The impact of early life permethrin exposure on development of neurodegeneration in adulthood

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

doi:10.1016/j.exger.2011.10.006

Cited by 62 publications

(46 citation statements)

References 55 publications

(61 reference statements)

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“…Studies conducted in our laboratory demonstrated that PERM exposure, at a dose of 34 mg/kg close to the NOAEL (25 mg/kg) during early life, induced, later in the life of rats, a significant neurodegeneration of the striatum (Str) characterized by a decrease of Nurr1 gene and protein expression, and an increased lipid peroxidation (Carloni et al, 2012). Lower DA levels and accelerated DA turnover following early life PERM treatment was also observed (Nasuti et al, 2007).…”

Section: Introductionmentioning

confidence: 92%

Effects of early life permethrin exposure on spatial working memory and on monoamine levels in different brain areas of pre-senescent rats

et al. 2013

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a b s t r a c tPesticide exposure during brain development could represent an important risk factor for the onset of neurodegenerative diseases. Previous studies investigated the effect of permethrin (PERM) administered at 34 mg/kg, a dose close to the no observable adverse effect level (NOAEL) from post natal day (PND) 6 to PND 21 in rats. Despite the PERM dose did not elicited overt signs of toxicity (i.e. normal body weight gain curve), it was able to induce striatal neurodegeneration (dopamine and Nurr1 reduction, and lipid peroxidation increase). The present study was designed to characterize the cognitive deficits in the current animal model. When during late adulthood PERM treated rats were tested for spatial working memory performances in a T-maze-rewarded alternation task they took longer to choose for the correct arm in comparison to age matched controls. No differences between groups were found in anxiety-like state, locomotor activity, feeding behavior and spatial orientation task. Our findings showing a selective effect of PERM treatment on the T-maze task point to an involvement of frontal cortico-striatal circuitry rather than to a role for the hippocampus. The predominant disturbances concern the dopamine (DA) depletion in the striatum and, the serotonin (5-HT) and noradrenaline (NE) unbalance together with a hypometabolic state in the medial prefrontal cortex area. In the hippocampus, an increase of NE and a decrease of DA were observed in PERM treated rats as compared to controls. The concentration of the most representative marker for pyrethroid exposure (3-phenoxybenzoic acid) measured in the urine of rodents 12 h after the last treatment was 41.50 g/L and it was completely eliminated after 96 h.

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Section: Introductionmentioning

confidence: 92%

Effects of early life permethrin exposure on spatial working memory and on monoamine levels in different brain areas of pre-senescent rats

et al. 2013

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“…Another pesticide, paraquat in combination with maneb, has also been shown to be more destructive in animal studies and leads to PD by dysfunction of nigrostriatal dopaminergic system as well as motor response abnormalities [66]. Likewise, permethrin, when administered to rats at age of 6–21 day results in glutamate, NO and calcium imbalance in brain hippocampus [67]. Despite accumulating evidence of the effect of pesticides in pathogenesis of neurodegeneration, very only fewer studies have integrated this aspect of investigation in understanding of brain disorders.…”

Section: Introductionmentioning

confidence: 99%

Role of early life exposure and environment on neurodegeneration: implications on brain disorders

Modgil

Lahiri

Sharma

et al. 2014

Transl Neurodegener

106

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Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Amyotrophic lateral sclerosis (ALS) and retinal degeneration have been studied extensively and varying molecular mechanisms have been proposed for onset of such diseases. Although genetic analysis of these diseases has also been described, yet the mechanisms governing the extent of vulnerability to such diseases remains unresolved. Recent studies have, therefore, focused on the role of environmental exposure in progression of such diseases especially in the context of prenatal and postnatal life, explaining how molecular mechanisms mediate epigenetic changes leading to degenerative diseases. This review summarizes both the animal and human studies describing various environmental stimuli to which an individual or an animal is exposed during in-utero and postnatal period and mechanisms that promote neurodegeneration. The SNPs mediating gene environment interaction are also described. Further, preventive and therapeutic strategies are suggested for effective intervention.

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“…For example, pesticide residues in foods have been associated with an increased risk for the development of neuronal damage [5,15] and obesity [16] according to individual genetic variations and the epigenetic modifications that may be induced and potentially inherited in the unexposed offspring [5,17,18]. In this regard, promoting the consumption of organic foods may be beneficial particularly during the sensitive window of epigenetic plasticity (i.e., early life) to prevent the risk of developing neuronal damage [5,8,14].…”

Section: Doi: 101159/000490751mentioning

confidence: 99%

“…Similarly, a maternal high-fat diet can contribute to proinflammatory cytokine production, and maternal obesity can promote changes in methylation patterns [4]. Finally, exposure to pesticides and metals during pregnancy and/or early life can promote inflammation, neurodevelopmental disorders, and progressive neurodegeneration later in life [7,8].…”

Section: Doi: 101159/000490751mentioning

confidence: 99%

The impact of early life permethrin exposure on development of neurodegeneration in adulthood

Cited by 62 publications

References 55 publications

Effects of early life permethrin exposure on spatial working memory and on monoamine levels in different brain areas of pre-senescent rats

Effects of early life permethrin exposure on spatial working memory and on monoamine levels in different brain areas of pre-senescent rats

Role of early life exposure and environment on neurodegeneration: implications on brain disorders

Modulation of the Epigenome by Nutrition and Xenobiotics during Early Life and across the Life Span: The Key Role of Lifestyle

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