Pyrethroid pesticide-induced alterations in dopamine transporter function

Elwan, Mohamed A.; Richardson, Jason R.; Guillot, Thomas S.; Caudle, W. Michael; Miller, Gary W.

doi:10.1016/j.taap.2005.06.003

Cited by 104 publications

(65 citation statements)

References 51 publications

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“…However, the effect of long-term exposure to low-level PYRs on human health has been little characterized. A number of epidemiological studies have suggested the relationship between Parkinson's disease (PD) and environmental exposure to pesticides (Tanner and Langston, 1990;Gorell et al, 1998;Priyadarshi et al, 2001); a recent experimental study corroborated the possible underlying mechanism that in vivo exposure to PYRs, deltamethrin and permethrin, increases dopamine transporter and transporter-mediated dopamine uptake in the striatal synaptosome (Elwan et al, 2006). Also revealed by a recent study was the estrogenicity of PYR metabolites (McCarthy et al, 2006).…”

Section: Introductionmentioning

confidence: 94%

Urinary excretion of 3-phenoxybenzoic acid in middle-aged and elderly general population of Japan

Ueyama¹,

Kimata²,

Kamijima³

et al. 2009

Environmental Research

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Limited data are available on the background levels of exposure to synthetic pyrethroid (PYR) in Japan despite their frequent application for agriculture and indoor extermination and possible effects of chronic and/or low-dose PYR exposure on human health. This study was conducted to describe the level and distribution of one of the major PYR metabolites, 3-phenoxybenzoic acid (3-PBA), in urine samples collected from a general population in Japan. The subjects were 535 individuals (184 men and 351 women; 61.5 ± 9.8 years of age, mean ± S.D.) residing in a town in Hokkaido, a dairy and agricultural area. Urinary 3-PBA was found detectable in 98% of samples above the limit of detection of 0.02 μg/L. The geometric mean values of urinary 3-PBA in occupationally exposed farmers (n = 87) and the remaining general group without occupational exposure (n = 448) were 0.38 μg/L and 0.29 μg/L, respectively, ranging from < LOD to 17.09 μg/L. No significant differences in urinary 3-PBA concentrations were shown between these two groups. Moreover, 3-PBA concentrations were found comparable to those reported in some countries. The present study is, to our knowledge, the first report of a biological monitoring study of urinary 3-PBA, which elucidated the background environmental exposure level of PYR in the Japanese general population without occupational exposure. Further nationwide studies covering different seasons and age distribution are needed to monitor the urinary 3-PBA levels in Japan.

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Section: Introductionmentioning

confidence: 94%

Urinary excretion of 3-phenoxybenzoic acid in middle-aged and elderly general population of Japan

Ueyama¹,

Kimata²,

Kamijima³

et al. 2009

Environmental Research

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“…Pyrethroid intoxication has long been known to cause neurological symptoms including salivation, tremor, choreoathetosis or coma, depending on the specific exposure. Several studies have reported the ability of pyrethroids, such as permethrin and deltamethrin, to increase DAT-mediated 3 H-dopamine uptake or cause neurotransmitter release [70,71]. Given the importance of DAT function to the dopamine neuron [72], this is an area of research that deserves more attention.…”

Section: Pyrethrins/pyrethroidsmentioning

confidence: 99%

Parkinson's disease and pesticides: a toxicological perspective

Hatcher

Pennell

Miller

2008

Trends in Pharmacological Sciences

295

176

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Environmental factors have been shown to contribute to the incidence of Parkinson's disease (PD). Pesticides, which represent one of the primary classes of environmental agents associated with PD, share the common feature of being intentionally released into the environment to control or eliminate pests. Pesticides consist of multiple classes and subclasses of insecticides, herbicides, rodenticides, fungicides, fumigants and others and exhibit a vast array of chemically diverse structures. In this review we examine the evidence regarding the ability of each of the major pesticide subclasses to increase the incidence of PD. We propose that, from a toxicological perspective, it would be beneficial to identify specific subclasses, common structural features and the propensity for widespread human exposure when considering the potential role in PD, rather than using the overly broad term of 'pesticides' to describe this diverse group of chemicals. Furthermore, these chemicals and their environmentally relevant combinations should be evaluated for their ability to promote or accelerate PD and not merely for being singular causative agents.

