Tandon S K, Khandelwal S, Jain V K, Mathur N
Industrial Toxicology Research Centre, Lucknow, India.
Sci Total Environ. 1994 Jun 6;148(2-3):167-73. doi: 10.1016/0048-9697(94)90393-x.
The influence of dietary iron deficiency on acute nickel, lead or cadmium toxicity as reflected by the induction of hepatic, renal, and intestinal metallothionein (MT), disposition of the metals and alterations in hematological parameters, was investigated in young rats to ascertain whether the toxic effects of these metals modify under anemic conditions. The administration of Cd induced hepatic, renal and intestinal MT while that of Ni or Pb induced hepatic MT only. While dietary Fe deficiency did not affect MT induction by Cd, it enhanced the synthesis of renal and intestinal MT by Ni and Pb. The accumulation of Pb in liver and kidney and that of Cd in liver only, were enhanced by Fe deficiency; the tissue deposition of Ni remained unaffected by Fe deficiency. The induction of hepatic MT by Ni, Pb or Cd appears to be related to the concomitant rise in the hepatic Zn, Ca and Fe levels in normal rats. However, dietary Fe deficiency increased the hepatic Zn in response to Ni or Cd and the hepatic Ca in response to Pb administration.
通过测定肝脏、肾脏和肠道金属硫蛋白（MT）的诱导情况、金属的分布以及血液学参数的变化，研究了膳食缺铁对急性镍、铅或镉毒性的影响，以确定在贫血条件下这些金属的毒性作用是否会发生改变。所用实验对象为幼鼠。镉的给药诱导了肝脏、肾脏和肠道的MT，而镍或铅的给药仅诱导了肝脏MT。虽然膳食缺铁不影响镉诱导MT，但它增强了镍和铅诱导的肾脏和肠道MT的合成。缺铁增强了铅在肝脏和肾脏中的蓄积以及镉仅在肝脏中的蓄积；镍在组织中的沉积不受缺铁影响。在正常大鼠中，镍、铅或镉诱导肝脏MT似乎与肝脏中锌、钙和铁水平的相应升高有关。然而，膳食缺铁会使大鼠肝脏对镍或镉的反应中锌含量增加，对铅给药的反应中钙含量增加。
