Metal deposition and functional neurotoxicity in rats after 3–6 weeks nasal exposure by two physicochemical forms of manganese

Oszlánczi, Gábor; Vezér, Tünde; Sárközi, Leila; Horváth, Edina; Szabó, Andrea; Horváth, Endre; Papp, András

doi:10.1016/j.etap.2010.04.006

Cited by 16 publications

(9 citation statements)

References 33 publications

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“…As shown in Table 1, a dramatic reduction in the horizontal and vertical exploratory behavior of rats illustrated that the locomotor activity of animals could be effectively diminished by AgNPs treatment. Consistent with the result from the literature on Mn (Oszlanczi et al, 2010), our data suggested that chronic treatment with AgNPs exerted an increase in the resting time as well as a decrease in the moving distance and moving velocity, revealing the depletion of horizontal activity in the rats. The difference of the rearing frequency between AgNPs-treated rats and the controls demonstrated that AgNPs exerted an inhibitory effect on the vertical exploratory behavior of animals, which was in line with preceding reports on the rats with sedation treatment (Sorensen et al, 2004).…”

Section: Discussionsupporting

confidence: 81%

Silver nanoparticle exposure induces rat motor dysfunction through decrease in expression of calcium channel protein in cerebellum

et al. 2015

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Silver nanoparticles cause cerebellar ataxia-like symptom in rats. Silver nanoparticles induce rat motor dysfunction. Silver nanoparticles decrease calcium channel protein expression in rat cerebellum. Silver nanoparticles (AgNPs) are currently used widely, however, their impact on central nervous system still remains ambiguous and needs to be elucidated. This study is performed to investigate the neurotoxicity of AgNPs and illustrate the potential molecular mechanism. Neonatal Sprague-Dawley (SD) rats are exposed to AgNPs by intranasal instillation for 14 weeks. It is demonstrated that AgNPs exposure causes cerebellar ataxia like symptom in rats, evidenced by dysfunction of motor coordination and impairment of locomotor activity. Observation of cerebellum section reveals that AgNPs can provoke destruction of cerebellum granular layer with concomitant activation of glial cells. AgNPs treatment decreases calcium channel protein (CACNA1A) levels in cerebellum without changing potassium channel protein (KCNA1) levels. The levels of silver in rat cerebellum tissue are correlated with exposure doses. In vitro experiments reveal that AgNPs treatment significantly reduces the protein and mRNA levels of CACNA1A in primary cultured cerebellum granule cells (CGCs). These findings suggest that AgNPs-induced rat motor dysfunction is associated with CACNA1A expression decrease, which reveals the underlying molecular mechanism for the neurotoxicity of AgNPs. Possible counteractions may accordingly be suggested to attenuate the unexpected harmful effects in biological applications of AgNPs.

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Section: Discussionsupporting

confidence: 81%

Silver nanoparticle exposure induces rat motor dysfunction through decrease in expression of calcium channel protein in cerebellum

et al. 2015

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“…Data from rodent studies generally offer conflicting reports on how Mn exposure affects neurochemistry and motor function. A general consensus regarding the effects of Mn on motor function is that hyperactivity is observed early in Mn toxicity in the young or after low cumulative doses, in both human and animal studies (Bouchard et al, 2007; Nachtman et al, 1986), and as the disease progresses and cumulative dose levels increase, patients and animals both tend to become hypoactive (Oszlanczi et al, 2010; Torrente et al, 2005). …”

