Methylmercury Poisoning in Common Marmosets—A Study of Selective Vulnerability Within the Cerebral Cortex

Neuropathological lesions found in chronic human Minamata disease tend to be localized in the calcarine cortex of occipital lobes, the pre- and postcentral lobuli, and the temporal gyri. The mechanism for the selective vulnerability is still not clear, though several hypotheses have been proposed. One hypothesi s is vascular and postulates that the lesions are the result of ischemia secondary to compression of sulcal arteries from methylmercury-induced cerebral edema. To test this hypothesis, we studied common marmosets because the cerebrum of marmosets has 2 distinct deep sulci, the calcarine and Sylvian fi ssures. MRI analysis, mercury assays of tissue specimens, histologic and histochemical studies of the brain are reported and discussed. Brains sacrifi ced early after exposure to methylmercury showed high contents of methylmercury and edema of the cerebral white matter. These results may explain the selective cortical degeneration along the deep cerebral fi ssures or sulci.

[1]  S. Ishiura,et al.  Expanded CTG repeats in myotonin protein kinase increase susceptibility to oxidative stress , 1998, Neuroreport.

[2]  T. Miyakawa,et al.  Late changes in human sural nerves in minamata disease and in nerves of rats with experimental organic mercury poisoning , 1976, Acta Neuropathologica.

[3]  K. Eto,et al.  HISTOCHEMICAL DEMONSTRATION OF MERCURY IN HUMAN TISSUE CELLS OF MINAMATA DISEASE BY USE OF AUTORADIOGRAPHIC PROCEDURE , 1975 .

[4]  Frank Henry Netter,et al.  The Ciba collection of medical illustrations , 1959 .

[5]  K. Nagashima,et al.  Apoptotic process of cerebellar degeneration in experimental methylmercury intoxication of rats , 1995, Acta Neuropathologica.

[6]  S. Bondy,et al.  Reactive oxygen species formation as a biomarker of methylmercury and trimethyltin neurotoxicity. , 1992, Neurotoxicology.

[7]  E. Luschei,et al.  Variability of neuropathologic lesions in experimental methylmercurial encephalopathy in primates. , 1975, The American journal of pathology.

[8]  J. Minckler Pathology of the nervous system , 1968 .

[9]  N. Imura,et al.  Microtubules: a Susceptible Target of Methylmercury Cytotoxicity , 1991 .

[10]  L. Goldwater,et al.  Determination of mercury in blood. , 1960, American Industrial Hygiene Association journal.

[11]  K. Nagashima,et al.  Review Article: A Review of Experimental Methylmercury Toxicity in Rats: Neuropathology and Evidence for Apoptosis , 1997, Toxicologic pathology.

[12]  Sarah D. Cramer,et al.  Pathology of the Nervous System , 2019, Toxicologic Pathology for Non-Pathologists.

[13]  A. Yasutake,et al.  Selective quantification of inorganic mercury in tissues of methylmercury-treated rats , 1990, Bulletin of environmental contamination and toxicology.

[14]  M. Mckee,et al.  Organometal-induced increases in oxygen reactive species: the potential of 2',7'-dichlorofluorescin diacetate as an index of neurotoxic damage. , 1990, Toxicology and applied pharmacology.

[15]  川崎 靖 Long-term toxicity study of methylmercury chloride in monkeys , 1987 .