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PubMed2005

Systemic exposure to paraquat and maneb models early Parkinson's disease in young adult rats.

In recent years, several lines of evidence have shown an increase in Parkinson's disease (PD) prevalence in rural environments where pesticides are widely used. Paraquat (PQ--herbicide) and maneb (MB--fungicide) are among the compounds suspected to induce neuronal degeneration and motor deficits characteristics of PD. Here, we investigated the effects of PQ and MB on dopaminergic (DA) neuron-glia cultures and in vivo in young adult rats. In vitro, PQ led to a loss of DA as compared to non-DA neurons and microglial activation in a dose-dependent manner. Addition of MB had no further effect nor did it lead to microglial activation when used alone. In vivo, 2-month old young adult rats were subjected to intraperitoneal injections of vehicle (n = 4), PQ alone (n = 8), or PQ in combination with MB (n = 8) twice a week for 4 weeks and were sacrificed the day following the last injection. Significant loss of nigral DA neurons was observed in both treatment groups, but a significant decrease in striatal DA fibers was not found. Microglial activation was seen in the nigra of rats subjected to PQ with or without MB. Behavioral analyses demonstrated a mixed pattern of motor impairments, which may have been related to early effects of nigral DA neuronal loss or systemic effects associated with MB exposure in addition to PQ. These results indicate that exposure to PQ with or without MB induces neurodegeneration which might occur via an early inflammatory response in young adult animals.

Age of Onset↗

PubMed2005

Modulation of antioxidant defense systems by the environmental pesticide maneb in dopaminergic cells.

A lack of evidence supporting a role of heritability in the development of idiopathic Parkinson's disease (PD) has implicated exposures to environmental contaminants in the disease etiology. Epidemiological and clinical studies, as well as animal models of the PD phenotype, have consistently linked agrichemical exposure with dopaminergic (DAergic) damage, particularly through oxidative stress mechanisms. Maneb (MB) is a dithiocarbamate (DTC) fungicide that has specifically been implicated to have adverse effects on dopamine (DA) systems, but the role MB plays in modulating the oxidative state of DAergic cells has not previously been described. Since glutathione (GSH) is a major cellular antioxidant, it was hypothesized that exposure to MB would disrupt this system. The current study primarily utilized the PC12 cell line, which displays a catecholaminergic phenotype. Low concentrations of MB (50-1000 ng/ml) had little effect on cell viability, as measured by LDH release. These same concentrations, however, led to increases in GSH and its oxidized form, GSSG. Effects on viability and GSH were correlated to a primary mesencephalic culture system. Furthermore, these effects were markedly different from those observed with the classical oxidative stressor and pesticide, paraquat (PQ). To determine how MB would affect cells in which antioxidant systems were compromised, PC12 cells were treated with L-buthionine-(S,R)-sulfoximine (BSO) to deplete cellular GSH, followed by treatment with MB. Results suggest that following an insult to the GSH antioxidant system, MB can act as an additional insult to the system and prevent the normal recovery of those defenses. Altered protein levels of heme oxygenase-1 (HO-1) further indicated an oxidative stress response elicited by MB in PC12 cells. DAergic neurons, as a population, are inherently vulnerable to oxidative stress, and the disruption of antioxidant systems by the fungicide MB may contribute to the neurodegeneration of these cells, especially with concurrent exposures to other environmentally relevant oxidative stressors, such as PQ.

Actins↗

PubMed2006

Acute neurotoxic effects of mancozeb and maneb in mesencephalic neuronal cultures are associated with mitochondrial dysfunction.

Recent studies suggest that exposure to agrochemicals may contribute to the development of idiopathic Parkinson's disease. Maneb (MB), a widely used Mn-containing ethylene-bis-dithiocarbamate (EBDC) fungicide, has been implicated in selective dopaminergic neurotoxicity. In this study, we examine the potential neurotoxicity of mancozeb (MZ), a widely used EBDC fungicide that is structurally similar to MB, but contains both Zn and Mn. Primary mesencephalic cells isolated from Sprague-Dawley embryonic day 15 rat embryos were exposed in vitro to either MZ or MB to compare their cytotoxic potential. Exposure to 10-120 microM MZ or MB for 24h resulted in a dose-dependent toxicity in both the dopamine (DA) and GABA mesencephalic populations as assessed by a functional assay for high affinity transporter activity. Consistent with this, cell viability as well as tyrosine hydroxylase-positive neurons decreased with increasing doses of MZ or MB. Toxic potencies for MZ and MB were similar and no difference in sensitivity between the DA and GABA populations was observed with the fungicides. Exposure to ethylene thiourea, the major metabolite of either MZ or MB, was not toxic, implicating the parent compound in toxicity. Both the organic and Mn metal components of the fungicides were found to contribute to toxicity. Non-toxic exposures to the fungicides decreased ATP levels in a dose-dependent manner suggesting impairment of energy metabolism. In whole mitochondrial preparations isolated from adult rat brains, MZ and MB inhibited NADH-linked state 3 respiration. Mild to moderate mitochondrial uncoupling was also observed in response to the fungicides. In conclusion, our findings indicate that acute exposure to high doses of MZ and MB produce equipotent toxic effects in both DA and GABA neurons that may be associated with perturbations in mitochondrial respiration.

Adenosine Triphosphate↗

PubMed2005

Neuroprotective effects of Polygonum multiflorum on nigrostriatal dopaminergic degeneration induced by paraquat and maneb in mice.

