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 delta-aminolevulinic acid dehydratase (delta-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 mu mol Pb/l kg b.w.); NiCl2 (96 mu mol Ni/l kg b.w.) or ZnSO4 (24 mu mol Zn/l kg b.w.). For the repeated exposure, mice were i.p. injected for 14 days (once a day) with Pb(CH3COO)(2) (48 mu mol Pb/l kg b.w.); NiCl2 (19 mu mol Ni/l kg b.w.) or ZnSO4 (24 mu mol Zn/l kg b.w.) solution. The control mice received i.p. injections of saline. The activity of delta-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 delta-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 delta-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 delta-ALAD activity by 73% and 92% respectively, while repeated NiCl2 administration suppressed enzyme activity only in the liver (by 32%). Repeated ZnSO4 administration did not affect the delta-ALAD activity neither in the liver nor in the blood, while Zn2+ pretreatment recovered Pb's suppressed enzyme activity in mice liver, as well as blood, respectively by 40% and 20%. After 14 days Zn2+ did not provide protection against Ni2+ induced delta-ALAD inhibition neither in the liver nor in the blood of mice.