Gene/Protein Disease Symptom Drug Enzyme Compound
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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.
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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

L-deprenyl protects neurons in a number of in vivo and in vitro models and it has been postulated that it ameliorates some neurodegenerative disorders. Superoxide dismutase (SOD) is one of the enzymes responsible for the inactivation of oxygen free radicals, and one of the mechanisms of the effect of L-deprenyl is thought to act by induction of SOD. In this study, PC12 cells were used to study the effect of L-deprenyl on gene regulation of SOD and its interaction with nerve growth factor (NGF). The results show that NGF induces SOD mRNA in a dose-dependent manner and that a similar effect was produced by L-deprenyl. In addition, L-deprenyl potentiates NGF effects. This study demonstrates that both L-deprenyl and NGF may be involved in common antioxidative mechanisms and that L-deprenyl may interact with neurotrophic factors.
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PMID:L-deprenyl potentiates NGF-induced changes in superoxide dismutase mRNA in PC12 cells. 967 80

Excessive brain Mn can produce toxicity with symptoms resembling parkinsonism. This syndrome, called "manganism," correlates with loss of dopamine in the striatum and cell death in the striatum and globus pallidus. A common hypothesis is that cell damage in Mn toxicity is caused by oxidation of important cell components by Mn3+. Determination of the amount of Mn3+ present, under a range of conditions, in neuronal cells and brain mitochondria represents an important step in evaluating the "damage through oxidation by Mn3+ hypothesis." In an earlier paper we used X-ray absorption near-edge structure (XANES) spectroscopy to determine the amount of Mn2+ and Mn3+ in brain mitochondria under a range of conditions. Here we extend the study to investigate the evidence for formation of Mn3+ through oxidation of Mn2+ by ROS in PC12 cells and in PC12 cells induced with nerve growth factor (NGF) to display a phenotype more like that of neurons. Although the results suggest that very small amounts of Mn3+ might be present at low Mn levels, probably in Mn superoxide dismutase, Mn3+ is not stabilized by complex formation in these cells and therefore does not accumulate to detectable amounts.
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PMID:Determining the oxidation states of manganese in PC12 and nerve growth factor-induced PC12 cells. 1596 8