Behavioral effects of subchronic inorganic manganese exposure in rats

Vezér, Tünde; Kurunczi, Anita; Náray, Miklós; Papp, András; Nagymajtényi, László

doi:10.1002/ajim.20485

Cited by 54 publications

(63 citation statements)

References 39 publications

(50 reference statements)

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“…For example, chronic exposure to Mn can lead to increased susceptibility toward developing pulmonary infections including pneumonia and bronchitis (Baader 1932;Davies and Harding 1949;Rodier 1955;Maigetter et al 1976;Bencko and Cikrt 1984;Roels et al 1987;Saric 1992;Saric and Piasek 2000;Jafari and Assari 2004;Bowler et al 2007;Antonini et al 2009). Similarly, hearing deficits have also been reported in occupations in which individuals are exposed to chronic high levels of Mn (Nikolov 1974;Khalkova and Kostadinova 1986;Korczynski 2000;Josephs et al 2005;Park et al 2006;Da Silva et al 2007;Vezér et al 2007;Bouchard et al 2008). Although Mn readily accumulates in both the lung and inner ear (Kalliomäki et al 1983;Park et al 2007;Ma et al 2008), few studies have actually attempted to characterize the specific biochemical and molecular mechanisms leading to malfunction in these organs.…”

Section: Introductionmentioning

confidence: 91%

Are There Common Biochemical and Molecular Mechanisms Controlling Manganism and Parkisonism

Roth

2009

Neuromol Med

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Over the past several decades there has been considerable progress in our basic knowledge as to the mechanisms and factors regulating Mn toxicity. The disorder known as manganism is associated with the preferential accumulation of Mn in the globus pallidus of the basal ganglia which is generally considered to be the major and initial site of injury. Because the area of the CNS comprising the basal ganglia is very complex and dependent on the precise function and balance of several neurotransmitters, it is not surprising that symptoms of manganism often overlap with that of Parkinson's disease. The fact that neurological symptoms and onset of Mn toxicity are quite broad and can vary unpredictably probably reflects specific genetic variance of the physiological and biochemical makeup within the basal ganglia in any individual. Differences in response to Mn overexposure are, thus, likely due to underlying genetic variability which ultimately presents in deviations in both susceptibility as well as the characteristics of the neurological lesions and symptoms expressed. Although chronic exposure to Mn is not the initial causative agent provoking Parkinsonism, there is evidence suggesting that persistent exposure can predispose an individual to acquire dystonic movements associated with Parkinson's disease. As noted in this review, there appears to be common threads between the two disorders, as mutations in the genes, parkin and ATP13A2, associated with early onset of Parkinsonism, may also predispose an individual to develop Mn toxicity. Mutations in both genes appear to effect transport of Mn into the cell. These genetic difference coupled with additional environmental or nutritional factors must also be considered as contributing to the severity and onset of manganism.

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Section: Introductionmentioning

confidence: 91%

Are There Common Biochemical and Molecular Mechanisms Controlling Manganism and Parkisonism

Roth

2009

Neuromol Med

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“…Thus, Mn exposure in young adult rats leads to a reduced behavioral response to amphetamines (Vezer et al, 2007). Interestingly, Mn-exposed rats show opposite locomotor responsiveness when challenged with different doses of cocaine (Reichel et al, 2006).…”

Section: Environmental Neurotoxicants and Drug Abusementioning

confidence: 99%

Interaction Between Exposure to Neurotoxicants and Drug Abuse

Carvajal¹,

Sanchez-Amate²,

Lerma-Cabrera³

et al. 2012

Environmental Health - Emerging Issues and Practice

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“…Rearing was recorded if beams at floor level and higher level were interrupted simultaneously. in earlier works of us [37] this method was found sensitive to metal-induced changes of motor activity.…”

Section: Open Field Behavioral Investigationmentioning

confidence: 99%

Rutin, a flavonoid phytochemical, ameliorates certain behavioral and electrophysiological alterations and general toxicity of oral arsenic in rats

Sárközi¹,

Papp²,

Máté³

et al. 2015

Acta Biologica Hungarica

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department of public health, university of szeged faculty of medicine, dóm tér 10, h-6720 szeged, hungary (Received: may 5, 2014; accepted: June 23, 2014) arsenic affects large populations and attacks, among others, the nervous system. Waterborne or occupational exposure causes electrophysiological alterations and motor disturbances in humans, and analogous effects were found in animals. certain phytochemicals may be protective against as-caused damages.In the present study it was investigated whether the flavonoid rutin, applied via the drinking water (2 g/L), ameliorates the effects of arsenic given by gavage (10 mg/kg b.w., in form of NaAsO 2 ) on open field motility, evoked cortical and peripheral electrophysiological activity, and body weight gain in adult male Wistar rats. Body weight gain was significantly reduced from the 4 th week of the 6 weeks arsenic treatment and this effect was largely abolished by rutin in the combination treatment group. Rats treated by arsenic alone showed decreased open field motility; latency of the cortical evoked potentials increased and peripheral nerve conduction velocity decreased. these functional alterations were also counteracted by co-administration of rutin, and both the antioxidant and the chelating activity of rutin might have contributed to the ameliorative effect. these results are apparently novel and support the potential role of natural agents in preserving human health in a contaminated environment.

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Behavioral effects of subchronic inorganic manganese exposure in rats

Abstract: Using complex methodology, new data were obtained regarding the relationship between the long-term effects of MnCl(2) at neuronal and behavioral level.

Cited by 54 publications

References 39 publications

Are There Common Biochemical and Molecular Mechanisms Controlling Manganism and Parkisonism

Are There Common Biochemical and Molecular Mechanisms Controlling Manganism and Parkisonism

Interaction Between Exposure to Neurotoxicants and Drug Abuse

Rutin, a flavonoid phytochemical, ameliorates certain behavioral and electrophysiological alterations and general toxicity of oral arsenic in rats

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