ِDezAzma

Metal-catalyzed oxidative systems represent central drivers of metal-catalyzed oxidative stress and core regulators of redox biology and disease mechanisms. In particular, iron and copper act as catalytic centers. They promote the Fenton reaction and Haber–Weiss reaction. Consequently, hydroxyl radicals are generated which are reactive oxygen species (ROS) and disrupts cellular redox homeostasis. Furthermore, oxidative injury […]

Administration of excessive Vitamin K1 (phylloquinone) produced a pronounced age-dependent oxidative stress response characterized by distinct alterations in plasma antioxidant capacity, lipid peroxidation, and liver injury biomarkers in adult and weanling rats. Quantification of ferric reducing ability of plasma (FRAP) demonstrated that total antioxidant capacity remained unchanged in adult animals despite escalating vitamin K1 doses […]

Maintenance of systemic redox homeostasis depends on the balance between antioxidant defense and oxidative injury, making plasma total antioxidant capacity a critical determinant of susceptibility to oxidative stress. Quantification of the ferric reducing ability of plasma (FRAP) demonstrated a significant increase in antioxidant capacity in suckling rats following administration of vitamin K1 (28, 56, or […]

Excessive pharmacological iron exposure represents a critical model of iron-induced oxidative stress and iron-mediated cellular toxicity, where uncontrolled redox reactions promote progressive molecular damage in circulating erythrocytes. The vulnerability of human red blood cells to oxidative injury is strongly associated with disruption of hemoglobin structure, impaired oxygen transport, and deterioration of membrane protein stability. Evaluation […]