Effects of low oral lead and cadmium exposure and zinc status of heme metabolites in weanling rats.

The effects of moderate zinc deficiency and low oral lead and cadmium exposure on metabolites of porphyrin synthesis were investigated in weanling rats. Groups of weanling Sprague-Dawley rats (6/group) were fed diets containing either zinc (Zn) deficient (Zn D), pair-fed (Zn PF), Zn high (Zn H) or control (Zn C) and given sodium (10 micrograms/mL as NaCl), lead (20 micrograms/mL as Pb acetate) or cadmium (5 micrograms/mL as CdCl2) in drinking water for 4 weeks. Porphyrins in tissues were analyzed by HPLC. Feeding of zinc deficient diets decreased food intake and body weight of rats; plasma and erythrocyte zinc levels were 60 and 27% less than the control group, respectively. Kidney was the target organ for lead and cadmium accumulation. The concentration of lead in tissues were about: kidney = 98 micrograms/g; liver = 74 micrograms/g; whole blood = 22 micrograms/mL. Porphyrin intermediates detected in tissues were: heptaporphyrin, pentaporphyrin, coproporphyrin and protoporphyrin. The Zn D diet increased protoporphyrin concentrations in the liver by nearly 100% (P < or = 0.05), but exposure to Pb or Cd decreased protoporphyrin to levels found in the Zn C group. Erythrocyte protoporphyrin concentrations were evaluated by 21% in Zn D rats; other metabolites were unchanged. In the kidney coproporphyrin was slightly higher in ZN D + Pb group. Low oral Cd exposure had no effect on porphyrin metabolites in all tissues. These results suggest that Zn deficiency triggers the accumulation of protoporphyrin in the liver and to some extent in the erythrocytes, and enhances renal coproporphyrin accretion in low lead exposed rats.