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Fig. 4. | Lipids in Health and Disease

Fig. 4.

From: Oxidative profiles of LDL and HDL isolated from women with preeclampsia

Fig. 4.

Mechanisms of oxidative damage in LDL-c and HDL-c. The main source of reactive species in PE is the placenta via the NADPH oxidase and xanthine oxidase production of O2 .- (a), which is dismutated by SOD to produce H2O2, which can be removed by CAT and GPx. GPx uses GSH as a reducing agent, and GSH is regenerated by GRd (b). When this antioxidant system is disrupted, excess O2 .- can react in two ways. It can interact with NO to produce ONOO via the Beckman-Radi-Freeman reaction, and ONOO can become protonated and rearrange to produce HO. Alternatively, SOD produces H2O2, which can interact with transition metals (Fenton reaction) to generate HO (c). HO can modify proteins and lipids from lipoproteins. Damage to proteins may occur via three oxidation mechanisms: 1) the modification of tyrosine residues to generate catechols (DOPA) when oxidized that then form orthoquinones that can reduce the nitroblue tetrazolium compound (NBT) (mild damage) (d), 2) the production of dimeric tyrosines (dityrosines) (severe damage) (e) or 3) the formation of carbonyl groups generated by direct free radical attack, interactions with transition metals, glycation and adduct formation between protein and lipoperoxidation products (f). HO may also oxidize lipids, which undergo molecular rearrangements to form conjugated dienes (mild damage) (g), lipohydroperoxides (moderate damage) (which may be hydrolysed by PON-I present on HDL) (h), and MDA (severe damage) (i). MDA can form adducts with apo B-100 of LDL and generate oxLDL, which is toxic to the vascular endothelium (j)

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