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- Manganese Intoxication in the Rat A neuropathologic study and distribution of manganese in rat brain.
- Tae Jung Jang, Jung Ran Kim, Jong Im Lee, Dong Hoon Kim, Ki Kwon Kim, Ji Yong Kim, Hae Kwan Cheong, Hyun Sul Lim
- Korean J Pathol. 1999;33(9):662-674.
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Abstract
PDF - We investigated a topographical distribution of managanese, and immunohistochemical density of tyrosine hydroxylase (TH), and histopathologic findings in globus pallidus and substantia nigra according to manganese dose and time course in the brain of rats which received MnCl2 intravenously. Topographical distribution of manganese was also investigated after injection of FeCl2. The manganese concentrations of brain in control and experimental group were highest in pituitary gland and thalamus, and lowest in the cerebral cortex. The manganese concentration of blood was increased proportionally to the dose administered, and the biological half-life of blood manganese was between 21 and 42 days. The manganese concentrations of brain were increased proportionally to the dose, and increase rate was highest in olfactory bulb, and the biological half-lives of brain manganese ranged from 42 days to 90 or more days; the longest were observed in pituitary gland, medulla oblongata and cerebral cortex. In case of administration of FeCl2, the manganese concentrations of brain were higher than that of control group in dose of 2.5 mg/kg, and decreased proportionally to the administered dose, resulting in lower level compared with control group in high dose of FeCl2 administered. Significantly decreased number of nerve cell and increased gliosis in globus pallidus were observed in experimental group, which were closely correlated with the duration after manganese injection, but no significant change of number of nerve cell expressing TH and gliosis were observed in substantia nigra. Density of immunohistochemical reaction for TH in globus pallidus made little difference between control and experimental group. These results suggest that pathology of manganese intoxication is caused by the loss of nerve cells in globus pallidus, and closely correlated with the duration after manganese exposure.
- Histopathologic Change and Apoptotic Profile in Basal Ganglia of Rat Induced by Manganese Administration.
- Chang Won Ha, Jong Im Lee, Jung Ran Kim, Tae Jung Jang, Ki Kwon Kim, Dong Hoon Kim
- Korean J Pathol. 2000;34(6):419-430.
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Abstract
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- Mn (manganese) is known to induce Parkinsonian neurological disorder. Several lines of evidence suggest that apoptosis is involved not only in physiological cell death during normal development but also in neurodegenerative disease. The mechanism of Mn induced cell death remains poorly understood. In the present study, we evaluated the morphologic changes and apoptotic profile in basal ganglia using rat model of Mn toxicity. The rats were divided into three groups: the first group was a control; the second group was subdivided by administration dosage of Mn into group A (5, 10 mg MnC12/ kg) and group B (20, 40 mg MnC12/kg). The rats of each subgroup received a injection of Mn via tail vein every week for 4 weeks. The second group received 4 repeated injection of 10 mg MnC12/kg in the same manner and the rats were sacrificed at day 1, 3 & 7 in group I and at day 10, 21, 42, and 90 in group II after the last injection. A significant loss of neuron and gliosis were observed in the basal ganglia in the experimental groups (p<0.05), which were more pronounced in group II than in the control or group I. No significant difference in number of nerve cells or degree of gliosis was identified in the substantia nigra. Apoptotic cells were also increased in basal ganglia of experimental groups and appeared among neurons (10%), glial cells (10%), and endothelial cells (60%). Apoptotic figures were consistently noted through the entire experimental period after Mn injection in basal ganglia. In conclusion, these results demonstrate that Mn-induced cytopathic insult affects various cell types in basal ganglia and shows variable sensitivity in the different regions of brain, especially in the apoptotic cell death of the neuron. The overaccumulation of Mn in the brain might be attributed from the breakdown of blood-brain barrier due to the injury through the apoptosis.
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