Protective effect of zinc ions against lead and nickel induced inhibition of δ-aminolevulinic acid dehydratase activity in mice liver

The present study was devoted to assess the ability of zinc (Zn) to protect heme synthesis system from Pb and Ni toxicity and to compare toxic effects of lead (Pb) and nickel (Ni) to the activity of one of heme synthesis enzymes δ-aminolevulinic acid dehydratase (δ-ALAD), after single and 2-week exposure. Material and methods: For the single metal exposure, mice were injected once i.p. with a solution of Pb(CH3COO)2 (242 μmol Pb/1 kg b.w.); NiCl2 (96 μmol Ni/1 kg b.w.) or ZnSO4 (24 μmol Zn/1 kg b.w.). For the repeated exposure, mice were i.p. injected for 14 days (once a day) with Pb(CH3COO)2 (48 μmol Pb/1 kg b.w.); NiCl2 (19 μmol Ni/1 kg b.w.) or ZnSO4 (24 μmol Zn/1 kg b.w.) solution. The control mice received i.p. injections of saline. The activity of δ-ALAD was examined according to the method of Sassa [1]. For the determination of reaction product porphobilinogen the modified Ehrlichs reagent was used. Absorbance was measured at the wavelength 555 nm. Statistical analysis was performed using a statistical software package (Statistica 6.0). p-value less than 0.05 was considered statistically significant. Results: Single exposure to Pb2+ decreased δ-ALAD activity in mice liver and blood by 74% and 99%, respectively, exposure to NiCl2 did so, however, not so drastically by 38% (in liver) and 53% (in blood). Though single exposure to ZnSO4 did not have any effect on the δ-ALAD activity neither in the liver, nor in the blood, Zn pre-treatment diminished the suppressing effect of Pb, increasing the liver and blood enzyme activity by 87% and 580%, respectively, as compared to the Pb treated mice group (p < 0.05). Single Zn2+ pre-treatment, 20 minutes before NiCl2 injections, completely restored enzyme activity to the control level in liver and blood of mice (Figure 1). Repeated administration of Pb(CH3COO)2 inhibited liver and blood δ-ALAD activity by 73% and 92% respectively, while repeated NiCl2 administration suppressed enzyme activity [...].