Table 3.

Heme oxygenase (HO)-1 as a therapy against heme toxicity in experimental disease models.

Experimental disease model	Therapeutic strategy	Specific protective effect	References
Glycerol-induced acute kidney injury in rat (Sprague Dawley)	Preconditioning of HO-1 using hemoglobin (30 mg/100 g body weight) 20 h prior to injection with glycerol	Protection from kidney failure Reduced mortality	Nath et al., 1992
Glycerol-induced acute kidney injury in mouse (C57BL/6)	Preconditioning of HO-1 using GM-CSF (200 mg/kg body weight) for 5 consecutive days prior to injection with glycerol	Reduced blood urea nitrogen levels Reduced tissue damage Reduced mortality	Wei et al., 2011
Exposure to bromine gas in mouse (C57BL/6)	Genetic overexpression of human HO-1 using (BAC)	Attenuated bromine-induced heme levels in plasma and lung Reduced bromine-induced cytokine/chemokine levels Reduced mortality	Nagy et al., 2010
Malaria PCC-infected mouse (DBA/2)	Liver-specific overexpression of HO-1 using recombinant adenovirus	Blocked hepatic failure indicated by the decrease in AST and reduced tissue necrosis Prevented mortality	Seixas et al., 2009
S+S-Antilles SCD mouse (C57BL/6)	Liver targeted rat HO-1 gene delivery by Sleeping Beauty transposase system	Reduced hypoxia-induced stasis in dorsal skin fold chambers	Belcher et al., 2006

AST, aspartate amino transferase; BAC, bacterial artificial chromosome.