Heme oxygenase induction - A possible factor in aluminum-associated anemia

Barbara Fulton, Elizabeth H. Jeffery

Research output: Contribution to journalArticlepeer-review


The effect of repeated parenteral administration of aluminum (Al) was investigated to determine if a relationship exists between the severity of anemia and increase in hepatic heme oxygenase activity. Female Swiss Webster mice were dosed for 11 d with 50 mg Al/kg, as Al lactate, and sodium lactate was given to control mice. On d 12, hematocrit, hemoglobin, blood smears, hepatic heme oxygenase activity, and cytochrome P450 levels were assessed. Significant decreases in hematocrit (39.1±0.7 vs 43.1±0.3% in controls) and hemoglobin (13.1±0.4 vs 14.2±0.2 g/dL in controls) were produced by Al administration. Blood smears from Al-treated mice consistently showed smaller, more irregular red cells. Cytochrome P450 content was significantly decreased (0.443±0.043 vs 0.665±0.055 nmol/mg) whereas hepatic heme oxygenase activity was significantly increased (2.75±0.34 vs 1.66±0.20 nmol/mg/h) in Al-treated animals. The production of mild anemia by parenteral aluminum correlated significantly with the increase in heme oxygenase activity, which, although only 66% greater than in control, preceded a significant loss of cytochrome P450. The increased heme oxygenase activity, with subsequent increased destruction of heme and/or heme proteins is discussed as a possible mechanism for the microcytic, hypochromic anemia associated with Al overload.

Original languageEnglish (US)
Pages (from-to)9-19
Number of pages11
JournalBiological Trace Element Research
Issue number1
StatePublished - Jan 1 1994


  • Aluminum
  • anemia
  • cytochrome P450
  • hematocrit
  • heme oxygenase
  • hemoglobin
  • mice

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Clinical Biochemistry
  • Biochemistry, medical
  • Inorganic Chemistry


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