Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P04179 (MnSOD)
 2,777 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Senescence-accelerated mice (SAM-P8) are characterized as mice in which aging is accelerated and memory disturbances occur. In several regions in the brain of SAM-P8 mice at 2, 4 and 8 months of age, we examined the concentrations of the beta-subunit of nerve growth factor (beta-NGF) and nine kinds of proteins such as S100 beta and alpha B-crystallin, and compared them with those in senescence-resistant mice (SAM-R1, as controls) at corresponding ages. Levels of beta-NGF in the hippocampus of SAM-R1 and SAM-P8 mice were reduced at 8 months of age. However, the decrease was more conspicuous in SAM-R1 than in SAM-P8, resulting in a significant difference between them (P < 0.01). The concentrations of beta-NGF in the cerebral cortex and cerebellum decreased to some extent with age in the control mice while it remained unchanged in the mutant mice. By contrast, the olfactory bulbs from SAM-R1 and SAM-P8 retained almost constant levels of beta-NGF during the first 8 months. However, its level was already higher in SAM-P8 at 2 months than in SAM-R1. Among nine proteins measured here, the acceleration of age-related increase was apparent in the levels of S100 beta and Mn-SOD in the cerebral cortex from SAM-P8. By contrast, the cerebral cortex and cerebellum from SAM-P8 showed tendencies to contain significantly high levels of alpha B-crystallin. These results suggest, at least, the presence of fibrous gliosis at quite an early age as well as the acceleration of senescence, in selected regions of the brain of SAM-P8.
 ...
PMID:Age-related changes in levels of the beta-subunit of nerve growth factor in selected regions of the brain: comparison between senescence-accelerated (SAM-P8) and senescence-resistant (SAM-R1) mice. 783 25

Superoxide dismutases (SODs) protect cells from damage by oxygen free radicals. Manganese (Mn) SOD is preferentially induced in terminally differentiating cells; induction of copper-zinc (CuZn) SOD is more closely associated with postnatal exposure to environmental sources of oxygen free radicals. The purpose of this study was to investigate ontogenetic changes in immunoreactivity for MnSOD and CuZnSOD relative to the expression of markers of neuronal and chemosensory differentiation in olfactory and vomeronasal receptor neurons (ORNs and VRNs, respectively), which mature with different time courses. Immunoreactivity for both SODs was detected in rat ORNs at embryonic day (E) 14, the earliest time point investigated, but not until E16 in vomeronasal neuroblasts. ORNs also expressed the neuronal marker protein gene product (PGP) 9.5 and the chemosensory cell marker olfactory marker protein (OMP) at E14; vomeronasal neuroblasts expressed PGP 9.5 at E16 but were not immunoreactive for OMP until postnatal day (P) 2. Immunoreactivity for MnSOD in ORNs and VRNs generally increased pre- and postnatally to a maximum at P11. Immunoreactivity for CuZnSOD did not increase markedly until after birth, reaching maximal levels at P11-P24. Within ORNs and VRNs, the most intense immunoreactivity was localized in the dendritic and supranuclear regions. The results indicate that in ORNs and VRNs, increases in MnSOD immunoreactivity during ontogeny parallel the ongoing differentiation and maturation of chemosensory receptor neurons; in contrast, the induction of immunoreactivity for CuZnSOD is associated with postnatal exposure to the ambient oxygen and xenobiotic environment.
 ...
PMID:Differential expression of manganese and copper-zinc superoxide dismutases in the olfactory and vomeronasal receptor neurons of rats during ontogeny. 908 17

Despite extensive interest in the rodent nasal cavity as a target organ for toxicity, there is very limited information regarding nasal defenses against oxidative stress and xenobiotic-derived oxidants. Using immunohistochemistry, we have examined the distribution of Cu,Zn and Mn superoxide dismutase (SOD), catalase, glutathione (GSH) peroxidase, and DT-diaphorase in rat nasal tissues. In addition, we have determined the concentrations of ascorbate and alpha-tocopherol and the activities of SOD (combined Cu,Zn and Mn forms), catalase, GSH peroxidase, GSH reductase, and DT-diaphorase in nasal respiratory epithelium (RE), olfactory epithelium (OE), and in lung. Immunohistochemistry demonstrated that all four enzymes were similarly distributed, with the greatest staining intensity in dorsal-medial regions of the nasal cavity. In respiratory epithelium, ciliated columnar cells and subepithelial glands stained positively, while in olfactory tissue the enzymes were detected in the sustentacular cells and Bowman's glands. With the exception of SOD, enzyme activities were higher in RE than OE, while concentrations of ascorbate and alpha-tocopherol were higher in OE than RE. With the exception of catalase, nasal activities were either higher than or comparable to those of the lung. Thus, the rat nasal cavity appears to be well protected against oxidative damage.
 ...
PMID:Antioxidant status of the rat nasal cavity. 1261 49

Manganese superoxide dismutase (MnSOD or SOD2) is a key mitochondrial enzymatic antioxidant. Arguably the most striking phenotype associated with complete loss of SOD2 in flies and mice is shortened life span. To further explore the role of SOD2 in protecting animals from aging and age-associated pathology, we generated a unique collection of Drosophila mutants that progressively reduce SOD2 expression and function. Mitochondrial aconitase activity was substantially reduced in the Sod2 mutants, suggesting that SOD2 normally ensures the functional capacity of mitochondria. Flies with severe reductions in SOD2 expression exhibited accelerated senescence of olfactory behavior as well as precocious neurodegeneration and DNA strand breakage in neurons. Furthermore, life span was progressively shortened and age-dependent mortality was increased in conjunction with reduced SOD2 expression, while initial mortality and developmental viability were unaffected. Interestingly, life span and age-dependent mortality varied exponentially with SOD2 activity, indicating that there might normally be a surplus of this enzyme for protecting animals from premature death. Our data support a model in which disruption of the protective effects of SOD2 on mitochondria manifests as profound changes in behavioral and demographic aging as well as exacerbated age-related pathology in the nervous system.
 ...
PMID:Reduced mitochondrial SOD displays mortality characteristics reminiscent of natural aging. 1807 70