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“…Uptake rates were calculated as specific uptake (total uptake minus non-specific uptake), with non-specific uptake defined by the inclusion of 10 μM nomifensine. Following determination of synaptosomal protein concentration (Bradford, 1976), uptake rates were calculated as pmol/ mg/min protein and expressed as percentage of control values.Determination of 3 H-WIN 35,428 binding to DAT was performed as previously described (Elwan et al, 2006). Binding studies were conducted with crude synaptosomes and a single concentration (10nM) of 3 H-WIN 35,428 in 25 mM sodium phosphate buffer (125 mM NaCl, 5 mM KCl; pH 7.4) for one hour at 4°C in 96-well plates.…”

mentioning

confidence: 99%

Dieldrin exposure induces oxidative damage in the mouse nigrostriatal dopamine system

Hatcher

Richardson

Guillot

et al. 2007

Experimental Neurology

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135

107

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Numerous epidemiological studies have shown an association between pesticide exposure and an increased risk of developing Parkinson's disease (PD). Here, we provide evidence that the insecticide dieldrin causes specific oxidative damage in the nigrostriatal dopamine (DA) system. We report that exposure of mice to low levels of dieldrin for 30 days resulted in alterations in dopamine-handling as evidenced by a decrease in dopamine metabolites, DOPAC (31.7% decrease) and HVA (29.2% decrease) and significantly increased cysteinyl-catechol levels in the striatum. Furthermore, dieldrin resulted in a 53% decrease in total glutathione, an increase in the redox potential of glutathione, and a 90% increase in protein carbonyls. α-Synuclein protein expression was also significantly increased in the striatum (25% increase). Finally, dieldrin caused a significant decrease in striatal expression of the dopamine transporter as measured by 3 H-WIN 35,428 binding and 3 H-dopamine uptake. These alterations occurred in the absence of dopamine neuron loss in the substantia nigra pars compacta. These effects represent the ability of low doses of dieldrin to increase the vulnerability of nigrostriatal dopamine neurons by inducing oxidative stress and suggest that pesticide exposure may act as a promoter of PD. *Corresponding Author: Gary W. Miller, Ph.D., Emory University -Center for Neurodegenerative Disease, Whitehead Biomedical Research Building 505K, 615 Michael Street Atlanta, GA 30322, Phone: 404.712.8582, Fax: 404.727.3728, Email: gary.miller@emory.edu Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Parkinson's disease (PD) is a chronic, progressive neurological disorder clinically characterized by resting tremor, bradykinesia, postural instability and rigidity (Marsden, 1984). Pathologically, PD presents as dopaminergic neuronal loss in the substantia nigra pars compacta (SNc), striatal depletion of the neurotransmitter dopamine (DA), the loss of neurochemical markers, such as the dopamine transporter (DAT), and the presence of Lewy bodies containing α-synuclein (Spillantini et al., 1997). Because only 5-10% of PD cases are thought to be primarily genetic in origin, investigation of the role of environmental factors in the pathogenesis of the disease is warranted (Dauer & Przedborski, 2003). NIH Public AccessNumerous epidemiological studies have shown an association between pesticide exposure and an increased risk of developing PD Le Couteur et al., 1999;Priyadarshi et al., 2000;Semchuk et al., 1991Semchuk et al., ,1992. In addition, a correlation between the presence of th...

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Pyrethroid pesticide-induced alterations in dopamine transporter function

Cited by 104 publications

References 51 publications

Urinary excretion of 3-phenoxybenzoic acid in middle-aged and elderly general population of Japan

Urinary excretion of 3-phenoxybenzoic acid in middle-aged and elderly general population of Japan

Parkinson's disease and pesticides: a toxicological perspective

Dieldrin exposure induces oxidative damage in the mouse nigrostriatal dopamine system

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