Early life permethrin exposure induces long-term brain changes in Nurr1, NF-kB and Nrf-2

Carloni, Manuel; Nasuti, Cinzia; Fedeli, Donatella; Montani, Maura; Vadhana, M.S. Dhivya; Amici, Augusto; Gabbianelli, Rosita

doi:10.1016/j.brainres.2013.03.048

Cited by 46 publications

(45 citation statements)

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“…Similarly, postnatal exposure increases blood-brain barrier permeability (Sinha and others 2004), causes oxidative stress (Gupta and others 1999b; Nasuti and others 2007; Sinha and others 2006) and impairs the cholinergic muscarinic, dopaminergic and noradrenergic systems (Ahlbom and others 1994; Carloni and others 2012; Carloni and others 2013; Eriksson and Nordberg 1990; Nasuti and others 2013; Nasuti and others 2007). However, several other effects were also identified.…”

Section: Pyrethroids (Pis)mentioning

confidence: 99%

“…These include unbalance between pro- and anti-inflammatory responses and impairment of the serotonergic system, decreased nitric oxide, glutamate and calcium in several brain regions even several months after the end of exposure (Carloni and others 2012; Carloni and others 2013; Nasuti and others 2013). As for behavioral effects, both locomotor activity and rearing are increased in response to early postnatal exposure (Ahlbom and others 1994; Nasuti and others 2007; Talts and others 1998), whereas spatial working memory (Carloni and others 2012; Carloni and others 2013; Nasuti and others 2013), and conditioned avoidance responses are decreased (Sinha and others 2006). Behavioral effects are identified even long after the end of exposure, in adult and aged rats, which suggests that early life exposure to type I PIs interferes with brain-aging processes.…”

Section: Pyrethroids (Pis)mentioning

confidence: 99%

“…In this regard, in addition to the decreased glutamate and calcium levels identified after postnatal exposures (Carloni and others 2012; Carloni and others 2013), in cultures of neonatal hippocampal neurons, the activity of glutamatergic neuronal networks and the spontaneous release of glutamate in synapses are decreased (Meyer and others 2008) and, recently, a NMDA receptor-mediated mechanism was suggested to play a role in PIs neurotoxic actions during development. Cao and collaborators (Cao and others 2014) demonstrated that, in primary cultures of neonatal cortical neurons, bifenthrin, at concentrations well below those that delay sodium channel inactivation and affect sodium current, alters spontaneous synchronized calcium oscillations that are essential for normal neuronal development (Dolmetsch and others 1998; Wayman and others 2006) and increases phosphorylated CREB and activity-dependent dendritic growth.…”

Section: Pyrethroids (Pis)mentioning

confidence: 99%

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Developmental neurotoxicity of succeeding generations of insecticides

Abreu‐Villaça

Levin

2017

Environment International

136

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Insecticides are by design toxic. They must be toxic to effectively kill target species of insects. Unfortunately, they also have off-target toxic effects that can harm other species, including humans. Developmental neurotoxicity is one of the most prominent off-target toxic risks of insecticides. Over the past seven decades several classes of insecticides have been developed, each with their own mechanisms of effect and toxic side effects. This review covers the developmental neurotoxicity of the succeeding generations of insecticides including organochlorines, organophosphates, pyrethroids, carbamates and neonicotinoids. The goal of new insecticide development is to more effectively kill target species with fewer toxic side effects on non-target species. From the experience with the developmental neurotoxicity caused by the generations of insecticides developed in the past advice is offered how to proceed with future insecticide development to decrease neurotoxic risk.

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Section: Pyrethroids (Pis)mentioning

confidence: 99%

Section: Pyrethroids (Pis)mentioning

confidence: 99%

Section: Pyrethroids (Pis)mentioning

confidence: 99%

See 1 more Smart Citation

Developmental neurotoxicity of succeeding generations of insecticides

Abreu‐Villaça

Levin

2017

Environment International

136

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“…In our previous study, we demonstrated that low-level, chronic permethrin exposure during the prenatal and early postnatal periods in mice has distinct effects on the male reproductive system (Saito, Hara, & Tanemura, 2017). Several previous studies have investigated the influence of permethrin in the developing nervous system (Carloni et al, 2012;Carloni et al, 2013;Imamura, Hasegawa, Kurashina, Matsuno, & Tsuda, 2002;Nasuti et al, 2007). Several previous studies have investigated the influence of permethrin in the developing nervous system (Carloni et al, 2012;Carloni et al, 2013;Imamura, Hasegawa, Kurashina, Matsuno, & Tsuda, 2002;Nasuti et al, 2007).…”

