EFFECT OF TREATMENT WITH MERCURY-CHLORIDE AND LEAD ACETATE DURING THE2ND STAGE OF RAPID POSTNATAL BRAIN GROWTH ON DELTA-AMINOLEVULINIC-ACID DEHYDRATASE (ALA-D) ACTIVITY IN BRAIN, LIVER, KIDNEY AND BLOOD OF SUCKLING RATS

The sensitivity of developing rodents to toxic metals differs consider ably from that of adults. In the present study, we investigated the in vivo and in vitro effects of inorganic mercury and lead on delta-amin olevulinic acid dehydratase (ALA-D) from brain, liver, kidney and bloo d of young rats. Eight day-old rats were injected with one or five dos es of lead acetate (0, 3.5, or 7.0 mg/kg) or HgCl2 (0, 2.5, or 5.0 mg/ kg). In vitro, the IC50 for mercury inhibition of cerebral, renal and hepatic ALA-D was in the 124 to 160 mu M range, while values for lead acetate was in the 7 to 12 mu M range. The IC50 of blood enzyme for le ad (0.8 mu M) and mercury (6.5 mu M) was significantly lower than that observed for the other tissues. A single dose of lead did not affect the enzyme activity, but a single dose of HgCl2 (5 mg/kg) caused a sig nificant inhibition of ALA-D from kidney (40%, P < 0.01) and liver (25 %, P < 0.05). Five doses of lead acetate (3.5 or 7 mg/kg) caused an in hibition of about 25 and 40%, respectively (P < 0.01), of hepatic ALA- D, and an increase of 1.4-fold (P < 0.05) and 2.6-fold (P < 0.01) of b lood enzyme, respectively. Treatment with five doses of HgCl2 (5 mg/kg ) caused an inhibition of about 25, 60, 50, and 80% of ALA-D from brai n, blood, liver and kidney, respectively (all P < 0.05). Five doses of 2.5 mg/kg HgCl2 caused an inhibition of ALA-D from liver (40%, P < 0. 01) and kidney (45%, P < 0.01). These results demonstrate that ALA-D f rom young rat tissues show different sensitivities to mercury and lead . The enzyme was more affected by mercury than by lead in vivo, while in vitro lead was more potent that mercury as an ALA-D inhibitor.