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Experimental lead neuropathy: Inorganic lead inhibits proliferation but not diffrentiation of Schwann cells
Author(s) -
Sobue Gen,
Pleasure David
Publication year - 1985
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410170508
Subject(s) - galactocerebroside , lead acetate , schwann cell , cyclic adenosine monophosphate , myelin , chemistry , endocrinology , medicine , sciatic nerve , wallerian degeneration , microbiology and biotechnology , adenosine , biochemistry , biology , neuroscience , toxicity , central nervous system , receptor , oligodendrocyte
Schwann cells were prepared from the sciatic nerves of newborn rats and cultured in a monolayer. Addition of lead acetate at concentrations between 0.4 and 10.0 μmUg/ml, levels comparable to those occurring in neural tissues and physiological fluids of lead‐intoxicated rats, diminished both the baseline rate of proliferation of the Schwann cells and their response to the mitogens, axolemmal fragment, glial growth factor, and the adenosine 3′:5′‐cyclic monophosphate (cAMP) analogues 8‐bromo‐cAMP and dibutyryl‐cAMP. This demonstrates a direct toxic effect of inorganic lead on Schwann cell. Lead acetate in this concentration range did not, however, inhibit the cAMP analogue‐induced appearance of the “myelin marker” lipid galactocerebroside on the surfaces of the cultured Schwann cells.