Widespread calcium deposits, as detected using the alizarin red S technique, in the nervous system of rats treated with dimethyl mercury
It has been reported that the alizarin red S technique may be used to visualize both intracellular and extracellular calcium deposits. Using this method histologic observations of the nervous system were made in rats that were given dimethyl mercury at 5 mg/kg per day for 12 consecutive days, and ki...
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| Published in | Neuropathology Vol. 20; no. 3; pp. 210 - 215 |
|---|---|
| Main Authors | , , |
| Format | Journal Article |
| Language | English |
| Published |
Melbourne, Australia
Blackwell Science Pty
01.09.2000
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0919-6544 1440-1789 |
| DOI | 10.1046/j.1440-1789.2000.00341.x |
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| Abstract | It has been reported that the alizarin red S technique may be used to visualize both intracellular and extracellular calcium deposits. Using this method histologic observations of the nervous system were made in rats that were given dimethyl mercury at 5 mg/kg per day for 12 consecutive days, and killed on days 1, 4, 7, 10, 12, 24, 32, 49, 100 and 140 (day 0 was the day that the final dose was administered). Neuronal degeneration with calcium deposition was found in the nervous system from day 4 onward. In the cerebellum alizarin red S‐positive granules became gradually larger with time after dimethyl mercury administration, and large calcospherites were observed from day 32 onward. In contrast, the visualization of calcium deposits in the cerebral cortex was restricted to days 10–12. Calcium deposits were found in the ascending axons of the dorsal root ganglion neurons (dorsal fascicles of the spinal cord), but not in their perikarya. These findings suggest that widespread calcium deposition could occur in the nervous system following dimethyl mercury exposure, and that in the rat the mechanism of calcium deposition differs depending upon the brain region. |
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| AbstractList | It has been reported that the alizarin red S technique may be used to visualize both intracellular and extracellular calcium deposits. Using this method histologic observations of the nervous system were made in rats that were given dimethyl mercury at 5 mg/kg per day for 12 consecutive days, and killed on days 1, 4, 7, 10, 12, 24, 32, 49, 100 and 140 (day 0 was the day that the final dose was administered). Neuronal degeneration with calcium deposition was found in the nervous system from day 4 onward. In the cerebellum alizarin red S-positive granules became gradually larger with time after dimethyl mercury administration, and large calcospherites were observed from day 32 onward. In contrast, the visualization of calcium deposits in the cerebral cortex was restricted to days 10-12. Calcium deposits were found in the ascending axons of the dorsal root ganglion neurons (dorsal fascicles of the spinal cord), but not in their perikarya. These findings suggest that widespread calcium deposition could occur in the nervous system following dimethyl mercury exposure, and that in the rat the mechanism of calcium deposition differs depending upon the brain region. It has been reported that the alizarin red S technique may be used to visualize both intracellular and extracellular calcium deposits. Using this method histologic observations of the nervous system were made in rats that were given dimethyl mercury at 5 mg/kg per day for 12 consecutive days, and killed on days 1, 4, 7, 10, 12, 24, 32, 49, 100 and 140 (day 0 was the day that the final dose was