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A Golgi and electron-microscopic study of cerebellum in methylmercury-poisoned neonatal mice
Abstract:
Neonatal C57BL/6J mice were injected with 5 mg/kg body weight of 203Hg-labeled methylmercuric chloride on postnatal days 3, 4, and 5, totaling 15 mg/kg body weight per animal. The experimental and control animals were sacrificed on postnatal by 15. Whole body radioactivity of 203Hg progressively increased during the 3-day injection period and reached the peak level and remained at peak levels until the time of sacrifice. This indicates a lack of clearance of 203Hg by neonatal mice during the period examined in this study. Golgi preparations of cerebella of MeHg-treated animals revealed significant reduction in dendritic arborization of Purkinje cells. Ultrastructurally, the vascular endothelium showed attenuation with increased electron density and frequent vacuolization of cytoplasm. Marked swelling of perivascular glia was noted in most of the capillaries throughout the cerebella of MeHg-treated animals.
Insights
Neonatal mice exposed to methylmercury (MeHg) showed no clearance of the toxin. This mercury accumulation caused significant damage to cerebellar Purkinje cells and associated vasculature.
Area of Science:
- Neuroscience
- Toxicology
- Developmental Biology
Background:
- Methylmercury (MeHg) is a potent neurotoxin.
- Neonatal exposure poses significant risks due to developing organ systems.
Purpose of the Study:
- To investigate the toxic effects of methylmercury on the developing cerebellum in neonatal mice.
- To assess the retention and distribution of methylmercury in neonatal mice.
Main Methods:
- Neonatal C57BL/6J mice were injected with 203Hg-labeled methylmercuric chloride over three days.
- Whole body radioactivity was measured to assess mercury clearance.
- Cerebellar tissue was analyzed using Golgi preparations and electron microscopy.
Main Results:
- 203Hg levels increased progressively and were retained in neonatal mice, indicating a lack of clearance.
- Significant reduction in dendritic arborization of Purkinje cells was observed.
- Ultrastructural changes included vascular endothelial attenuation, vacuolization, and swollen perivascular glia.
Conclusions:
- Neonatal exposure to methylmercury leads to significant accumulation in the body.
- Methylmercury exposure causes structural damage to cerebellar neurons and vasculature in developing mice.