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

Abstract

Neuropathologica l 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 methylmercuryinduced cerebral edema. To test this hypothesis, we studied common marmosets because the cerebrum of marmosets has 2 distinct deep sulci, the calcarine and Sylvian ssures. MRI analysis, mercury assays of tissue specimens, histologic and histochemical studies of the brain are reported and discussed. Brains sacri 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 ssures or sulci.

Methylmercury Retards the Repair of Wounded Monolayer of Human Brain Microvascular Endothelial Cells by Inhibiting Their Proliferation without Nonspecific Cell Damage

“…For example, Eto et al 3) demonstrated that acute MeHg exposure induces severe damage in the occipital lobes of the cerebrum of common marmosets. The concentration of MeHg was observed to be high in the edematous white matter of the cerebrum, suggesting that edema in the white matter is caused by MeHg, leading to secondary damage to the neurons.…”

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

“…Our attempt herein is to present an overview of the pathological ndings in the central and peripheral nervous system of Minamata disease patients through a case presentation, and to reemphasize the occurrence of peripheral neuropathy in human Minamata disease patients and in common marmosets, which show lesions very similar to those of human patients (6). Whereas methylmercury-treated common marmosets showed lesions in the cerebrum, cerebellum, and peripheral nerves, Macaca mulatta showed lesions from methylmercury poisoning in the cerebrum excluding the cerebellum and no lesions in the peripheral nerves (24)(25)(26).…”

Increased expression of aquaporin-4 with methylmercury exposure in the brain of the common marmoset

“…Takeuchi and Eto reported edema in the perivascular space of the brains of patients with Minamata disease that was accentuated in the boundary zones of the cerebral hemispheres (Takeuchi and Eto, 1999). It was hypothesized that the most vulnerable sites in experimental MeHg intoxication are in the cortices along deep sulci and fissures, and cerebral edema in the early stages might cause ischemia followed by acceleration of the neuronal injury around deep sulci (Shaw et al, 1979;Eto et al, 2001). MeHg-treated common marmosets showed lesions in the cerebrum, cerebellum, and peripheral nerves (Eto et al, 2001(Eto et al, , 2002.…”