Ik. Grundt et al., DEFENSE-MECHANISMS PROTECTING GLIAL-CELL CULTURES AGAINST THE TOXICITY OF LEAD, ATLA. Alternatives to laboratory animals, 23(4), 1995, pp. 513-520
Several defence mechanisms against the toxicity of triethyllead (TEL)
in cultures of glial cells have been studied. In contrast to cultures
of glioma C-6 cells, primary cultures of glial cells generated a resis
tance to the toxicity of TEL, which increased with the age of the cult
ures. When the time of exposure of glial cells was extended from 24 ho
urs to 6 days and the cells were exposed to increasing doses of TEL, t
he activities of several metabolic enzymes were stimulated by concentr
ations of TEL over 10-(7)M. Among these were glucose-6-phosphate-dehyd
rogenase and acid phosphatase. On the other hand, lactate dehydrogenas
e activity was not significantly affected under these experimental con
ditions. When the cultures were exposed to 10(-8)M. TEL, the cellular
calcium content increased and the potassium content fell. This indicat
es that the activation of metabolic enzymes is a response to early eve
nts in the toxic process, which include disturbances in calcium metabo
lism. When glial cells were incubated with lead and selenium simultane
ously, the uptake of lead into the cells was reduced, and the cellular
calcium content was increased by selenium.