administered). Neuronal degeneration with calcium deposition was found in the nervous system from day 4 onward. In the cerebellum alizarin red S-positive granules became gradually larger with time after dimethyl mercury administration, and large calcospherites were observed from day 32 onward. In contrast, the visualization of calcium deposits in the cerebral cortex was restricted to days 10-12. Calcium deposits were found in the ascending axons of the dorsal root ganglion neurons (dorsal fascicles of the spinal cord), but not in their perikarya. These findings suggest that widespread calcium deposition could occur in the nervous system following dimethyl mercury exposure, and that in the rat the mechanism of calcium deposition differs depending upon the brain region.It has been reported that the alizarin red S technique may be used to visualize both intracellular and extracellular calcium deposits. Using this method histologic observations of the nervous system were made in rats that were given dimethyl mercury at 5 mg/kg per day for 12 consecutive days, and killed on days 1, 4, 7, 10, 12, 24, 32, 49, 100 and 140 (day 0 was the day that the final dose was administered). Neuronal degeneration with calcium deposition was found in the nervous system from day 4 onward. In the cerebellum alizarin red S-positive granules became gradually larger with time after dimethyl mercury administration, and large calcospherites were observed from day 32 onward. In contrast, the visualization of calcium deposits in the cerebral cortex was restricted to days 10-12. Calcium deposits were found in the ascending axons of the dorsal root ganglion neurons (dorsal fascicles of the spinal cord), but not in their perikarya. These findings suggest that widespread calcium deposition could occur in the nervous system following dimethyl mercury exposure, and that in the rat the mechanism of calcium deposition differs depending upon the brain region. |
| Author | Wakabayashi, Koichi Tanji, Kunikazu Mori, Fumiaki |
| Author_xml | – sequence: 1 givenname: Fumiaki surname: Mori fullname: Mori, Fumiaki organization: Department of Neuropathology, Institute of Brain Science, Hirosaki University School of Medicine, Hirosaki, Japan – sequence: 2 givenname: Kunikazu surname: Tanji fullname: Tanji, Kunikazu organization: Department of Neuropathology, Institute of Brain Science, Hirosaki University School of Medicine, Hirosaki, Japan – sequence: 3 givenname: Koichi surname: Wakabayashi fullname: Wakabayashi, Koichi organization: Department of Neuropathology, Institute of Brain Science, Hirosaki University School of Medicine, Hirosaki, Japan |
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| Cites_doi | 10.1007/BF02889124 10.1016/0006-8993(95)01208-7 10.3181/00379727-80-19661 10.1111/j.1749-6632.1994.tb44406.x 10.1146/annurev.pa.32.040192.002313 10.1111/j.1440-1789.1997.tb00039.x 10.1007/BF00685743 10.1016/0041-008X(76)90023-5 10.1111/j.1365-2990.1984.tb00360.x 10.1016/0041-008X(87)90271-7 10.1007/BF00691435 10.1111/j.1440-1789.1996.tb00178.x 10.1016/0006-8993(85)91219-3 10.1016/S0006-8993(00)01964-8 10.1111/j.1600-0773.1996.tb00203.x 10.1007/BF00689565 10.1007/BF00304634 10.1016/S0022-510X(98)00030-6 10.1136/jnnp.17.4.235 10.1016/0041-008X(74)90036-2 10.1006/taap.1998.8383 10.1007/BF00684597 10.1111/j.1440-1789.1998.tb00138.x |
