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Jennifer M. Sandbach, Pinar E. Coscun, Hans E. Grossniklaus, Jason E. Kokoszka, Nancy J. Newman, Douglas C. Wallace; Ocular Pathology in Mitochondrial Superoxide Dismutase (Sod2)–Deficient Mice. Invest. Ophthalmol. Vis. Sci. 2001;42(10):2173-2178.
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purpose. To characterize the pathologic features in retina, optic nerve, and
extraocular muscle of mitochondrial superoxide dismutase
(Sod2)–deficient mice, a model of increased mitochondrial production
of reactive oxygen species.
methods. Morphometric and ultrastructural study of eyes of 43 homozygous
sod2tm1Cje−/− mice and wild-type control animals. For
retinal morphometric analysis, 32 manganese 5,10,15,20-tetrakis
(4-benzoic acid) porphyrin (MnTBAP)–treated animals aged either 9 to
10 days or 20 to 21 days were studied. Ultrastructural examination was
performed on tissue from the treated animals, and 11 additional
untreated mutant and control animals.
results. In treated Sod2-deficient animals, the photoreceptor layer was thinner
centrally at 9 to 10 days than in control animals (mean 8.8 vs. 14.7μ
m). By 20 to 21 days, all retinal layers apart from the outer
nuclear layer and retinal pigment epithelium (RPE) were thinner
centrally in mutant animals (total retinal thickness, 233.2 vs. 272.6μ
m; combined nerve fiber layer, ganglion cell layer, and inner
plexiform layer, 86.2 vs. 103.4 μm; inner nuclear layer, 51.8 vs.
60.3 μm; photoreceptors, 26.7 vs. 35.6 μm). Optic nerve
cross-sectional area was less in 20- to 21-day-old treated
Sod2-deficient animals than in control animals. Mitochondrial
morphologic abnormalities (swelling, pale matrix, and disorganized
cristae) were found predominantly in older mutant animals’ (16 and 20
to 21 days) RPE and in extraocular muscle of a 16-day-old untreated
conclusions. In sod2tm1Cje−/− mice, there is relative progressive
retinal thinning, with particular involvement of the inner retinal
layers and an early effect on the photoreceptor layer, as well as
mitochondrial morphologic abnormalities, all consistent with
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