The neuroprotective effects of Polygonum multiflorum extract (PME) and its two fractions, ethanol-soluble PME (PME-I) and -insoluble PME (PME-II), on the degeneration of nigrostriatal dopaminergic neurons induced by a combination of paraquat and maneb (PQMB) were investigated in male C57BL/6 mice. The mice were treated twice a week for 6 weeks with intraperitoneal injections of PQMB. This combination caused a reduction of spontaneous locomotor activity, motor incoordination, and declines of dopamine level in the striatum and tyrosine hydroxylase-positive neurons in the substantia nigra. Administration of PME and PME-I once daily for 47 days during 6 weeks of PQMB treatment and last 8 days after PQMB significantly attenuated the impairment of behavioral performance and the decrease in striatal dopamine level and substantia nigral tyrosine hydroxylase-positive neurons in the PQMB-treated animals, whereas the administration of PME-II had no effect on these behavioral, neurochemical and histological indices. The present findings suggest that PME has a beneficial influence on parkinsonism induced by PQMB and that the effects of PME are attributable to some substance(s) included in the ethanol-soluble fraction of PME (PME-I).

3,4-Dihydroxyphenylacetic Acid↗

PubMed2002

Developmental exposure to the pesticides paraquat and maneb and the Parkinson's disease phenotype.

Idiopathic Parkinson's disease (PD) is associated with advanced age, but it is still unclear whether dopaminergic neuronal death results from events initiated during development, adulthood, or represents a cumulative effect across the span of life. This study hypothesized that paraquat (PQ) and maneb (MB) exposure during critical periods of development could permanently change the nigrostriatal dopamine (DA) system and enhance its vulnerability to subsequent neurotoxicant challenges. C57BL/6 mice were treated daily with saline, 0.3 mg/kg PQ, 1 mg/kg MB or PQ + MB from post-natal (PN) days 5 to 19. At 6 weeks, a 20% decrease in activity was evident only in the PQ + MB group, with a further decline (40%) observed at 6 months. A subset of mice were re-challenged as adults with saline, 10 mg/kg PQ, 30 mg/kg MB, or PQ + MB 2 x a week for 3 weeks. Mice exposed developmentally to PQ + MB and rechallenged as adults were the most affected, showing a 70% reduction in motor activity 2 weeks following the last rechallenge dose. Striatal DA levels were reduced by 37% following developmental exposure to PQ + MB only, butfollowing adult re-challenge levels were reduced by 62%. A similar pattern of nigral dopaminergic cell loss was observed, with the PQ + MB treated group exhibiting the greatest reduction, with this loss being amplified by adult re-challenge. Developmental exposure to PQ or MB alone produced minimal changes. However, following adult re-challenge, significant decreases in DA and nigral cell counts were observed, suggesting that exposure to either neurotoxicant alone produced a state of silent toxicity that was unmasked following adult re-exposure. Taken together, these findings indicate that exposure to pesticides during the PN period can produce permanent and progressive lesions of the nigrostriatal DA system, and enhanced adult susceptibility to these pesticides, suggesting that developmental exposure to neurotoxicants may be involved in the induction of neurodegenerative disorders and/or alter the normal aging process.

Aging↗

PubMed1975

[Changes in the gonads and reproductive capacity of white rats after oral maneb poisoning].

Changes in the gonads and reproduction capacity of white rats following oral intoxication with maneb are studied. The preparation at doses 1/10, 1/50, 1/100 and 1/5000 LD50 is administered to the starting generation of white rats twice weekly. Changes in the gonads--biochemical, histological, histoenzymatic and electron microscopic--are established, as well as a capacity for reproduction of the starting I and II offspring. The results show a clearcut gonadotropic effect of the preparation, manifested by morphological changes in the starting generation, and by changes in fertility, gestation, survival and lactation of the starting I and II offspring.

Administration, Oral↗

PubMedDate not supplied

Gas chromatographic determination of lindane (gamma isomer of BHC) in maneb-lindane liquid pesticide formulations.

Lindane from liquid insecticide-fungicide formulations containing lindane with maneb can be determined by gas chromatography using 3% OV-1 or 5% SE-30 columns. Lindane is extracted with acetone, and an aliquot is diluted to volume with anhydrous methanol and injected on-column. The internal standard, diethyl phthalate, has a retention time of 6 min and lindane has a retention time of 12 min, allowing injection every 15 min. Within-laboratory analysis of 3 typical formulations indicates good precision with coefficients of variation ranging from 0.45 to 1.58%. The method can be easily adapted to other liquid or dust formulations of lindane.

Chromatography, Gas↗

PubMedDate not supplied

Acute renal failure and nephrotic syndrome after maneb exposure. A new case with light and electron microscopic study.

A new case of nephrotoxic effect of Maneb is related. The patient used this product as fungicide and developed a progressive illness with acute renal failure. The study by light and electron microscopy revealed severe tubular lesions that disappeared some months later with tubular cell regeneration. However, in spite of the renal function returning to normal, a steroid-dependent nephrotic syndrome persisted with glomerular minimal change like lesions.

Acute Kidney Injury↗

PubMedDate not supplied

Simple method for distinguishing maneb, zineb, mancozeb, and selected mixtures.

Maneb, zineb, mancozeb, and arbitrarily selected mixtures of those can be differentiated by a simple method. Compounds are differentiated on the basis of colors produced after treatment of saturated solutions of the fungicides in n-propanol-acetone mixture (1 + 1 v/v), first with dithizone and then with monosodium dihydrogen phosphate solution in the same solvent. The color depends on the type and concentration of metal present in the sample.

Colorimetry↗

PubMed1972