Cross-linked hemoglobin (alpha alpha-Hb) may be a useful red blood cell substitute if it can be
administered safely. However, cell-free hemoglobin has inherent properties that may cause oxidant-mediated toxicity.
We investigated whether alpha alpha-Hb induces oxidative or inflammatory responses that lead to liver damage.
alphaalpha-Hb (0.5 or 1.0 gm/kg) was infused into rats, and indices of liver injury, inflammation, and oxidative
stress were examined. Although focal hepatic necrosis was noted at 24 hours, plasma alanine aminotransferase
activity was not increased and lesions were resolved by 48 hours. Modest neutrophil accumulation in hepatic vessels,
but not sinusoids, occurred at 24 hours. Heme oxygenase-1 (HO-1) protein and activity were induced in a dose- and time-dependent
manner, with maximal induction at 24 hours. Plasma tumor necrosis factor alpha levels were not significantly increased. Additional
cytokine- and oxidant-mediated events such as nuclear transcription factor-kappaB activation and nitric oxide synthase induction
were not observed. These results suggest that alphaalpha-Hb-derived products such as heme and ferric iron (Fe3+), potent inducers
of HO-1, are responsible for increasing HO-1. HO-1 induction may be a protective response by the liver to metabolize excess heme
and Fe3+, thereby providing antioxidative products to counter the potentially damaging oxidants produced by Fe3+-catalyzed reactions.
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