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| References | Su M, Kakita A, Wakabayashi K, Yamada M, Takahashi H, Ikuta F. Degeneration of spinal dorsal root ganglia in adult rats treated with methylmercury: Chronological observations on the cell bodies, centrally directed axons and presynaptic terminals. Neuropathology 1997; 17: 201 207. Hunter D, Bomford RR, Russell DS. Poisoning by methyl mercury compounds. Q J Med 1940; 9: 193 219. Dahl LK. A simple and sensitive histochemical method for calcium. Proc Soc Exp Biol NY 1952; 80: 474 479. Wakabayashi K, Kakita A, Sakamoto M, Su M, Iwanaga K, Ikuta F. Variability of brain lesions in rats administered methylmercury at various postnatal development phases. Brain Res 1995; 705: 267 272. Evans MC, Griffiths T, Meldrum BS. Kainic acid seizures and the reversibility of calcium loading in vulnerable neurons in the hippocampus. Neuropathol Appl Neurobiol 1984; 10: 285 302. Hunter D & Russell DS. Focal cerebral and cerebellar atrophy in a human subject due to organic mercury compounds. J Neurol Neurosurg Psychiatry 1954; 17: 235 241. Marty MS & Atchison WD. Elevations of intracellular Ca2+ as a probable contributor to decreased viability in cerebellar granule cells following acute exposure to methylmercury. Toxicol Appl Pharmacol 1998; 150: 98 105. Siesjö BK. Calcium-mediated processes in neuronal degeneration. Ann NY Acad Sci 1994; 747: 140 161. Sztriha L, Joó F, Szerdahelyi P. Accumulation of calcium in the rat hippocampus during kainic acid seizures. Brain Res 1985; 360: 51 57. Cavanagh JB & Chen FCK. The effects of methyl-mercury-dicyandiamide on the peripheral nerves and spinal cord of rats. Acta Neuropathol 1971; 19: 208 215. Paxinos G & Watson C. The Rat Brain in Stereotaxic Coordinates, 3rd edn. San Diego: Academic Press, 1997. Su M, Kakita A, Yamada M, Takahashi H, Ikuta F. Degeneration of the synaptic boutons of parallel fibers in rats treated with methylmercury: Chronological observations. Neuropathology 1996; 16: 172 177. Takeuchi T, Morikawa N, Matsumoto H, Shiraishi Y. A pathological study of Minamata disease in Japan. Acta Neuropathol 1962; 2: 40 57. Eto K & Takeuchi T. Pathological changes of human sural nerves in Minamata disease (methylmercury poisoning): Light and electron microscopic studies. Virchows Arch B Cell Pathol 1977; 23: 109 128. Eto K & Takeuchi T. A pathological study of prolonged cases of Minamata disease, with particular reference to 83 autopsy cases. Acta Pathol Jpn 1978; 28: 565 584. Sakamoto M, Ikegami N, Nakano A. Protective effects of Ca2+ channel blockers against methyl mercury toxicity. Pharmacol Toxicol 1996; 78: 193 199. Chou SM & Fukuhara N. EM studies on calcospherites induced in cerebellar granular layers of rats by chronic methyl mercury poisoning. J Neuropathol Exp Neurol 1973; 32: 175 176. Kobayashi Y, Sawa H, Watanabe M, Furuoka H, Matsui T, Nagashima K. Calbindin D immunoreactivity and chronic lesions of rat cerebella in methylmercury chloride intoxication. Neuropathology 1998; 18: 402 407. Komulainen H & Bondy SC. Increased free intrasynaptosomal Ca2+ by neurotoxic organometals: Distinctive mechanisms. Toxicol Appl Pharmacol 1987; 88: 77 86. Sztriha L, Joó F, Szerdahelyi P. Time-course of changes in water, sodium, potassium and calcium contents of various brain regions in rats after systemic kainic acid administration. Acta Neuropathol 1986; 70: 169 176. Nitsch C & Scotti AL. Ibotenic acid-induced calcium deposits in rat substantia nigra. Ultrastructure of their time-dependent formation. Acta Neuropathol 1992; 85: 55 70. Kakita A, Wakabayashi K, Su M, Sakamoto M, Ikuta F, Takahashi H. Distinct pattern of neuronal degenera-tion in the fetal rat brain induced by consecutive transplacental administration of methylmercury. Brain Res 2000; 859: 233 239. Charbonneau SM, Munro IC, Nera EA et al. Subacute toxicity of methylmercury in the adult cat. Toxicol Appl Pharmacol 1974; 27: 569 581. Hare MF, McGinnis KM, Atchison WD. Methylmercury increases intracellular concentrations of Ca++ and heavy metals in NG108-15 cells. J Pharmacol