21 days of cessation of EB feeding. Histologically, dose-dependent alterations like granular layer degeneration, spongiosis, necrotized areas in the stratum album centrale, stratum griserum centrale stratum griseum superficiale, and stratum marginale and stratum opticum degeneration in the brain tissues were documented. The neuron cells were scattered or degenerated and stretched with a shrunken nucleus in the treated groups. The revocable alterations in acetylcholinesterase and brain histoarchitecture upon the termination of dosing indicated that the fry can able to tolerate and mount adaptive responses to overcome the EB toxicity.