Klauder D S, Petering H G
J Nutr. 1977 Oct;107(10):1779-85. doi: 10.1093/jn/107.10.1779.
Lead-induced anemia in rats, which is of a microcytic, hypochromic type, has been shown to be a result of an interference with the metabolism of copper and iron. In this complex interaction, copper may be the target upon which ingested lead has its antagonistic effect on hematopoiesis. The depressions in hematocrit and hemoglobin levels resulting from exposure to lead may occur secondarily to the effects of a lead-induced copper deficiency on iron mobilization and utilization. The metabolic fault induced by lead is seen in a reduction of serum iron, elevation of serum iron binding capacity, and increase in liver iron, all manifestations of systemic effects related to an interference with copper metabolism. These results relate many of the characteristics of the lead-induced anemia to those found in the copper-deficiency anemia.
大鼠铅诱导的贫血属于小细胞低色素型,已被证明是铜和铁代谢受到干扰的结果。在这种复杂的相互作用中,铜可能是摄入的铅对造血产生拮抗作用的靶点。接触铅导致的血细胞比容和血红蛋白水平降低,可能继发于铅诱导的铜缺乏对铁动员和利用的影响。铅引起的代谢缺陷表现为血清铁降低、血清铁结合能力升高和肝脏铁增加,所有这些都是与铜代谢干扰相关的全身效应的表现。这些结果将铅诱导贫血的许多特征与铜缺乏性贫血中的特征联系起来。