1. Date of download: 11/12/2016 Copyright © 2016 American Medical Association. All rights reserved. From: Use of Mitochondrial Antioxidant Defenses for Rescue of Cells With a Leber Hereditary Optic Neuropathy–Causing Mutation Arch Ophthalmol. 2007;125(2):268-272. doi:10.1001/archopht.125.2.268 Illustrations of the control adeno-associated viral (AAV) vector plasmid (pTR-UF12) (A) and the AAV containing the superoxide dismutase gene (SOD2) (B). Immunoblots of mitochondrial SOD (C) show that, relative to uninfected Leber hereditary optic neuropathy cells (lane 1) or controls infected with AAV–green fluorescent protein (GFP) (lane 2), manganese SOD (MnSOD) (24 kDa) is increased in cybrid cell cultures infected with AAV-SOD2 (lane 3). Expression of β-actin (42 kDa) is relatively comparable in each of the 3 lanes.CBA indicates chicken β-actin; CMV, cytomegalovirus enhancer; IRES, internal ribosomal entry site; and iTR, inverted terminal repeat. Figure Legend:

2. Date of download: 11/12/2016 Copyright © 2016 American Medical Association. All rights reserved. From: Use of Mitochondrial Antioxidant Defenses for Rescue of Cells With a Leber Hereditary Optic Neuropathy–Causing Mutation Arch Ophthalmol. 2007;125(2):268-272. doi:10.1001/archopht.125.2.268 Micrographs show decreased superoxide-induced dihydroethidium (DHE) fluorescence with adeno-associated viral vector containing the superoxide dismutase gene (AAV-SOD2) (A) relative to AAV–green fluorescent protein (GFP) infection (B), after 1 day in the galactose medium. After 2 days in galactose medium, decreased DHE fluorescence is also evident with AAV-SOD2 infection (C) relative to AAV infection (D) (original magnification ×100). The histogram (E)shows that the mean ± SD intensity of superoxide-induced DHE fluorescence is diminished with AAV-SOD2 infection relative to infection with AAV-GFP. Figure Legend:

3. Date of download: 11/12/2016 Copyright © 2016 American Medical Association. All rights reserved. From: Use of Mitochondrial Antioxidant Defenses for Rescue of Cells With a Leber Hereditary Optic Neuropathy–Causing Mutation Arch Ophthalmol. 2007;125(2):268-272. doi:10.1001/archopht.125.2.268 Micrographs of TUNEL (terminal deoxynucleotidyl transferase–mediated biotin–deoxyuridine triphosphate nick-end labeling) fluorescence show decreased TUNEL-positive cells with adeno-associated viral vector containing the superoxide dismutase gene (AAV-SOD2) (A) relative to AAV–green fluorescent protein (GFP) infection (B) after 1 day in the galactose medium. After 2 days in galactose medium,a decrease in TUNEL-positive cells is also evident with AAV-SOD2 infection (C) relative to AAV infection (D) (original magnification ×100). The histogram (E) shows that the mean ± SD intensity of TUNEL-induced fluorescence is diminished with AAV-SOD2 infection relative to infection with AAV-GFP. Figure Legend:

4. Date of download: 11/12/2016 Copyright © 2016 American Medical Association. All rights reserved. From: Use of Mitochondrial Antioxidant Defenses for Rescue of Cells With a Leber Hereditary Optic Neuropathy–Causing Mutation Arch Ophthalmol. 2007;125(2):268-272. doi:10.1001/archopht.125.2.268 Micrographs show an increase in Leber hereditary optic neuropathy (LHON) cell survival with adeno-associated viral vector containing the superoxide dismutase gene (AAV-SOD2) treatment (A) relative to AAV–green fluorescent protein (GFP)infection (B) after 2 days in galactose medium (original magnification ×100).The histogram (C) shows that the mean ± SD LHON cell survival is increased with AAV-SOD2 relative to AAV-GFP infection after 2 and 3 days of growth in the galactose medium (C). Figure Legend: