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Methionine sulfoxide reductase B3 deficiency causes hearing loss due to stereocilia degeneration and apoptotic cell death in cochlear hair cells.

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Methionine sulfoxide reductase B3 (MsrB3) is a protein repair enzyme that specifically reduces methionine-R-sulfoxide to methionine. A recent genetic study showed that the MSRB3 gene is associated with autosomal recessive hearing loss in human deafness DFNB74. However, the precise role of MSRB3 in

Methionine sulfoxide reductase A as a marker for isolating subpopulations of stem and progenitor cells used in regenerative medicine.

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The essence of cell therapies is to transplant stem and progenitor cells for repairing and/or replacing damaged tissues. Transplanted cells need adapt to the injured site, where they are subjected to high levels of oxidative stress and the failure of those transplanted cells to combat the oxidative

Protection from oxidative stress by methionine sulfoxide reductases in RPE cells.

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We investigated the role of methionine sulfoxide reductases (Msrs) in oxidant-stress-induced cell death in retinal pigmented epithelial (RPE) cells. In RPE cells exposed to varying doses of H(2)O(2), gene expression of MsrA and hCBS-1 (the human analog of MsrB2) increased in a dose-dependent and

Mitochondrial function and redox control in the aging eye: role of MsrA and other repair systems in cataract and macular degenerations.

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Oxidative stress occurs when the level of prooxidants exceeds the level of antioxidants in cells resulting in oxidation of cellular components and consequent loss of cellular function. Oxidative stress is implicated in wide range of age-related disorders including Alzheimer's disease, Parkinson's

Methionine sulfoxide reductase A: Structure, function and role in ocular pathology.

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Methionine is a highly susceptible amino acid that can be oxidized to S and R diastereomeric forms of methionine sulfoxide by many of the reactive oxygen species generated in biological systems. Methionine sulfoxide reductases (Msrs) are thioredoxin-linked enzymes involved in the enzymatic

Methionine sulfoxide reductase A, B1 and B2 are likely to be involved in the protection against oxidative stress in the inner ear.

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The methionine sulfoxide reductase (Msr) family of proteins is a class of repair enzymes that reduce methionine-S (MsrA) or methionine-R (MsrB) sulfoxide to methionine. Recent studies have reported that mutations in the MSRB3 gene cause autosomal recessive hearing loss in humans, and in mice MsrB3

Evidence for participation of the methionine sulfoxide reductase repair system in plant seed longevity.

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Seeds are in a natural oxidative context leading to protein oxidation. Although inevitable for proper progression from maturation to germination, protein oxidation at high levels is detrimental and associated with seed aging. Oxidation of methionine to methionine sulfoxide is a common form of damage

Methionine Sulfoxide Reductase B3-Targeted In Utero Gene Therapy Rescues Hearing Function in a Mouse Model of Congenital Sensorineural Hearing Loss.

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OBJECTIVE Methionine sulfoxide reductase B3 (MsrB3), which stereospecifically repairs methionine-R-sulfoxide, is an important Msr protein that is associated with auditory function in mammals. MsrB3 deficiency leads to profound congenital hearing loss due to the degeneration of stereociliary bundles

Resveratrol preconditioning increases methionine sulfoxide reductases A expression and enhances resistance of human neuroblastoma cells to neurotoxins.

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Methionine sulfoxide reductases A (MsrA) has been postulated to act as a catalytic antioxidant system involved in the protection of oxidative stress-induced cell injury. Recently, attention has turned to MsrA in coupling with the pathology of Parkinson's disease, which is closely related to

Production of hydrogen peroxide in cancerous tissue by intravenous administration of sodium 5,6-benzylidene-L-ascorbate.

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We investigated whether the antitumor action of sodium 5,6-benzylidene-L-ascorbate (SBA) is mediated via oxidation-involved mechanism, in three different systems: 3'-methyl-4-dimethylaminoazobenzene (DAB)-induced rat hepatocellular carcinoma (in vivo), its homogenate (semi in vivo), and cultured

Kinetic modeling of storage effects on biomarkers related to B vitamin status and one-carbon metabolism.

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BACKGROUND Biomarkers and metabolites related to B vitamin function and one-carbon metabolism have been studied as predictors of chronic diseases in studies based on samples stored in biobanks. For most biomarkers, stability data are lacking or fragmentary. METHODS Degradation and accumulation

Mitochondrial gene expression in the human annulus: in vivo data from annulus cells and selectively harvested senescent annulus cells.

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BACKGROUND Mitochondrial dysfunction is recognized during cell senescence and apoptosis, two important components of human disc aging/degeneration. We hypothesize that mitochondrial dysfunction is present in the degenerating and senescent annulus cells. The objective of the present study was to

Key role of cysteine residues and sulfenic acids in thermal- and H2O2-mediated modification of β-lactoglobulin.

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Oxidation results in protein deterioration in mammals, plants, foodstuffs and pharmaceuticals, via changes in amino acid composition, fragmentation, aggregation, solubility, hydrophobicity, conformation, function and susceptibility to digestion. This study investigated whether and how individual or

Association between Advanced Glycation End Products and Impaired Fasting Glucose: Results from the SALIA Study.

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Advanced glycation end products (AGEs) may contribute to the development of type 2 diabetes and related complications, whereas their role in the early deterioration of glycaemia is unknown. While previous studies used antibody-based methods to quantify AGEs, data from tandem mass spectrometry

Comparative study of the antitumor action between sodium 5,6-benzylidene-L-ascorbate and sodium ascorbate (minireview).

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This review summarizes our comparative study of the antitumor action of sodium 5,6-benzylidene-L-ascorbate (SBA) and sodium ascorbate. Both SBA and ascorbate produced ascorbate radicals during decomposition, elevated oxidation potential and oxidized methionine to methionine sulfoxide, in the regular

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