ATLA::Alternatives to Laboratory Animals

Volume 23, Number 4

Defence mechanisms protecting glial cell cultures against the toxicity of lead.

ATLA 23, 513-520, July/August 1995

Inger K. Grundt, Marvelyn Rise and Harald Nyland

Department of Clinical Biology, Division of Biochemistry and Department of Neurology University of Bergen, Haukeland Sykehus, N-5021 Bergen, Norway

SUMMARY

Several defence mechanisms against the toxicity of triethyllead (TEL) in cultures of glial cells have been studied. In contrast to cultures of glioma C6 cells, primary cultures of glial cells generated a resistance to the toxicity of TEL, which increased with the age of the cultures.

When the time of exposure of glial cells was extended from 24 hours to 6 days and the cells were exposed to increasing doses of TEL, the activities of several metabolic enzymes were stimulated by concentrations of TEL over 10^-7 M. Among these were glucose-6-phosphatedehydrogenase and acid phosphatase. On the other hand, lactate dehydrogenase activity was not significantly affected under these experimental conditions.

When the cultures were exposed to 10^-8 M TEL, the cellular calcium content increased and the potassium content fell. This indicates that the activation of metabolic enzymes is a response to early events in the toxic process, which include disturbances in calcium metabolism. When glial cells were incubated with lead and selenium simultaneously, the uptake of lead into the cells was reduced, and the cellular calcium content was increased by selenium.

Keywords: glial cells, lead toxicity, glucose-6-phosphate-dehydrogenase, acid phosphatase, calcium, selenium