9.2. Protein-Based Hg(II) Detectors 3467 9.3. Oligonucleotide-Based Hg(II) Detector 3467 9.4. DNAzyme-Based Hg(II) Detectors 3469 9.5. Antibody-Based Hg(II) Detector 3469 10. Mercury Detectors Based on Materials 3469 10.1. Soluble and Fluorescent Polymers 3469 10.2. Membranes, Films, and Fibers 3471 10.3. Micelles 3473 10.4. Nanoparticles 3473 11. Perspectives 3474 12. Addendum 3475 12.1. Small Molecules 3475 12.2. Biomolecules 3477 12.3. Materials 3477 13. List of Abbreviations 3477 14. Acknowledgments 3478 15. References 3478

Tools and tactics for the optical detection of mercuric ion.

This review covers the toxicology of mercury and its compounds. Special attention is paid to those forms of mercury of current public health concern. Human exposure to the vapor of metallic mercury dates back to antiquity but continues today in occupational settings and from dental amalgam. Health risks from methylmercury in edible tissues of fish have been the subject of several large epidemiological investigations and continue to be the subject of intense debate. Ethylmercury in the form of a preservative, thimerosal, added to certain vaccines, is the most recent form of mercury that has become a public health concern. The review leads to general discussion of evolutionary aspects of mercury, protective and toxic mechanisms, and ends on a note that mercury is still an "element of mystery."

The Toxicology of Mercury and Its Chemical Compounds

Minamata disease (M. d.) is methylmercury (MeHg) poisoning that occurred in humans who ingested fish and shellfish contaminated by MeHg discharged in waste water from a chemical plant (Chisso Co. L...

Minamata disease: methylmercury poisoning in Japan caused by environmental pollution

Biogeochemistry of the Human Environment.- The Biosphere.- Soils.- Waters.- Air.- Plants.- Humans.- Biogeochemistry of Trace Elements.- Trace Elements of Group 1 (Previously Group Ia).- Trace Elements of Group 2 (Previously Group IIa).- Trace Elements of Group 3 (Previously Group IIIb).- Trace Elements of Group 4 (Previously Group IVb).- Trace Elements of Group 5 (Previously Group Vb).- Trace Elements of Group 6 (Previously Group VIb).- Trace Elements of Group 7 (Previously Group VIIb).- Trace Elements of Group 8 (Previously Part of Group VIII).- Trace Elements of Group 9 (Previously Part of Group VIII).- Trace Elements of Group 10 (Previously Part of Group VIII).- Trace Elements of Group 11 (Previously Group Ib).- Trace Elements of Group 12 (Previously Group IIb).- Trace Elements of Group 13 (Previously Group IIIa).- Trace Elements of Group 14 (Previously Group IVa).- Trace Elements of Group 15 (Previously Group Va).- Trace Elements of Group 16 (Previously Group VIa).- Trace Elements of Group 17 (Previously Group VIIa).

/pdf/trace-elements-from-soil-to-human-gyujylwhl8.pdf

Trace Elements From Soil to Human

Cognitive Deficit in 7-year-old Children With Prenatal Exposure to Methylmercury

Clinical and pathological features of the disease process in 2 children who were affected by a congenital form of cerebral palsy are reported. Both children were born near Minamata bay in families in which cases of Minamata disease had occurred. Pathological examination of the central nervous system showed lesions very similar in type and distribution to those found in adult patients suffering from Minamata disease. The disease is caused by intoxication with alkyl-mereury compounds and is contracted by rating fish from Minamata bay, the waters of which contain mercury originating from industrial wastes. Since the 2 children never ate fish or shellfish, it is concluded that cerebral palsy was caused by mercury intoxication acquired prenatally from the mother, although the mothers did not show manifestations of Minamata disease.

Fetal Minamata disease. A neuropathological study of two cases of intrauterine intoxication by a methyl mercury compound.

