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Anders Behndig, Kurt Karlsson, Bengt O. Johansson, Thomas Brännström, Stefan L. Marklund; Superoxide Dismutase Isoenzymes in the Normal and Diseased Human Cornea. Invest. Ophthalmol. Vis. Sci. 2001;42(10):2293-2296.
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purpose. The human cornea, a tissue much exposed to oxidative stress, is
rich in extracellular superoxide dismutase (SOD). In this study, the
contents and distributions of the SOD isoenzymes in the normal human
cornea were compared with those in corneas affected by keratoconus and
methods. The central and peripheral parts of normal human corneas were analyzed
separately. Central corneal buttons were obtained from patients with
keratoconus and bullous keratopathy who were undergoing primary
keratoplasty or retransplantation. SOD enzymatic activities were
determined by a direct spectrophotometric method, and extracellular SOD
and the cytosolic Cu- and Zn-containing SOD (CuZn-SOD) proteins were
determined with ELISA and studied with immunohistochemistry.
results. The total SOD content, and particularly the extracellular SOD content,
was lower in the central than in the peripheral normal cornea. CuZn-SOD
and extracellular SOD were demonstrated in all three corneal layers.
CuZn-SOD was found in cells, whereas extracellular SOD appeared to be
localized on cell surfaces, in basal membranes, and in the stroma. In
keratoconus, corneal levels of extracellular SOD were half those in the
control corneas, whereas CuZn-SOD and the mitochondrial Mn-containing
SOD levels were normal. In bullous keratopathy, apart from edematous
dilution, SOD isoenzyme levels were essentially normal. In a remarkable
finding, the same pattern in SOD isoenzyme levels as in the original
disease was also found at retransplantation.
conclusions. Extracellular SOD and CuZn-SOD show markedly different distribution
patterns within the human cornea. Extracellular SOD activity in the
central cornea is halved in keratoconus, compared with that in normal
control corneas. The finding of a similar reduction at
retransplantation in keratoconus suggests reduced corneal extracellular
SOD synthesis in cells of the host as a cause of the low enzyme
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