Section: Introductionmentioning

confidence: 99%

Subacute manganese exposure in rats is a neurochemical model of early manganese toxicity

et al. 2014

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Manganese (Mn) is an essential trace element, but excess exposure leads to accumulation in biological tissues, including the brain. Chronically high Mn levels in the brain are neurotoxic and can result in a progressive, irreversible neurological disorder known as manganism. Manganism has signs and symptoms similar to, but distinguishable from idiopathic Parkinson’s disease, which include both psychological and motor disturbances. Evidence suggests that Mn exposure impacts neurotransmitter levels in the brain. However, it remains unclear if subacute, low-level Mn exposure resulted in alterations in neurotransmitter systems with concomitant behavioral deficits. The current study used high performance liquid chromatography to quantify neurotransmitter levels in rat striatum (STR), substantia nigra (SN), and hippocampus (HP). Subacute Mn exposure via i.p. injection of 15 mg Mn/kg as MnCl2 caused significantly increased dopamine (DA) levels in the STR. The enhancement was accompanied by significantly elevated levels of the DA metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), in the STR. In addition, levels of HVA were significantly increased in the SN and HP. These data indicate that subacute, low-level Mn exposure disrupts multiple neurotransmitter systems in the rat brain which may be responsible, in part, for observed locomotor deficits.

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“…Mn was detected in their lung and brain tissues indicating that the instilled NMs had crossed from the airways to the brain (Sarkozi et al ., 2009). Subchronic exposure of MnO 2 ‐NPs to rats by intra‐nasal and intra‐tracheal routes, showed a significant increase in Mn levels in the brain and blood as well as functional alterations (Oszlanczi et al ., , ).…”

Section: Introductionmentioning

confidence: 99%

Toxicity assessment of manganese oxide micro and nanoparticles in Wistar rats after 28 days of repeated oral exposure

Singh

Kumari

et al. 2013

J of Applied Toxicology

107

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In the near future, nanotechnology is envisaged for large-scale use. Hence health and safety issues of nanoparticles (NPs) should be promptly addressed. Twenty-eight-day oral toxicity, genotoxicity, biochemical alterations, histopathological changes and tissue distribution of nano and microparticles (MPs) of manganese oxide (MnO2 ) in Wistar rats was studied. Genotoxicity was assessed using comet, micronucleus and chromosomal aberration assays. The results demonstrated a significant increase in DNA damage in leukocytes, micronuclei and chromosomal aberrations in bone marrow cells after exposure of MnO2 -NPs at 1000, 300 mg kg(-1) bw per day and MnO2 -MPs at the dose of 1000 mg kg(-1) bw per day. Our findings showed acetylcholinestrase inhibition at 1000 as well as at 300 mg kg(-1) bw per day in blood and with all the doses in the brain indicating the toxicity of MnO2 -NPs. Further, the doses significantly inhibited different ATPases in the brain P2 fraction. Significant changes were observed in aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) in the liver, kidney and serum in a dose-dependent manner. MnO2 -MPs at 1000 mg kg(-1) bw per day were found to induce significant alterations in biochemical enzymes. A significant distribution was found in all the tissues in a dose-dependent manner. MnO2 -NPs showed a much higher absorptivity and tissue distribution as compared with MnO2 -MPs. A large fraction of MnO2 -NPs and MnO2 -MPs was cleared by urine and feces. Histopathological analysis revealed that MnO2 -NPs caused alterations in liver, spleen, kidney and brain. The MnO2 -NPs induced toxicity at lower doses compared with MnO2 -MPs. Further, this study did not display gender differences after exposure to MnO2 -NPs and MnO2 -MPs. Therefore, the results suggested that prolonged exposure to MnO2 has the potential to cause genetic damage, biochemical alterations and histological changes.

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Metal deposition and functional neurotoxicity in rats after 3–6 weeks nasal exposure by two physicochemical forms of manganese

Cited by 16 publications

References 33 publications

Silver nanoparticle exposure induces rat motor dysfunction through decrease in expression of calcium channel protein in cerebellum

Silver nanoparticle exposure induces rat motor dysfunction through decrease in expression of calcium channel protein in cerebellum

Subacute manganese exposure in rats is a neurochemical model of early manganese toxicity

Toxicity assessment of manganese oxide micro and nanoparticles in Wistar rats after 28 days of repeated oral exposure

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