The outbreak of methylmercury poisoning in the geographic areas around Minamata Bay, Kumamoto, Japan in the 1950s has become known as Minamata disease. Based on earlier reports and extensive pathological studies on autopsied cases at the Kumamoto University School of Medicine, destructive lesions in the anterior portion of the calcarine cortex and depletion predominantly of granular cells in the cerebellar cortex came to be recognized as the hallmark and diagnostic yardstick of methylmercury poisoning in humans. As the number of autopsy cases of Minamata disease increased, it became apparent that the cerebral lesion was not restricted to the calcarine cortex but was relatively widespread. Less severe lesions, believed to be responsible for the motor symptoms of Minamata patients, were often found in the precentral, postcentral, and lateral temporal cortices. These patients also frequently presented with signs of sensory neuropathy affecting the distal extremities. Because of few sufficiently comprehensive studies, peripheral nerve degeneration has not been universally accepted as a cause of the sensory disturbances in Minamata patients. The present paper describes both biopsy and autopsy findings of the peripheral nerves in a male fisherman who died at the age of 64 years and showed the characteristic central nervous system lesions of Minamata disease at autopsy. A sural nerve biopsy with electron microscopy performed 1 month prior to his death showed endoneurial fibrosis and regenerated myelin sheaths. At autopsy the dorsal roots and sural nerve showed endoneurial fibrosis, loss of nerve fibers, and presence of Bungner's bands. The spinal cord showed Wallerian degeneration of the fasciculus gracilis (Goll's tract) with relative preservation of neurons in sensory ganglia. These findings support the contention that there is peripheral nerve degeneration in Minamata patients due to toxic injury from methylmercury.

https://journals.sagepub.com/doi/pdf/10.1080/01926230290166805

An Autopsy Case of Minamata Disease (Methylmercury Poisoning)—Pathological Viewpoints of Peripheral Nerves

Details are given of the mercury level and deposition in a human brain with Minamata disease following a twenty-six year clinical course after the first severe attack in 1956. This is the first report of a case in which the methylmercury level within the brain has returned to normal limits in a severely affected victim. However, the total mercury remained high in the brain, and mercury was clearly demonstrated histochemically in microglial cells or macrophages over wide areas of the brain and in neurons of specific brain areas. Bergmann's glial cells also contained mercury deposits, whereas Purkinje's cells had relatively little or no deposition. Mild deposition of the metal was demonstrable in the epithelial cells of the choroid plexus.

Mercury level and histochemical distribution in a human brain with Minamata disease following a long-term clinical course of twenty-six years.

Minamata is a small industrial town with a total population of about 50,000. It is near the south west coast of Kyushu, the most southerly of the main Japanese islands. There is an old large artificial-fertilizer factory, the effluent from which empties into a small Minamata Bay. In this factory, a small amount of vinyl chloride compounds were experimentally manufactured during 1949-1951, and their production on a large scale has been opened since 1952 to 1953, separately from the fertilizer production. From the end of 1953 a mysterious nervous illness began sporadically to affect the villagers, especially the fishermen, and was called the “Minamata Disease ”. The outbreak was investigated by several departments of our University. The pathologic investigations and experiments were made by us. It was explained that the illness was caused from the eating of a large amount of fish and shellfish contaminated by the effluent of the new industrial department. The toxic agent seems to have some relation to the manufacturing of the vinyl chloride compounds.

Pathologic observations of the Minamata disease.

This study consists of 83 autopsy cases including 64 prolonged cases of Minamata disease. Lesions were severe in the prolonged cases with an acute onset, while they tended to be mild in those with chronic onset. Cerebral cortex showed loss of nerve cells in many of the former, with the cortex often being in a loosening or spongy state, while the thinning-out or decrease of neurons not exceeding 30% of all cells was frequent in the latter. Glial reaction was also intense in the former, but relatively weak in the latter; gradual loss of degenerative neurons without glial reaction was not rare. A given selectivity was found in the localization of lesions of the cerebral cortex, but it was not so conspicuous in those with a chronic onset as in those with an acute onset. Secondary changes corresponding to the lesions of the cortex appeared in the medulla. Cerebellar lesions in the chronic onset cases, as compared with those in the acute onset ones, were milder. The selectively localized area was diminished; the nodulus, uvula and lingula of the vermis and the medial surface of the semilunar lobules were the most likely to be damaged. Of the spinal peripheral nerves, damages to the spinal sensory nerve were found, which were more predominant than those to the motor nerve system, and in which was noted prominent regeneration and repair. The deposited mercury found in organs tended to remain in the nervous system and the kidneys during the prolonged course of this disease, and the prolonged accumulation of mercury in the nervous system appeared to have an influence on the pathogenesis of chronic Minamata disease.

Tadao Takeuchi

Papers

Fetal Minamata disease. A neuropathological study of two cases of intrauterine intoxication by a methyl mercury compound.

An Autopsy Case of Minamata Disease (Methylmercury Poisoning)—Pathological Viewpoints of Peripheral Nerves

Mercury level and histochemical distribution in a human brain with Minamata disease following a long-term clinical course of twenty-six years.

Pathologic observations of the Minamata disease.

A Pathological Study of Prolonged Cases of Minamata Disease--With Particular Reference to 83 Autopsy Cases