mentioning

confidence: 98%

“…Moreover, we proposed the importance of assessing the effects of low-level, chronic exposure to environmental chemicals in early life. Several previous studies have investigated the influence of permethrin in the developing nervous system (Carloni et al, 2012;Carloni et al, 2013;Imamura, Hasegawa, Kurashina, Matsuno, & Tsuda, 2002;Nasuti et al, 2007). In the developing brain, various neuronal signals must be activated appropriately for the construction of the neural network, and exposure to chemical substances in this period can induce developmental neurotoxicity (Rice & Barone, 2000).…”

mentioning

confidence: 99%

Early‐life exposure to low levels of permethrin exerts impairments in learning and memory with the effects on neuronal and glial population in adult male mice

Saito

Hara

Tominaga

et al. 2019

J of Applied Toxicology

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Permethrin, a pyrethroid chemical, is widely used as a pesticide because of its rapid insecticidal activity. Although permethrin is considered to exert very low toxicity in mammals, the effects of early, low‐level, chronic exposure on the adult central nervous system are unclear. In this study, we investigated the effects of low‐level, chronic permethrin exposure in early life on the brain functions of adult mice, using environmentally relevant concentrations. We exposed mice to the acceptable daily intake level of permethrin (0.3 ppm) in drinking water during the prenatal and postnatal periods. We then examined the effects on the central nervous system in adult male offspring. In the permethrin group, we detected behavior that displayed incomplete adaptation to a novel environment, as well as an impairment in learning and memory. In addition, immunohistochemical analysis revealed an increase in doublecortin‐ (an immature neuron marker) positive cells in the hippocampal dentate gyrus in the permethrin exposure group compared with the control group. Additionally, in the permethrin exposure group there was a decrease in astrocyte number in the hilus of the dentate gyrus, and remaining astrocytes were often irregularly shaped. These results suggest that exposure to permethrin at low levels in early life affects the formation of the neural circuit base and behavior after maturation. Therefore, in the central nervous system of male mice, low‐level, chronic permethrin exposure during the prenatal and postnatal periods has effects that were not expected based on the known effects of permethrin exposure in mature animals.

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Trans‐ovo permethrin exposure affects growth, brain morphology and cardiac development in quail

Curtis

Nogueiro

Schneider

et al. 2021

Environmental Toxicology

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Permethrin is a commonly used, highly effective pesticide in poultry agriculture, and has recently been trialed in conservation efforts to protect Galápagos finch hatchlings from an invasive ectoparasite. Although permethrin is considered safe for adults, pesticides can have health consequences when animals are exposed during early life stages. The few studies that have examined permethrin's effects in embryonic chicks and rats have shown hydrocephaly, anencephaly, reduced cellular energy conversion, and disruption of developing heart muscle. To test whether trans‐ovo exposure of permethrin affects early development in birds, we exposed Japanese quail (Coturnix japonica) eggs to cotton treated with 1% permethrin that was incorporated into nests in two amounts (0.2, 0.8 g), each with a paired untreated cotton control group. When measured on incubation Day 15, we found permethrin‐treated developing birds were smaller and showed signs of microcephaly, although mortality rates were the same. Despite no difference in heart mass, ventricular tissue was less compact, cardiac arteries were reduced and heart rates were slower in permethrin‐treated birds. Differences in heart development were also observed at 5 days of incubation, indicating that abnormalities are present from early in cardiac development. Future studies are needed to examine permethrin's effects on developmental pathways and to determine if these effects persist after hatching to affect offspring health. This study provides evidence that permethrin can cross the eggshell to cause non‐lethal but adverse effects on embryonic development, and studies should look beyond hatching when monitoring the efficacy of permethrin on wild bird populations.

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Early life permethrin exposure induces long-term brain changes in Nurr1, NF-kB and Nrf-2

Cited by 46 publications

References 61 publications

Developmental neurotoxicity of succeeding generations of insecticides

Developmental neurotoxicity of succeeding generations of insecticides

Early‐life exposure to low levels of permethrin exerts impairments in learning and memory with the effects on neuronal and glial population in adult male mice

Trans‐ovo permethrin exposure affects growth, brain morphology and cardiac development in quail

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