Disease relevance of Mercury Poisoning, Nervous System

• The contents of urinary renal tubular epithelial antigen and beta-2-microglobulin, and the ratios of these proteins to albumin in individuals with Minamata disease were significantly different from the levels in healthy control subjects (P less than 0.05) were identical to those found in patients with tubular and the values, proteinuria [1].
• Congenital Minamata disease is due to transplacental fetal toxicity caused by accidental ingestion of methyl mercury [2].
• Nearly three decades have passed since the first outbreak of Minamata disease (methyl mercury poisoning) [3].
• Patients with Minamata disease (methylmercury intoxication) usually suffer from the glove and stocking type hypesthesia in the extremities [4].
• The well-known Minamata disease was caused by mercury; the Itai-Itai disease by cadmium; and lead poisoning by gasoline additives [5].

High impact information on Mercury Poisoning, Nervous System

• The therapeutic use of 2,3-dimercaptopropane-1-sulfonate in two cases of inorganic mercury poisoning [6].
• Methylmercury poisoning (e.g., Minamata disease) and tumor development in rats after exposure to dimethylarsinic acid or tributyltin oxide are just some examples [7].
• Most reported cases of inorganic mercury poisoning are from mercuric chloride [8].
• In Japan, human contamination by mercury, which causes Minamata disease, has been successfully treated by the metal scavenger thiola (N-2 mercaptopropionylglycine) [9].
• Widespread neuronal degeneration in rats following oral administration of methylmercury during the postnatal developing phase: a model of fetal-type minamata disease [10].

Chemical compound and disease context of Mercury Poisoning, Nervous System

• Cerebellar neurons in primary culture were exposed to methylmercury, a well-established neurotoxicant known as a cause of Minamata disease, at 0.1-1.0 microM for up to 72 hours and compared with the neurons undergoing apoptosis induced by withdrawing K+ from the medium [11].
• We looked at regional cerebellar blood flow in patients with Minamata disease (MD) using technetium-99m ethyl cysteinate dimer (99m-Tc-ECD) [12].
• 5. Thus, both the composition of the sulfur-containing radical and the steroid moiety are important for protection against inorganic mercury poisoning [13].
• In order to prove or disprove that industrial waste from the Chisso Factory was the culprit in Minamata disease, a total of ten cats were fed food mixed with industrial waste produced in the acetaldehyde-producing plant [14].
• Autopsy specimens from the historic cat experiment were recently discovered in a storage area at the Kumamoto University School of Medicine. The specimens were from an experiment prompted by physicians in the Chisso Minamata Plant following the announcement made by the Study Group for Minamata disease [14].

Anatomical context of Mercury Poisoning, Nervous System

• Methylmercury dose estimation from umbilical cord concentrations in patients with Minamata disease [15].
• Ultrastructural changes of human sural nerves in the neuropathy induced by intrauterine methylmercury poisoning (so-called fetal Minamata disease) [16].

Gene context of Mercury Poisoning, Nervous System

• DMSA-ERCH appears to be much more effective than BAL and haemodialysis in the treatment of acute inorganic mercury poisoning [17].
• But, we could not observe drastic degeneration in their brains which mimicked Fetal Minamata Disease in human [18].

References