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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 […]

Human plasma total antioxidant capacity (TAC) represents the integrated cumulative ability of circulating enzymatic and nonenzymatic antioxidants to neutralize reactive oxygen and nitrogen species, thereby reflecting the overall human plasma total antioxidant capacity of extracellular redox defense rather than the concentration of individual antioxidants alone. As a comprehensive oxidative stress biomarker, TAC incorporates the collective […]

Lipid peroxidation represents a central biochemical mechanism underlying oxidative stress, characterized by the free radical-mediated oxidation of polyunsaturated fatty acids within biological membranes, ultimately compromising membrane architecture, cellular homeostasis, and tissue function. The process is initiated when excessive reactive oxygen species (ROS), particularly the hydroxyl radical, abstract hydrogen atoms from membrane phospholipids to generate lipid […]

Phylloquinone, the primary dietary form of Vitamin K1, is an essential fat-soluble micronutrient that serves as the indispensable cofactor for γ-glutamyl carboxylase, enabling the Vitamin K cycle and the post-translational activation of multiple Vitamin K-dependent proteins through γ-carboxylation of glutamate residues. Adequate phylloquinone metabolism ensures the biological activity of osteocalcin, matrix Gla protein (MGP), coagulation […]

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 […]

Accurate evaluation of predicting the antioxidant status of human plasma by artificial neural network analysis represents an important advancement in clinical biochemistry, oxidative stress assessment, and precision medicine, particularly because simultaneous measurement of multiple oxidative and antioxidant biomarkers is labor-intensive, costly, and unsuitable for high-throughput clinical laboratories. To establish a reliable computational strategy, blood samples […]

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 […]

In a metal-catalyzed oxidative system, iron effects is driven by continuous Fenton reaction, in which cycling of the Fe2+/Fe3+ redox pair sustains the generation of reactive oxygen species, predominantly hydroxyl radicals, resulting in progressive oxidative damage to plasma proteins. Within this system, ascorbate redox modulation acts as a concentration-dependent regulator of iron redox cycling and […]

Occupational exposure to aluminum represents a significant source of aluminum-induced oxidative stress, where disruption of redox homeostasis accelerates oxidative injury to circulating blood components and compromises systemic antioxidant defense. Evaluation of blood samples obtained from hospital operating room personnel demonstrated that aluminum-mediated metal-catalyzed oxidation profoundly altered the biochemical balance between oxidants and antioxidants. Ferric reducing […]

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 […]