## 3 Oxidative Stress Biomarkers Involved in Psoriasis Inflammation
### Myeloperoxidase (MPO)  
Myeloperoxidase (MPO) serves as a pivotal enzyme primarily derived from neutrophils, key players in the immune response, and, to a lesser extent, from monocytes. It plays a crucial role in the innate immune system's defense against pathogens, particularly bacteria and fungi. Upon activation, neutrophils release MPO, which catalyzes the conversion of hydrogen peroxide (H\({}_{2}\)O\({}_{2}\)) and chloride ions (Cl\({}^{-}\)) into hypochlorous acid (HOCI), a potent oxidizing agent, thereby generating reactive oxygen species (ROS) to combat invading pathogens and support host defense mechanisms [19]. The production of ROS and hypochlorous acid (HOCI) during an inflammatory response via MPO contributes to oxidative stress that damages mitochondrial DNA and impairs mitochondrial function within the skin [20]. Given that MPO serves as a biomarker for the activation of neutrophils and monocytes, the oxidative stress caused by elevated MPO can worsen mitochondrial dysfunction, thereby contributing to the psoriasis etiopathogenesis [20]. In the context of psoriasis, dysregulated immune responses result in the infiltration of activated neutrophils into affected skin lesions. Elevated MPO levels have been observed in psoriasis-related skin lesions, indicating heightened inflammation and neutrophil activation. Excessive or dysregulated MPO activity can lead to tissue damage and contribute to the pathogenesis of various inflammatory conditions, including autoimmune diseases like psoriasis [20]. A study conducted observed that the MPO levels were greater in psoriasis patients' serum and skin compared to controls [20]. A study on children with psoriasis showed that they had significantly higher MPO levels and activity than healthy controls [21]. A study also observed that psoriatic lesions have elevated MPO levels, which positively correlate with the severity of the illness [22]. This heightened MPO activity can lead to tissue damage and exacerbate the inflammatory processes underlying psoriasis. Figure 1: Summary of oxidative stress biomarkers in psoriasis inflammation. This figure illustrates key oxidative stress biomarkers involved in the inflammatory processes of psoriasis. The biomarkers depicted, including myeloperoxidase (MPO), paraoxonase (PON), sirtuins (SIRTs), superoxide dismutase (SOD), and catalase (CAT), are emerging as critical indicators of psoriasis pathogenesis. The red arrows indicate decreasing, while green arrow represent increasing. MPO-derived ROS contribute to oxidative damage to lipids, proteins, and DNA, crucial steps in psoriasis pathogenesis that perpetuate inflammatory processes. Tracking MPO activity and levels provides insights into the extent of oxidative stress and inflammation in psoriasis, serving as potential biomarkers for disease severity and progression. Targeting MPO expression or activity presents a potential therapeutic approach to mitigate inflammation and oxidative damage in psoriasis and other inflammatory conditions. In a study using a mouse model of plaque psoriasis induced by Aldara (imiquimod) cream, researchers investigated the impact of MPO inhibition on psoriatic skin lesions [23]. Researchers created an innovative method for evaluating the severity of psoriasis in mice. They discovered that administering MPO inhibitors, both through the bloodstream and directly to the affected area, resulted in a decrease in psoriasis severity [23]. This finding indicates that targeting oxidative damage might be a promising therapeutic strategy for treating psoriasis. Research shows that MPO gene mutations affect neutrophil activity, inflammation control, and skin inflammation resolution, highlighting the genetic basis of generalized pustular psoriasis (GPP) and related disorders. Variants that cause MPO deficit and decrease MPO protein function have been found in individuals with acute generalized exanthematous pustulosis (AGEP), acral pustular psoriasis (APP), and GPP.