Abstract

Oxidative stress results from an imbalance between the formation and neutralization of reactive oxygen species (ROS), and it is imposed on cells because of one or more of the following factors: an increase in oxidant generation, a decrease in antioxidant protection, or a failure to repair oxidative damage. There is controversy about the susceptibility of cells to lipid peroxidation in iron deficiency anemia (IDA)—some investigators have claimed there is no difference in lipid peroxidation among patients with IDA compared with controls, but others have reported that among patients with IDA oxidants are increased and antioxidants decreased, so the oxidative/antioxidative balance is shifted toward the oxidative side. This apparent discrepancy may be due to different concentrations of ROS and antioxidant enzymes in the tissues studied, the subjects of the study, the severity of the iron deficiency, and the methods used for the assessment of the oxidative stress. However, in humans, where the degree of iron deficiency is not very high, it is accepted that iron deficiency increases oxidative stress, a fact that can also be attributed to the repletion process with several sources of iron. Several authors have reported increased lipid peroxidation products in patients with iron-deficiency anemia, which may be attributed to overproduction of ROS and a deficiency of antioxidant defense. Decreased superoxide dismutase (SOD) activity in iron-deficiency anemia may be linked to increased oxidative stress, because it is well known that ROS inhibits SOD activity. On the other hand, goat milk has beneficial effects, reducing oxidative stress and protecting cell bioconstituents from free radicals. Caprine milk alters the activities of enzymes that improve the total antioxidative defense capacity of the organism, a fact that limits the oxidative damage to the main biomolecules (lipids, protein DNA, and prostaglandins).

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