ABSTRACT
<p><b>OBJECTIVES</b>To study the effect of lead acetate on the expression of nerve growth factor (NGF) protein in rat brain and the regulation of thyroid hormone.</p><p><b>METHODS</b>Lead acetate was given to SD rats intraperitoneally ip. at the dosage of 25, 50 and 100 mg/kg respectively. 6-n-propyl-2-thiouracil (PTU) was used to make a hypothyroid model and then lead acetate was given at the dosage of 50 mg/kg body weight through i.p. The NGF protein expression in rat brain was observed by immunohistochemistry Triiodothyronine (T3), thyroxin (T4), TSH in serum and T3, T4 in brain tissue were determined by radio immunoassays (RIAs).</p><p><b>RESULTS</b>The average gray value of NGF protein in cerebral cortex of 50 mg, 100 mg treated groups (180.49 +/- 10.33, 169.72 +/- 19.75, respectively) were lower than the control (200.75 +/- 3.27, P<0.01). The area density of NGF protein in hippocampus of three treated groups (0.08 +/- 0.14, 0.12 +/- 0.02, 0.13 +/- 0.04, respectively) were significantly different from the control (0.025 +/- 0.015, P<0.05). The area density and the average gray value of NGF protein in lead acetate treated hypothyroid rat brain were of no significant changes. The levels of serum T3 in three treated groups [(0.68 +/- 0.02), (0.57 +/- 0.04), (0.54 +/- 0.02) microg/L respectively] and T4 [(28.30 +/- 1.83), (27.35 +/- 2.55), (24.00 +/- 3.01) microg/L] in serum were significantly lower while TSH [(6.34 +/- 1.13), (7.74 +/- 0.79), (9.16 +/- 0.77) IU] higher than those in the control [T3 (0.97 +/- 0.14) microg/L, T4 (54.50 +/- 3.70) microg/L and TSH (4.62 +/- 2.16) IU], and there was a good dose-response relationship. The levels of T3 in cerebral cortex of three treated groups [(13.26 +/- 0.81), (11.49 +/- 0.10), (10.42 +/- 1.19) pg/mg pro respectively] and T4 [(0.50 +/- 0.03), (0.49 +/- 0.13), (0.42 +/- 0.01) ng/mg pro] were significantly lower than those in control [(20.85 +/- 11.01) pg/mg pro, (0.76 +/- 0.14) ng/mg pro, P<0.05, P<0.01].</p><p><b>CONCLUSION</b>Lead could increase the NGF protein expression in rat brain, which may be regulated by thyroid hormone.</p>