THE EFFECT OF LEAD-EXPOSURE AND SERUM DEPRIVATION ON MESENCEPHALIC PRIMARY CULTURES

The effect of Pb2+ was studied in embryonic mesencephalic primary cult ures that contain neurons and glia. Pb2+ exposure in absence of serum, damaged more efficaciously the cultured cells than Pb2+ exposure in p resence of serum. In serum-free medium, Pb2+ elicited mainly necrosis and apoptosis in maximally 13 % of the cells in culture. The glial fib rillary acidic protein (GFAP) content was decreased by Pb2+ exposure i n serum-containing medium. The abundance of GFAP was also decreased by serum deprivation that was augmented by the addition of 12.5 mu M Pb2 + in, serum-free medium. A 6h exposure to 6 mu M Pb2+ in serum-free me dium also lowered the low affinity H-3-D-aspartate uptake. A 6h exposu re of mesencephalic cells to 3-25 mu M Pb2+ in serum-free medium faile d to alter the number of tyrosine hydroxylase-and calretinin-immunorea ctive cells, whereas, 50 mu M Pb2+ obliterated both cell types. A 6h e xposure of cells to 3 mu M Pb2+ in serum-free medium decreased H-3-dop amine uptake by 50 % and 12.5 mu M Pb2+ obliterated it. Addition of al bumin to serum-free medium failed to prevent the Pb2+-elicited inhibit ion of [H-3]-dopamine uptake suggesting that the serum-afforded delay of cell death may not be due to a removal of reactive Pb2+ by protein/ chelate formation but rather to the Pb2+-scavenging function of glial cells. Serum deprivation may exacerbate the Pb2+-induced neurotoxicity presumably by impairing the metal scavenging function of astrocytes. (C) 1997 Inter Press, Inc.