Exp Ther 1993; 266: 1626 1635. Nicotera P, Bellomo G, Orrenius S. Calcium-mediated mechanisms in chemically induced cell death. Ann Rev Pharmacol Toxicol 1992; 32: 449 470. Carmichael N, Cavanagh JB, Rodda RA. Some effects of methyl mercury salts on the rabbit nervous system. Acta Neuropathol 1975; 32: 115 125. Su M, Wakabayashi K, Kakita A, Ikuta F, Takahashi H. Selective involvement of large motor neurons in the spinal cord of rats treated with methylmercury. J Neurol Sci 1998; 156: 12 17. World Health Organization. Environmental Health Criteria 101. Methylmercury. Geneva: World Health Organization, 1990. Berthoud HR, Garman RH, Weiss B. Food intake, body weight, and brain histopathology in mice following chronic methylmercury treatment. Toxicol Appl Pharmacol 1976; 36: 19 30. 2000; 859 1986; 70 1973; 32 1962; 2 1997 1977; 23 1975; 32 1992; 32 1996; 16 1998; 156 1985; 360 1998; 150 1993; 266 1996; 78 1974; 27 1987; 88 1998; 18 1976; 36 1990 1971; 19 1952; 80 1995; 705 1984; 10 1997; 17 1978; 28 1954; 17 1994; 747 1940; 9 1992; 85 Eto K (e_1_2_6_12_2) 1977; 23 e_1_2_6_30_2 Eto K (e_1_2_6_13_2) 1978; 28 Paxinos G (e_1_2_6_27_2) 1997 e_1_2_6_18_2 e_1_2_6_19_2 World Health Organization (e_1_2_6_8_2) 1990 e_1_2_6_10_2 e_1_2_6_11_2 e_1_2_6_16_2 e_1_2_6_17_2 e_1_2_6_14_2 e_1_2_6_15_2 Chou SM (e_1_2_6_23_2) 1973; 32 e_1_2_6_20_2 e_1_2_6_7_2 Hunter D (e_1_2_6_22_2) 1940; 9 e_1_2_6_9_2 e_1_2_6_29_2 e_1_2_6_4_2 Hare MF (e_1_2_6_5_2) 1993; 266 e_1_2_6_3_2 e_1_2_6_6_2 e_1_2_6_24_2 e_1_2_6_2_2 e_1_2_6_21_2 e_1_2_6_28_2 e_1_2_6_26_2 e_1_2_6_25_2 |
| References_xml | – reference: Paxinos G & Watson C. The Rat Brain in Stereotaxic Coordinates, 3rd edn. San Diego: Academic Press, 1997. – reference: Marty MS & Atchison WD. Elevations of intracellular Ca2+ as a probable contributor to decreased viability in cerebellar granule cells following acute exposure to methylmercury. Toxicol Appl Pharmacol 1998; 150: 98 105. – reference: Eto K & Takeuchi T. A pathological study of prolonged cases of Minamata disease, with particular reference to 83 autopsy cases. Acta Pathol Jpn 1978; 28: 565 584. – reference: Kakita A, Wakabayashi K, Su M, Sakamoto M, Ikuta F, Takahashi H. Distinct pattern of neuronal degenera-tion in the fetal rat brain induced by consecutive transplacental administration of methylmercury. Brain Res 2000; 859: 233 239. – reference: Berthoud HR, Garman RH, Weiss B. Food intake, body weight, and brain histopathology in mice following chronic methylmercury treatment. Toxicol Appl Pharmacol 1976; 36: 19 30. – reference: Hunter D & Russell DS. Focal cerebral and cerebellar atrophy in a human subject due to organic mercury compounds. J Neurol Neurosurg Psychiatry 1954; 17: 235 241. – reference: World Health Organization. Environmental Health Criteria 101. Methylmercury. Geneva: World Health Organization, 1990. – reference: Wakabayashi K, Kakita A, Sakamoto M, Su M, Iwanaga K, Ikuta F. Variability of brain lesions in rats administered methylmercury at various postnatal development phases. Brain Res 1995; 705: 267 272. – reference: Kobayashi Y, Sawa H, Watanabe M, Furuoka H, Matsui T, Nagashima K. Calbindin D immunoreactivity and chronic lesions of rat cerebella in methylmercury chloride intoxication. Neuropathology 1998; 18: 402 407. – reference: Nicotera P, Bellomo G, Orrenius S. Calcium-mediated mechanisms in chemically induced cell death. Ann Rev Pharmacol Toxicol 1992; 32: 449 470. – reference: Siesjö BK. Calcium-mediated processes in neuronal degeneration. Ann NY Acad Sci 1994; 747: 140 161. – reference: Sakamoto M, Ikegami N, Nakano A. Protective effects of Ca2+ channel blockers against methyl mercury toxicity. Pharmacol Toxicol 1996; 78: 193 199. – reference: