Methods PC12 cells were exposed to 0μmol/L, 12.5μmol/L, 25μmol/L, 50μmol/L, 100μmol/L, 200μmol/L, 400μmol/L, 800μmol/L and 1600μmol/L lead acetate for 24 hours. The IC_ 50 value was measured by MTT assay.
Methods PC12 cells were exposed to 0(control), 62.5, 125.0, 250.0, and 500.0 μmol/L lead acetate for 12, 24, 36, 48, 60, 72 hours, respectively, and then caspase-6 and -9 activities were determined by colorimetric assay.
Results When PC12 cells were exposed to 250.0 μmol/L lead acetate for 24 hours, caspase-6 activity increased, and reaching its peak at 48 hours (5.75-fold of control group, P < 0.01) and was still significantly higher than that of control group at 72th hour( P < 0.01).
In this study ,changes of cellular vitalities ,cellular K +contents,supernatant LDH and r-GT activity of cullured LLC-PK1 cell induced by 1,5,10,50 ,100μmol/L acetate lead (Pb) were investigeted ,the results showed that the cellular vitality decreased signiffcantly after 32 hours of 50and 100μmol/L. Pb treatment;
Methods: Chronic lead treated animal models were acquired by feeding the male postwean Wistar rats with 0.015%,0.10%,0.15% acetate lead in drinking water for 3 months,[Ca 2+ ] i was determined after LTP of hippocampus was induced by high frequency stimulation (HFS).
After the weanling male Wistar rats were fed 0.2% acetate lead water for 90～108 days,blood lead and brain blood lead,the induction rate of LTP,the concentration of Ca 2+ and the activities of protein kinase C(PKC) in the neurons of rat hippocampal dentate gyrus(DG) were measured in order to probe into the mechanisms of lead induced impairment on learning and memory functions.