The intracellular free calcium (Ca2+) or lead (Pb(i)2+) ions were measured by using 19F-NMR and 1,2-bis(2-amino-5-fluorophenoxy)ethane-N,N,N',N'-tetraacetic acid in brain slices obtained from control rats and rats chronically exposed to 1 mg/kg.day or 100 mg/kg.day dose of Pb acetate ingestion. The basal Ca(i)2+ values obtained in this study were comparable to the values reported previously for brain neurons by using the Fura-2 method (Singh, 1993a). The concentrations of total Pb in blood samples obtained from 2-week old rats exposed to 1 and 100 mg/kg.day doses of lead acetate were 31 and 521 μg/dl respectively. The concentrations of total Pb in brain samples obtained from 2-week old rats exposed to 1 and 100 mg/kg.day doses of lead acetate were 150 and 2700 ng/g respectively. The concentration of Pb in neonatal and adult samples did not differ significantly. Free Pb2+ was not detected in samples obtained from the rats exposed to a Pb dose of 1 mg/kg.day; however, a small concentration (ranging from 100 to 300 pM) of the ion was detected in samples obtained from the rats exposed to a Pb dose of 100 mg/kg.day. This suggests that either a small proportion of total Pb is ionized in brain or there is an efflux of Pb2+ from intracellular fluid into the incubation medium. Depolarization caused significant increase in Ca(i)2+ in cortical slices obtained both from control and Pb-exposed rats. However, depolarization increased Pb(i)2+ only in samples obtained from rats exposed to a Pb dose of 100 mg/kg.day. Chronic Pb exposure significantly reduced the effects of depolarization on Ca(i)2+ levels. Since there is very little extracellular Pb2+ remaining in the slices, the observed decrease in depolarization-induced Ca(i)2+ may not be because of the inhibition by Pb2+ in the influx of Ca2+ but because of long-term changes in cellular metabolism.
|Original language||English (US)|
|Number of pages||6|
|State||Published - Jan 1 1995|
- brain slices
- intracellular calcium
- intracellular lead