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Review

The role of manganese superoxide dismutase in skin aging

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Pages 232-235 | Received 26 Mar 2012, Accepted 13 Aug 2012, Published online: 01 Jul 2012

Figures & data

Figure 1. Accelerated aging phenotype in mice with conditional deficiency for mitochondrial superoxide dismutase in the connective tissue. (A) The mutant mice (mut) revealed kyphosis and a prominent progeroid forehead compared with littermates of SOD2 competent (co) mice at the age of 47 d. The intrinsically aged control mice (co) of 900 d also exhibited incidence of kyphosis similar to mutant mice. (B) Representative hematoxylin-eosin stained sections of the skin from control (co), heterozygous (h), mutant (mut) and intrinsically aged control (old) mice. Mutant mice at an age of 6 weeks revealed a severe atrophy of the dermis, the subcutaneous fat tissue and the muscle fibers of the panniculus carnosus compared with SOD2 competent mice (co). Only minor changes in SOD2 heterozygous mice (h) were evident compared with SOD2 competent mice (co). Intrinsically aged control mice (old) of 900 d also show skin atrophy similar to mutant mice. E, epidermis; D, dermis; H, hair follicle; SC, subcutaneous fat tissue; PC, panniculus carnosus. Scale bars, 20 µm. (C) X-ray analysis from dissected femur bone of SOD2 competent mice (co), SOD2 heterozygous mice (h) and mutant mice (mut) revealed an osteoporosis-like phenotype in mutant mice. Scale bars, 0.5 cm. (D) Significantly reduced survival time of mutant mice (median 444 d) compared with SOD2 competent control mice (median 784 d) (***p < 0.0001, log-rank test stratified for gender). No statistically significant difference was found between SOD2 competent (co) and SOD2 heterozygous (h) mice (p = 0.65). The maximal life span for mutant mice was 837 d compared with 971 d in SOD2 competent mice and 932 d in SOD2 heterozygous mice. Figure modified from Treiber et al., 2011.50

Figure 1. Accelerated aging phenotype in mice with conditional deficiency for mitochondrial superoxide dismutase in the connective tissue. (A) The mutant mice (mut) revealed kyphosis and a prominent progeroid forehead compared with littermates of SOD2 competent (co) mice at the age of 47 d. The intrinsically aged control mice (co) of 900 d also exhibited incidence of kyphosis similar to mutant mice. (B) Representative hematoxylin-eosin stained sections of the skin from control (co), heterozygous (h), mutant (mut) and intrinsically aged control (old) mice. Mutant mice at an age of 6 weeks revealed a severe atrophy of the dermis, the subcutaneous fat tissue and the muscle fibers of the panniculus carnosus compared with SOD2 competent mice (co). Only minor changes in SOD2 heterozygous mice (h) were evident compared with SOD2 competent mice (co). Intrinsically aged control mice (old) of 900 d also show skin atrophy similar to mutant mice. E, epidermis; D, dermis; H, hair follicle; SC, subcutaneous fat tissue; PC, panniculus carnosus. Scale bars, 20 µm. (C) X-ray analysis from dissected femur bone of SOD2 competent mice (co), SOD2 heterozygous mice (h) and mutant mice (mut) revealed an osteoporosis-like phenotype in mutant mice. Scale bars, 0.5 cm. (D) Significantly reduced survival time of mutant mice (median 444 d) compared with SOD2 competent control mice (median 784 d) (***p < 0.0001, log-rank test stratified for gender). No statistically significant difference was found between SOD2 competent (co) and SOD2 heterozygous (h) mice (p = 0.65). The maximal life span for mutant mice was 837 d compared with 971 d in SOD2 competent mice and 932 d in SOD2 heterozygous mice. Figure modified from Treiber et al., 2011.50