Dissociation into dimers (Chang, 1988; Elmer et al., 2012) | • Overloading the renal tubular cells (renal failure) |
Nitric oxide (NO) stealing property mainly from the endothelial cell layer (Doherty et al., 1998; Olson et al., 2004; Cabrales and Friedman, 2013; Alayash, 2014) | • Systemic and pulmonary vasoconstriction (myocardial damage pulmonary hypertension) |
| • Lack of mediator of thrombocyte aggregation and adhesion (impaired clotting) |
| • Gastrointestinal side effects |
Local hyperoxia due to decreased oxygen affinity (no diffusion barrier existent) (McCarthy et al., 2001; Alayash, 2014) | • Systemic hypertension |
Auto-oxidation (Buehler et al., 2010; Scurtu et al., 2013; Alayash, 2014) | • Nonfunctional hemoglobin |
| • Formation of superoxide ions |
| • Altering transcriptional activity of heme oxygenase and other antioxidant enzymes |