A series of antioxidant enzymes and numerous endogenous and dietary antioxidant compounds maintain defenses against oxidative stress by scavenging ROS. The susceptibility of cells to oxidative stress is the function of the overall balance between the degree of ROS formation and their antioxidant defense capability. Overproduction of ROS depletes enzymatic and nonenzymatic antioxidants leading to additional ROS accumulation and cellular damage [ 27 ] . The primary antioxidant enzymes include, but are not limited to, superoxide dismutase (SOD), catalase, and glutathi-one and thioredoxin peroxidases. The nonenzymatic antioxidants include, among others, vitamin C (ascorbic acid), vitamin E (a-tocopherol), b-carotene, and reduced glutathione [28].

Superoxide is converted spontaneously or by SOD to hydrogen peroxide. SOD exists in three isoforms: cytoplasmic copper-zinc (SOD1), mitochondrial manganese (SOD2), and extracellular copper-zinc (SOD3), the latter being the main vascular SOD. Catalase catalyzes the decomposition of hydrogen peroxide to water and molecular oxygen. Glutathione peroxidases (GPx) are selenium-containing enzymes which reduce hydrogen peroxide to water and lipid peroxides to their corresponding alcohols. Thioredoxin peroxidase (TrPx) is a member of the peroxiredoxin family, which reduces hydrogen peroxide [28] .

Numerous nonspecific antioxidants scavenge ROS. Vitamin Eisa lipid-soluble antioxidant, which protects LDL against oxidation. Vitamin C is the water-soluble antioxidant, which very effectively scavenges a wide array of ROS, and also prevents oxidation of BH4, an essential NOS cofactor [22].

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