TY - JOUR
T1 - Delayed behavioral toxicity of lead with increasing exposure concentration
AU - Cory-Slechta, Deborah A.
AU - Weiss, Bernard
AU - Cox, Christopher
N1 - Funding Information:
’ This work was supported in part by Grants ES-O 1247, ES-O 1248, ES-03054, and Postdoctoral Fellowship ES-01577 from the National Institute of Environmental Health Sciences and by contract No. DE-ACOZ-76EV03490 with the U.S. Department of Energy at the University of Rochester Department of Radiation Biology and Biophysics and has been assigned Report No. UR-3490-2 19 1. We thank Deena Burdick for technical assistance. 2 Author to whom reprint requests should be sent.
PY - 1983/12
Y1 - 1983/12
N2 - Twenty-one-day-old male Long-Evans hooded rats were exposed chronically to drinking solutions containing 500 ppm sodium acetate (controls) or 50, 100, or 500 ppm lead acetate. Performance on a fixed interval 1-min schedule of food reinforcement was assessed over 155 sessions. Blood lead values were monitored serially and brain lead determinations made at the end of testing (335 days of lead exposure). The lowest concentration of lead in the drinking water was associated with increases in the rate of fixed-interval responding over the first 30 sessions. At the two higher concentrations, response rate values similar to controls over the first 40 sessions were followed by rate increases. The latency to maximum rate depended on concentration; the highest concentration was associated with the longest latency. Response rates of rats exposed to 50 ppm lead gradually returned to control levels after 120 sessions, while increased rates were sustained in rats at 100 and 500 ppm lead, even 100 days after lead exposure was terminated. Marked individual differences in susceptibility to lead-induced rate increases were observed in all treatment groups. Serial blood lead values were related both to exposure concentration and duration. Brain lead values also reflected exposure concentrations. Blood-brain ratios averaged 0.743 to 0.913, which agree with other data for the rat and human. These results confirm the vulnerability to lead of rats beyond the neonatal period, and extend the range of conditions under which such effects occur.
AB - Twenty-one-day-old male Long-Evans hooded rats were exposed chronically to drinking solutions containing 500 ppm sodium acetate (controls) or 50, 100, or 500 ppm lead acetate. Performance on a fixed interval 1-min schedule of food reinforcement was assessed over 155 sessions. Blood lead values were monitored serially and brain lead determinations made at the end of testing (335 days of lead exposure). The lowest concentration of lead in the drinking water was associated with increases in the rate of fixed-interval responding over the first 30 sessions. At the two higher concentrations, response rate values similar to controls over the first 40 sessions were followed by rate increases. The latency to maximum rate depended on concentration; the highest concentration was associated with the longest latency. Response rates of rats exposed to 50 ppm lead gradually returned to control levels after 120 sessions, while increased rates were sustained in rats at 100 and 500 ppm lead, even 100 days after lead exposure was terminated. Marked individual differences in susceptibility to lead-induced rate increases were observed in all treatment groups. Serial blood lead values were related both to exposure concentration and duration. Brain lead values also reflected exposure concentrations. Blood-brain ratios averaged 0.743 to 0.913, which agree with other data for the rat and human. These results confirm the vulnerability to lead of rats beyond the neonatal period, and extend the range of conditions under which such effects occur.
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U2 - 10.1016/0041-008X(83)90021-2
DO - 10.1016/0041-008X(83)90021-2
M3 - Article
C2 - 6658785
AN - SCOPUS:0021026882
SN - 0041-008X
VL - 71
SP - 342
EP - 352
JO - Toxicology and Applied Pharmacology
JF - Toxicology and Applied Pharmacology
IS - 3
ER -