Assessing Effects of Neurotoxic Pollutants by Biochemical Markers

Manzo, Luigi; Castoldi, Anna Federica; Coccini, Teresa; Prockop, Leon D.

doi:10.1006/enrs.2000.4039

Cited by 38 publications

(25 citation statements)

References 36 publications

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“…Neurochemical changes may represent early and reversible indicators of neurological harm because they occur prior to the onset of overt functional or structural damage (Manzo et al 2001). Among the documented neurochemical changes characteristic of MeHg exposure are disruption of glutamate uptake by astrocytes (Brookes and Kristt 1989) and inhibition of ligand binding to synaptic muscarinic cholinergic (mACh) receptors (Castoldi et al 1996;Basu et al 2005a).…”

Section: Introductionmentioning

confidence: 99%

Relationships among mercury, selenium, and neurochemical parameters in common loons (Gavia immer) and bald eagles (Haliaeetus leucocephalus)

et al. 2007

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Fish-eating birds can be exposed to levels of dietary methylmercury (MeHg) known or suspected to adversely affect normal behavior and reproduction, but little is known regarding Hg's subtle effects on the avian brain. In the current study, we explored relationships among Hg, Se, and neurochemical receptors and enzymes in two fish-eating birds--common loons (Gavia immer) and bald eagles (Haliaeetus leucocephalus). In liver, both species demonstrated a wide range of total Hg (THg) concentrations, substantial demethylation of MeHg, and a co-accumulation of Hg and Se. In liver, there were molar excesses of Se over Hg up to about 50-60 microg/g THg, above which there was an approximate 1:1 molar ratio of Hg:Se in both species. However, in brain, bald eagles displayed a greater apparent ability to demethylate MeHg than common loons. There were molar excesses of Se over Hg in brains of bald eagles across the full range of THg concentrations, whereas common loons often had extreme molar excesses of Hg in their brains, with a higher proportion of THg remaining as MeHg compared with eagles. There were significant positive correlations between brain THg and muscarinic cholinergic receptor concentrations in both species studied; whereas significant negative correlations were observed between N-methyl-D-aspartic acid (NMDA) receptor levels and brain Hg concentration. There were no significant correlations between brain Se and neurochemical receptors or enzymes (cholinesterase and monoamine oxidase) in either species. Our findings suggest that there are significant differences between common loons and bald eagles with respect to cerebral metabolism and toxicodynamics of MeHg and Se. These interspecies differences may influence relative susceptibility to MeHg toxicity; however, neurochemical responses to Hg in both species were similar.

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Section: Introductionmentioning

confidence: 99%

Relationships among mercury, selenium, and neurochemical parameters in common loons (Gavia immer) and bald eagles (Haliaeetus leucocephalus)

et al. 2007

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“…However, unlike with experimental models and wildlife, direct assessment of brain neurochemistry in humans is challenging. There is some promise that peripheral neurochemical markers in blood (e.g., platelet monoamine oxidase activity, lymphocyte muscarinic receptor levels, red cell cholinesterase activity) may refl ect brain activity (Manzo et al 2001 ) . For example, mercury-associated decreases in monoamine oxidase were measured in the brain tissues of rats (Chakrabarti et al 1998 ) , salmon (Berntssen et al 2003 ) , and river otters (Basu et al 2007c ) , as well as blood platelets of humans (Stamler et al 2006 ) .…”

Section: Health Effects Of Methylmercurymentioning

confidence: 99%

Piscivorous Mammalian Wildlife as Sentinels of Methylmercury Exposure and Neurotoxicity in Humans

Basu

2012

Methylmercury and Neurotoxicity

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The purpose of this chapter is to provide an overview of how piscivorous (fi sh-eating) wildlife can be used to complement existing public health strategies to assess the neurotoxic risks of methylmercury. A brief introduction concerning the use of wildlife as model sentinel organisms in the fi eld of environmental neurotoxicology is provided. Next, selected scientifi c examples are detailed that illustrate how data from piscivorous wildlife may provide pertinent, real-world information on the bioavailability of methylmercury and environmental exposures. Information concerning methylmercury's subclinical (e.g., perturbations in brain neurochemistry and neuroendocrine hormones) and clinical (structural and functional defi cits) neurological effects across organisms is also discussed.

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“…These results further substantiate the theory that the mechanism of toxicity between the two species is different. (Charleston etal., 1996) (Charleston et al, 1996) There is increasing literature investigating the use of neurochemical endpoints as biomarkers for toxicity due to their limited invasiveness and time utilization (Manzo et al, 2001). Basu et al (2005a) studied the inhibitory effects of Hg on muscarinic acetylcholine (ACh) and dopamine (D2) receptors in wild river otter.…”

Section: In Vitromentioning

confidence: 99%

Characterization of methylmercury demethylation in the central nervous system.

Shapiro¹

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Assessing Effects of Neurotoxic Pollutants by Biochemical Markers

Cited by 38 publications

References 36 publications

Relationships among mercury, selenium, and neurochemical parameters in common loons (Gavia immer) and bald eagles (Haliaeetus leucocephalus)

Relationships among mercury, selenium, and neurochemical parameters in common loons (Gavia immer) and bald eagles (Haliaeetus leucocephalus)

Piscivorous Mammalian Wildlife as Sentinels of Methylmercury Exposure and Neurotoxicity in Humans

Characterization of methylmercury demethylation in the central nervous system.

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