• MastellaMoisés HenriqueMHGraduate Program of Pharmacology, Federal University of Santa Maria, Santa Maria, Brazil; Biogenomics Lab, Health Sciences Center, Federal University of Santa Maria, Santa Maria, Brazil., Isabel Roggia, TurraBárbara OsmarinBOGraduate Program of Pharmacology, Federal University of Santa Maria, Santa Maria, Brazil; Biogenomics Lab, Health Sciences Center, Federal University of Santa Maria, Santa Maria, Brazil., TeixeiraCibele FerreiraCFGraduate Program of Pharmacology, Federal University of Santa Maria, Santa Maria, Brazil; Biogenomics Lab, Health Sciences Center, Federal University of Santa Maria, Santa Maria, Brazil., AssmannCharles EliasCEBiogenomics Lab, Health Sciences Center, Federal University of Santa Maria, Santa Maria, Brazil; Graduate Program of Toxicological Biochemistry, Federal University of Santa Maria, Santa Maria, Brazil., Luciano Morais-Pinto, Taís Vidal, Cinthia Melazzo, JungIvo Emílio da CruzIEDCBiogenomics Lab, Health Sciences Center, Federal University of Santa Maria, Santa Maria, Brazil., Fernanda Barbisan, and da CruzIvana Beatrice MânicaIBMGraduate Program of Pharmacology, Federal University of Santa Maria, Santa Maria, Brazil; Biogenomics Lab, Health Sciences Center, Federal University of Santa Maria, Santa Maria, Brazil; Graduate Program of Gerontology, Fede.
• Graduate Program of Pharmacology, Federal University of Santa Maria, Santa Maria, Brazil; Biogenomics Lab, Health Sciences Center, Federal University of Santa Maria, Santa Maria, Brazil.
• Neuroscience. 2022 Oct 15; 502: 25-40.

BackgroundSome studies have suggested that mitochondrial dysfunction and a superoxide imbalance could increase susceptibility to chronic stressful events, contributing to the establishment of chronic inflammation and the development of mood disorders. The mitochondrial superoxide imbalance induced by some molecules, such as rotenone, could be evolutionarily conserved, causing behavioral, immune, and neurological alterations in animals with a primitive central nervous system.ObjectiveBehavioral, immune, and histological markers were analyzed in Eisenia fetida earthworms chronically exposed to rotenone for 14 days.MethodsEarthworms were placed in artificial soil containing 30 nM of rotenone distributed into a plastic cup that allowed the earthworms to leave and return freely into the ground. Since these organisms prefer to be buried, the model predicted that the earthworms would necessarily have to return to the rotenone-contaminated medium, creating a stressful condition. The effect on survival behavior in the immune and histological body wall and ventral nervous ganglia (VNG) structures, as well as gene expression related to inflammation and mitochondrial and neuromuscular changes.ResultsRotenone-induced loss of earthworm escape behavior and immune alterations indicated a chronic inflammatory state. Some histological changes in the body wall and VNG indicated a possible earthworm reaction aimed at protecting against rotenone. Overexpression of the nicotinic acetylcholine receptor gene (nAChR α5) in neural tissues could also help earthworms reduce the degenerative effects of rotenone on dopaminergic neurons.ConclusionThese data suggest that mitochondrial dysfunction could be an evolutionarily conserved element that induces inflammatory and behavioral changes related to chronic stress.Copyright © 2022 IBRO. Published by Elsevier Ltd. All rights reserved.

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