1. Oxidative stress in cataracts
Joe A. Vinson 
Pathophysiology 
Volume 13, Issue 3, Pages (August 2006)
DOI: /j.pathophys
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2. Fig. 1 Illustrations of the types of cataracts and lens anatomy.
Pathophysiology  , DOI: ( /j.pathophys )
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3. Fig. 2
Relation between the prevalence of nuclear lens opacities and the healthy eating index quartiles (ranging from low to high) in 479 female nurses [15].
Pathophysiology  , DOI: ( /j.pathophys )
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4. Fig. 3 Chemical structure of lutein and zeaxanthin.
Pathophysiology  , DOI: ( /j.pathophys )
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5. Fig. 4 Risk of cataracts and alcohol consumption [32].
Pathophysiology  , DOI: ( /j.pathophys )
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6. Fig. 5 Chemical structure of aminoguanidine.
Pathophysiology  , DOI: ( /j.pathophys )
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7. Fig. 6
Correlations between lens glucose and the three pathological mechanisms in a tea-supplemented animal diabetes model.
Pathophysiology  , DOI: ( /j.pathophys )
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8. Fig. 7
Mitochondrial oxidative damage. The mitochondrial respiratory chain (top) passes electrons from the electron carriers NADH and FADH2 through the respiratory chain to oxygen. This leads to the pumping of protons across the mitochondrial inner membrane to establish a proton electrochemical potential gradient (DmH+), negative inside: only the membrane potential (Dym) component of DmH+ is shown. The DmH+ is used to drive ATP synthesis by the FoF1ATP synthase. The exchange of ATP and ADP across the inner membrane is catalysed by the adenine nucleotide transporter (ANT) and the movement of inorganic phosphate (Pi) is catalysed by the phosphate carrier (PC) (top left). There are also proton leak pathways that dissipate DmH+ without formation of ATP (top right). The respiratory chain also produces superoxide (O2−) which can react with and damage iron sulfur proteins such as aconitase thereby ejecting ferrous iron. Superoxide also reacts with nitric oxide (NO) to form peroxynitrite (ONOO−). In the presence of ferrous iron, hydrogen peroxide forms the very reactive hydroxyl radical (OH). Both peroxynitrite and hydroxyl radical can cause extensive oxidative damage (bottom right). The defenses against oxidative damage (bottom left) include superoxide dismutase (MnSOD) and the hydrogen peroxide it produces is degraded by glutathione peroxidase (GPX) and peroxiredoxin III (PrxIII). Glutathione (GSH) is regenerated from glutathione disulfide (GSSG) by the action of glutathione reductase (GR) and the NADPH for this is in part supplied by a transhydrogenase (TH).
Pathophysiology  , DOI: ( /j.pathophys )
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9. Fig. 8
Chemical structure of triphenylphosphonium adduct of Coenzyme Q10.
Pathophysiology  , DOI: ( /j.pathophys )
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