Plant growth under abiotic stress conditions significantly enhances intracellular generation of reactive oxygen species (ROS). Oxidative status of plant cells is directly affected by the modulation of iron homeostasis. Among mammals and plants, heme oxygenase-1 (HO-1) is a well-known antioxidant enzyme. It catalyzes oxygenation of heme, thereby producing Fe2+, CO and biliverdin as byproducts. The antioxidant potential of HO-1 is primarily due to its catalytic reaction byproducts. Biliverdin and bilirubin possess conjugated π-electrons which escalate the ability of these biomolecules to scavenge free radicals. CO also enhances the ROS scavenging ability of plants cells by upregulating catalase and peroxidase activity. Enhanced expression of HO-1 in plants under oxidative stress accompanies sequestration of iron in specialized iron storage proteins localized in plastids and mitochondria, namely ferritin for Fe3+ storage and frataxin for storage of Fe-S clusters, respectively. Nitric oxide (NO) crosstalks with HO-1 at multiple levels, more so in plants under oxidative stress, in order to maintain intracellular iron status. Formation of dinitrosyl-iron complexes (DNICs) significantly prevents Fenton reaction during oxidative stress. DNICs also release NO upon dissociation in target cells over long distance in plants. They also function as antioxidants against superoxide anions and lipidic free radicals. A number of NO-modulated transcription factors also facilitate iron homeostasis in plant cells. Plants facing oxidative stress exhibit modulation of lateral root formation by HO-1 through NO and auxin-dependent pathways. The present review provides an in-depth analysis of the structure-function relationship of HO-1 in plants and mammals, correlating them with their adaptive mechanisms of survival under stress.

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