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THE EFFECT OF CHRONIC DOSING WITH MERCURIC CHLORIDE ON DORSAL ROOT AND TRIGEMINAL GANGLIA OF RATS
Author(s) -
JACOBS JEAN M.,
CAVANAGH J. B.,
CARMICHAEL N.
Publication year - 1975
Publication title -
neuropathology and applied neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.538
H-Index - 95
eISSN - 1365-2990
pISSN - 0305-1846
DOI - 10.1111/j.1365-2990.1975.tb00656.x
Subject(s) - neurotoxicity , mercury (programming language) , endoplasmic reticulum , chemistry , sciatic nerve , mercury poisoning , ultrastructure , toxicity , pathogenesis , axon , pathology , anatomy , biology , medicine , biochemistry , computer science , programming language
Rats have been dosed repeatedly with 1.08 mg/kg of HgCl 2 for up to 70 days and studied ultrastructurally. After two weeks, focal areas of disruption of endoplasmic reticulum (ER) occur in the neurons of the spinal ganglia; other features are present that are found also in methyl mercury intoxication in this species. At 1 month and longer on this dosing schedule a constant finding is loss of ribosomes from the rough ER of some neurons which persisted throughout the study. Occasional axon degeneration was found in the sciatic nerves of those animals having received the largest doses of HgCl 2 . Alterations in vascular endothelial cells and enlargement and other abnormalities in mitochondria of the neurones of spinal ganglia were also found. Because of similarities in the ultrastructural changes in the early phases of methyl mercury intoxication and those in chronic HgCl 2 intoxication, it is suggested that degraded inorganic mercury may be important in the pathogenesis of the intracellular disturbances in methyl mercury poisoning. It is suggested that the excessive neurotoxicity of methyl mercury compounds may reside in the lipid solubility of these compounds and hence their ready capacity to enter cells.