NICKEL TOXICITY TO HUMAN TERM PLACENTA - IN-VITRO STUDY ON LIPID-PEROXIDATION

It has been reported that nickel (Ni) crosses the human placenta and p roduces teratogenesis and embryotoxicity. In the present study, the ef fects of nickel on human term placentas were investigated. In time-cou rse experiments, placental tissue was incubated for 3, 6, 12, or 24 h with 2.5 mM Ni. The viability as determined by glucose consumption rat e did not show any significant change from 3 to 12 h, whereas the perm eability, lipid peroxidation, and Ni concentration were significantly increased compared to the control. In concentration-response studies, placental explants were incubated with 0.5, 1.0, 2.5, or 5 mM Ni for 1 2 h. The viability did not change significantly, except for 5 mM Ni, b ut the permeability and lipid peroxidation increased markedly in a con centration-dependent manner. Treatment with ascorbic acid or Zn decrea sed placental lipid peroxidation and permeability induced by Ni, but h ad no effect on lowering the Ni tissue content. Data show that Ni is t oxic as evidenced by lipid peroxidative damage to placental membrane, and this metabolic change may be responsible for decreased placental v iability, altered permeability, and potential subsequent embryotoxicit y.