Carmichael N, Cavanagh JB, Rodda RA. Some effects of methyl mercury salts on the rabbit nervous system. Acta Neuropathol 1975; 32: 115 125. – reference: Komulainen H & Bondy SC. Increased free intrasynaptosomal Ca2+ by neurotoxic organometals: Distinctive mechanisms. Toxicol Appl Pharmacol 1987; 88: 77 86. – reference: Chou SM & Fukuhara N. EM studies on calcospherites induced in cerebellar granular layers of rats by chronic methyl mercury poisoning. J Neuropathol Exp Neurol 1973; 32: 175 176. – reference: Sztriha L, Joó F, Szerdahelyi P. Accumulation of calcium in the rat hippocampus during kainic acid seizures. Brain Res 1985; 360: 51 57. – reference: Su M, Kakita A, Wakabayashi K, Yamada M, Takahashi H, Ikuta F. Degeneration of spinal dorsal root ganglia in adult rats treated with methylmercury: Chronological observations on the cell bodies, centrally directed axons and presynaptic terminals. Neuropathology 1997; 17: 201 207. – reference: Hare MF, McGinnis KM, Atchison WD. Methylmercury increases intracellular concentrations of Ca++ and heavy metals in NG108-15 cells. J Pharmacol Exp Ther 1993; 266: 1626 1635. – reference: Cavanagh JB & Chen FCK. The effects of methyl-mercury-dicyandiamide on the peripheral nerves and spinal cord of rats. Acta Neuropathol 1971; 19: 208 215. – reference: Nitsch C & Scotti AL. Ibotenic acid-induced calcium deposits in rat substantia nigra. Ultrastructure of their time-dependent formation. Acta Neuropathol 1992; 85: 55 70. – reference: Takeuchi T, Morikawa N, Matsumoto H, Shiraishi Y. A pathological study of Minamata disease in Japan. Acta Neuropathol 1962; 2: 40 57. – reference: Evans MC, Griffiths T, Meldrum BS. Kainic acid seizures and the reversibility of calcium loading in vulnerable neurons in the hippocampus. Neuropathol Appl Neurobiol 1984; 10: 285 302. – reference: Charbonneau SM, Munro IC, Nera EA et al. Subacute toxicity of methylmercury in the adult cat. Toxicol Appl Pharmacol 1974; 27: 569 581. – reference: Su M, Kakita A, Yamada M, Takahashi H, Ikuta F. Degeneration of the synaptic boutons of parallel fibers in rats treated with methylmercury: Chronological observations. Neuropathology 1996; 16: 172 177. – reference: Su M, Wakabayashi K, Kakita A, Ikuta F, Takahashi H. Selective involvement of large motor neurons in the spinal cord of rats treated with methylmercury. J Neurol Sci 1998; 156: 12 17. – reference: Dahl LK. A simple and sensitive histochemical method for calcium. Proc Soc Exp Biol NY 1952; 80: 474 479. – reference: Eto K & Takeuchi T. Pathological changes of human sural nerves in Minamata disease (methylmercury poisoning): Light and electron microscopic studies. Virchows Arch B Cell Pathol 1977; 23: 109 128. – reference: Sztriha L, Joó F, Szerdahelyi P. Time-course of changes in water, sodium, potassium and calcium contents of various brain regions in rats after systemic kainic acid administration. Acta Neuropathol 1986; 70: 169 176. – reference: Hunter D, Bomford RR, Russell DS. Poisoning by methyl mercury compounds. 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| SubjectTerms | alizarin red S Animals Anthraquinones Calcium - analysis calcium deposition dimethylmercury Dose-Response Relationship, Drug Female Mercury Poisoning, Nervous System - pathology Methylmercury Compounds - toxicity Microscopy, Electron Nerve Degeneration - pathology Nervous System - pathology Nervous System - ultrastructure Neurons - pathology Neurons - ultrastructure neurotoxicity rat Rats Rats, Wistar ultrastructure |
| Title | Widespread calcium deposits, as detected using the alizarin red S technique, in the nervous system of rats treated with dimethyl mercury |
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