Effects of 2,4-dichlorophenoxyacetic acid (2,4-D) on open-field behaviour and neurochemical parameters of rats

Oliveira, Georgino Honorato de; Palermo-Neto, João

doi:10.1016/0378-4274(94)90367-0

Cited by 4 publications

(8 citation statements)

References 14 publications

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“…Previous studies in animals have suggested that the central nervous system (CNS) is one of the principal targets of 2,4-D toxicity (Drill and Hiratzka, 1953;Bage et aL, 1973;Duffard et al, 1987;Oliveira and Neto, 1993;Evangelista de Duffard et al, 1995;Bortolozzi et al, 1998;Rosso et al, 1997). For example, neonatal rats exposed to 2,4-D showed a delay in CNS development with concomitant biochemical and neurobehavioral alterations (Rosso et al, 1997;.…”

Section: Discussion O R G a N O C H L O R I N E P E S T I C mentioning

confidence: 95%

Acute exposure to organochlorine pesticides does not affect striatal dopamine in mice

2001

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The purpose of this study was to evaluate the possible association between the risk of developing Parkinson's disease (PD) and exposure to organochlorine pesticides in the mouse model. Animals were treated with a single subcutaneous injection of either dieldrin (40 and 80 mg/kg) or 2,4-dichlorophenoxyacetic acid (100 and 200 mg/kg, 2,4-D) and levels of dopamine (DA) and DA metabolites were measured in the striatum at the 7-day time point. Dieldrin exposure did not affect the striatal concentrations of DA, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA). Administration of 2,4-D did not produce any changes with the exception of a slight (15%), but statistically significant decrease in DOPAC using the higher dose of the pesticide. No neurochemical signs of dopaminergic injury were found following the combined treatment with either dieldrin or 2,4-D plus diethyldithiocarbamate (DDC), a compound known to potentiate the effects of the dopaminergic toxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Furthermore, neither dieldrin nor 2,4-D caused additional damage in animals previously lesioned with MPTP. Data failed to support the hypothesis that acute exposure to organochlorine compounds or synergistic interactions involving these pesticides may cause significant damage to dopaminergic terminals and therefore contribute to nigrostriatal degeneration in PD.

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Section: Discussion O R G a N O C H L O R I N E P E S T I C mentioning

confidence: 95%

Acute exposure to organochlorine pesticides does not affect striatal dopamine in mice

2001

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“…Using tests of neurobehavioral parameters (such as the Functional Observational Battery), decreased activity levels, behavioral changes, and motor skill abnormalities have been reported in rats at doses greater than 60 mg/kg body weight/day and in rabbits at doses of approximately 30 mg/kg body weight/day de Duffard et al, 1990b;Duffard et al, 1995;Hoberman, 1990;Jeffries et al, 1994;Liberacki et al, 1991;Martin, 1991;Mattsson et al, 1994Mattsson et al, , 1997Oliveira and Palermo-Neto, 1993;Rodwell, 1991;Schulze and Dougherty, 1988;Zablotny et al, 1991). In acute studies conducted using beagle dogs, clinical signs of central nervous system depression and/or abnormalities in electroencephalograms were only reported at doses of 175 mg/kg or greater .…”

Section: Neurotoxicitymentioning

confidence: 93%

“…Rats exposed to high doses of 2,4-D n-butyl ester were reported to display alterations in neurotransmitter concentrations in the brain (de Duffard et al, 1990a;Elo and MacDonald, 1989;Oliveira and Palermo-Neto, 1993). These neurochemical alterations have been hypothesized to result from compromise of the blood-brain barrier by high doses of 2,4-D (Elo et al, 1988;Tyynela et al, 1986).…”

Section: Neurotoxicitymentioning

confidence: 96%

“…Several investigators have reported accumulation of 2,4-D in the brain or cerebrospinal fluid, following administration of high doses (40 to 300 mg/kg body weight) of 2,4-D Ylitalo, 1977, 1979;Kim et al, 1988;Oliveira and Palermo-Neto, 1993;Tyynela et al, 1990). Kim et al (1988) suggested that the increased accumulation of 2,4-D in the brain at high doses was likely not the result of increased permeability of the blood-brain barrier since the entry of the organic solute, 2-deoxyglucose, into rabbit brain was unaffected by 2,4-D pretreatment.…”

Section: Neurotoxicitymentioning

confidence: 99%

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Phenoxy Herbicides (2,4-D)

Kennepohl¹,

Munro

Bus

2010

Hayes' Handbook of Pesticide Toxicology

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“…The current annual US consumption of 2,4-D is approximately 20000 tons (Hileman, 1996), and the extensive use of these compounds is recognized as an environmental and toxicological hazard. Chlorophenoxyacetic acids are teratogenic and mutagenic (Grant, 1979) and cause a variety of adverse neurological symptoms (El0 et al, 1988;Oliveira & Palermo-Neto, 1993). Furthermore, chlorophenoxyacetic acids suppress the immune system, thereby increasing the vulnerability of mammals to infectious diseases and cancers (Hileman, 1996).…”

Section: Introductionmentioning

confidence: 99%

Degradation of chlorophenoxyacetic acids by the lignin-degrading fungus Dichomitus squalens

Reddy¹,

Joshi²,

Gold³

1997

Microbiology

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We have examined the degradation of 14C ring-and side-chain-labelled 2,4,5-trichlorophenoxyacetic acid by Dichomitus squalens and Phanerochaete chrysosporium. The effects of Mn2+ on the degradation of these radiolabelled substrates by D. squalens and the effect of nitrogen limitation on their degradation by P. chrysosporium suggested that in both fungi, side-chain cleavage was catalysed by a mechanism independent of the lignin degradation system, whereas the degradation of the aromatic ring was dependent on the lignin degradative system. Using unlabelled substrates, a pathway for the degradation of chlorophenoxyacetic acids was elucidated in D. squalens. Time courses for the degradation of unlabelled chlorophenoxyacetic acids by D. squalens demonstrated that the corresponding chlorophenol was the initial product formed. The chlorophenol intermediate was xylosylated to form the chlorophenolxyloside. In turn, the chlorophenolxyloside could be hydrolysed by an intracellular p-xylosidase to regenerate the chlorophenol. The chlorophenol product of the xylosidase reaction was oxidatively dechlorinated to form 2-chloro-p-benzoquinone which could undergo subsequent further dechlorination and ring-opening reactions, as has been reported previously for P. chrysosporium.

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Effects of 2,4-dichlorophenoxyacetic acid (2,4-D) on open-field behaviour and neurochemical parameters of rats

Cited by 4 publications

References 14 publications

Acute exposure to organochlorine pesticides does not affect striatal dopamine in mice

Acute exposure to organochlorine pesticides does not affect striatal dopamine in mice

Phenoxy Herbicides (2,4-D)

Degradation of chlorophenoxyacetic acids by the lignin-degrading fungus Dichomitus squalens

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