Astroglial reaction during the early phase of acute lead toxicity in the adult rat brain.
The developing nervous system is susceptible to lead (Pb) exposure but less is known about the effect of this toxic agent in adult rat brain. Since astrocytes serve as a cellular Pb deposition site, it is of importance to investigate the response of astroglial cells in the adult rat brain in a model of acute lead exposure (25 mg/kg b.w. of lead acetate, i.p. for 3 days). An increased immunoreactivity of glial fibrillary acidic protein (GFAP) on Western blots was noticeable in fractions of astroglial origin-glial plasmalemmal vesicles (GPV) and in homogenates from the hippocampus and cerebral cortex but not in the cerebellum. The features of enhanced astrocytic reactivity (i.e. large accumulation of mitochondria, activated Golgi apparatus and increment of gliofilaments) were observed in electron microscopy studies in the same tissues. Total glutathione levels increased both in GPV fractions and in brain homogenates-in the cerebellum (120% above control) and in hippocampus (30% above control). The results of current studies indicate that acute lead exposure is accompanied by astrocyte activation connected with the presence of the enhanced expression of GFAP. It may indicate lead-induced neuronal injury. At the same time, a regional enhancement of detoxicative mechanisms (GSH) was noticed, suggesting activation of astrocyte-mediated neuroprotection against toxic Pb action.
Struzyñska
L
L
Department of Neurochemistry, Laboratory of Pathobiochemistry of the Central Nervous System, Medical Research Centre, Polish Academy of Sciences, 5 Pawiñskiego St., 02-106, Warsaw, Poland. lidkas@cmdik.pan.pl
Bubko
I
I
Walski
M
M
Rafałowska
U
U
D000208:Acute Disease; D000818:Animals; D001253:Astrocytes / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology*; D015153:Blotting, Western; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D008658:Inactivation, Metabolic; D020263:Lead Poisoning, Nervous System / Q000378:metabolism / Q000473:pathology*; D008297:Male; D008854:Microscopy, Electron; D009942:Organometallic Compounds / Q000097:blood / Q000493:pharmacokinetics / Q000633:toxicity; D051381:Rats; D017208:Rats, Wistar
D005904:Glial Fibrillary Acidic Protein; D009942:Organometallic Compounds; D005978:Glutathione; C008261:lead acetate