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Exposure to Sub-Lethal Doses of Permethrin Is Associated with Neurotoxicity: Changes in Bioenergetics, Redox Markers, Neuroinflammation and Morphology.

ABSTRACT: Permethrin (PERM) is a member of the class I family of synthetic pyrethroids. Human use has shown that it affects different systems, with wide health dysfunctions. Our aim was to determine bioenergetics, neuroinflammation and morphology changes, as redox markers after subacute exposure to PERM in rats. We used MDA determination, protein carbonyl assay, mitochondrial O₂ consumption, expression of pro-inflammatory cytokines and a deep histopathological analysis of the hippocampus. PERM (150 mg/kg and 300 mg/kg body weight/day, o.v.) increased lipoperoxidation and carbonylated proteins in a dose-dependent manner in the brain regions. The activities of antioxidant enzymes glutathione peroxidase, reductase, S-transferase, catalase, and superoxide dismutase showed an increase in all the different brain areas, with dose-dependent effects in the cerebellum. Cytokine profiles (IL-1β, IL-6 and TNF-α) increased in a dose-dependent manner in different brain tissues. Exposure to 150 mg/kg of permethrin induced degenerated and/or dead neurons in the rat hippocampus and induced mitochondrial uncoupling and reduction of oxidative phosphorylation and significantly decreased the respiratory parameters state 3-associated respiration in complex I and II. PERM exposure at low doses induces reactive oxygen species production and imbalance in the enzymatic antioxidant system, increases gene expression of pro-inflammatory interleukins, and could lead to cell damage mediated by mitochondrial functional impairment.

SUBMITTER: Lopez-Aceves TG

PROVIDER: S-EPMC8704605 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Permethrin (PM) is a synthetic pyrethroid insecticide widely used as domestic repellent. Damage effects to nontarget organisms have been reported, particularly in the early stages of development. Studies indicate redox unbalance as secondary PM effect. Therefore, our goal was to investigate the acute PM effects on larval zebrafish. Larvae (6 days postfertilization) were exposed to PM (25-600 ?g/L) during 24 hours, and 50% lethal concentration was estimated. For subsequent assays, the sublethal PM concentrations of 25 and 50 ?g/L were used. PM increased anxiety-like behaviors according to the Novel Tank and Light-Dark tests. At the molecular level, PM induced increased ROS, which may be related to the increased lipid peroxidation, DNA damage, and apoptosis detected in PM-exposed organisms. In parallel, upregulation of the antioxidant system was detected after PM exposure, with increased superoxide dismutase, glutathione S-transferase and glutathione reductase activities, and thiol levels. The increased of Nrf2 target genes and the activation of an electrophile response element-driven reporter Tg(EPRE:LUC-EGFP) suggest that the Nrf2 pathway can mediate a fast response to PM, leading to antioxidant amplification. By using high-resolution respirometry, we found that exposure to PM decreased the oxygen consumption in all respiratory stages, disrupting the oxidative phosphorylation and inhibiting the electron transfer system, leading to decrease in bioenergetics capacity. In addition, PM led to increases of residual oxygen consumption and changes in substrate control ratio. Glucose metabolism seems to be affected by PM, with increased lactate dehydrogenase and decreased citrate synthase activities. Taken together, our results demonstrated the adverse effects of acute sublethal PM concentrations during larval development in zebrafish, causing apparent mitochondrial dysfunction, indicating a potential mechanism to redox unbalance and oxidative stress, which may be linked to the detected cell death and alterations in normal behavior patterns caused by acute PM exposure.

Project description:Permethrin is increasingly used for parasite control in bird nests, including nests of threatened passerines. We present the first formal evaluation of the effects of continued permethrin exposure on the reproductive success and liver function of a passerine, the zebra finch (Taeniopygia guttata), for two generations. We experimentally treated all nest material with a 1% permethrin solution or a water control and provided the material to breeding finches for nest building. The success of two consecutive clutches produced by the parental generation and one clutch produced by first-generation birds were tracked. Finches in the first generation were able to reproduce and fledge offspring after permethrin exposure, ruling out infertility. Permethrin treatment had no statistically significant effect on the number of eggs laid, number of days from clutch initiation to hatching, egg hatch rate, fledgling mass or nestling sex ratio in either generation. However, treating nest material with permethrin significantly increased the number of hatchlings in the first generation and decreased fledgling success in the second generation. Body mass for hatchlings exposed to permethrin was lower than for control hatchlings in both generations, but only statistically significant for the second generation. For both generations, an interaction between permethrin treatment and age significantly affected nestling growth. Permethrin treatment had no effect on liver function for any generation. Permethrin was detected inside 6 of 21 exposed, non-embryonated eggs (28.5% incidence; range: 693-4781 ng of permethrin per gram of dry egg mass). Overall, results from exposing adults, eggs and nestlings across generations to permethrin-treated nest material suggest negative effects on finch breeding success, but not on liver function. For threatened bird conservation, the judicious application of this insecticide to control parasites in nests can result in lower nestling mortality compared to when no treatment is applied. Thus, permethrin treatment benefits may outweigh its sub-lethal effects.

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Exposure to Sub-Lethal Doses of Permethrin Is Associated with Neurotoxicity: Changes in Bioenergetics, Redox Markers, Neuroinflammation and Morphology.

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