Table 2.
Effects of ROS | Result | Biological evidence(s) |
---|---|---|
Protein oxidation | Increased protein carbonyl content | Increased protein oxidation in frontal pole and occipital pole [113] Decreased ratio of (MAL-6)/(W/S) in AD hippocampus and inferior parietal lobule, decreased the W/S ratio in in vitro models of human synaptosomes oxidation by ROS [114] |
| ||
DNA oxidation | Direct damage to DNA structure | 3-fold increase in mitochondrial DNA oxidation in parietal cortex in AD [115] Increase in oxidative damage to nuclear DNA in AD compared with age-matched control subjects [116] 8-hydroxy-2-deoxyguanosine as a marker of DNA oxidation increases in AD [117] |
| ||
Lipid peroxidation | Brain phospholipid damage | Increased TBARS levels in AD in hippocampus, piriform cortex, and amygdala [118] Increased lipid peroxidation of AD brain homogenates in vitro due to Fe-H2O2 [119] Increased apoptosis in cultured DS and AD neurons inhibited by antioxidant enzymes [112, 120] Decrease in PC, PE, phospholipid precursors, choline, and ethanolamine in hippocampus and inferior parietal lobule in AD [121] Increased aldehydes as a cytotoxic agent in the brain of AD patients [122] |
| ||
Antioxidant enzymes | Changes in enzymes contents | Elevated GSH-Px, GSSG-R, and CAT activity in hippocampus and amygdala in AD [118] Many studies showed no elevation in enzyme activity [123, 124] or decrease in activity [125] |
| ||
AGE formation | Pathological changes in protein structure and action | Accelerates aggregation of soluble nonfibrillar Aβ and tau [126] |
MAL-6: weakly immobilized protein bound spin label; W/S: strongly immobilized protein bound spin label; TBARS: thiobarbituric acid reactive substances; DS: Down syndrome; PC: phosphatidylcholine; PE: phosphatidylethanolamine; GSH-Px: glutathione peroxidase; GSSG-R: glutathione reductase; CAT: catalase; AGE: advanced glycation end products.