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Citation |
Roos PM, Dencker L. Basic Clin. Pharmacol. Toxicol. 2012; 111(2): 126-132. |
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Affiliation |
Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; Department of Clinical Neurophysiology, Oslo University Hospital, Oslo, Norway. |
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Copyright |
(Copyright © 2012, Nordic Pharmacological Society, Publisher John Wiley and Sons) |
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DOI |
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PMID |
22364490 |
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Abstract |
Amyotrophic lateral sclerosis (ALS) affects anterior horn cells of the spinal cord causing an indolent slow and steady deterioration of muscle strength leading inevitably to death in respiratory failure. ALS is a model condition for neurodegenerative disorders. Exposure to different agents dispersed in the environment has been suggested to cause neurodegeneration but no convincing evidence for such a link has yet been presented. Respiratory exposure to metallic mercury (Hg(0) ) from different sources may be suspected. Body distribution of metallic mercury is fast and depends on solubility properties. Routes of transport, metabolism, excretion and biological half-time determine the overall toxic effects. Inhalation experiments were performed in 1984 where small marmoset monkeys (Callithrix jacchus) were exposed to (203) Hg(0 vapour) mixed into the breathing air (4-5μg/liter). After one hour of exposure, they were killed and whole body autoradiograms prepared to study the distribution of mercury within organs. Autoradiograms showed that Hg was deposited inside the spinal cord. Areas of enhanced accumulation anatomically corresponding to motor nuclei could be observed. This paper describes a reinvestigation, with new emphasis on the spinal cord, of these classical metal exposure data in a primate, focusing on their relevance for the causation of neurodegenerative disorders. A comparison with more recent rodent experiments with similar findings is included. The hypothesis that long-time low-dose respiratory exposure to metals e.g., Hg contributes to neurodegenerative disorders is forwarded and discussed. Language: en |