methionine sulfoxide/necroză

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Characterization of macrophage phenotype, redox, and purinergic response upon chronic treatment with methionine and methionine sulfoxide in mice.

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Hypermethioninemia is a disorder characterized by high plasma levels of methionine (Met) and its metabolites such as methionine sulfoxide (MetO). Studies have reported associated inflammatory complications, but the mechanisms involved in the pathophysiology of hypermethioninemia are still uncertain.

Oxidative modification of IkappaB by monochloramine inhibits tumor necrosis factor alpha-induced NF-kappaB activation.

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We have previously reported that monochloramine (NH(2)Cl), a neutrophil-derived oxidant, inhibited tumor necrosis factor alpha (TNFalpha)-induced expression of cell adhesion molecules and nuclear factor-kappaB (NF-kappaB) activation (Free Radical Research 36 (2002) 845-852). Here, we studied the

Methionine and/or Methionine Sulfoxide Alter Ectoenzymes Activities in Lymphocytes and Inflammatory Parameters in Serum from Young Rats: Acute and Chronic Effects.

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In this study we investigated the effect of acute and chronic treatment with Met and/or methionine sulfoxide (MetO) on ectonucleotidases and cholinesterases activities from lymphocytes and purine derivatives compounds, C-protein reactive, interleukin-10, interleukin-6, and tumor necrosis factor-α

Methionine sulfoxide reductase A (MsrA) modulates cells and protects against Mycoplasma genitalium induced cytotoxicity.

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Methionine sulfoxide reductase A (MsrA) is a ubiquitous antioxidant repair enzyme which specifically reduces the oxidized methionine (Met-O) in proteins to methionine (Met). Previous studies have shown that lack of or overexpression of MsrA in cells affects the function of proteins and can lead to

Suppression of the TNFalpha-induced increase in IL-1alpha expression by hypochlorite in human corneal epithelial cells.

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OBJECTIVE In response to injury, activated neutrophils release tumor necrosis factor (TNF)-alpha and myeloperoxidase (MPO). TNFalpha in turn causes human corneal epithelial cells to secrete interleukin (IL)-1alpha, whereas MPO results in formation of HClO/OCl(-). The effect of HClO/OCl(-) on the

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

Effects of Sodium Selenite on Oxidative Damage in the Liver, Kidney and Brain in a Selenite Cataract Rat Model.

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Selenite cataracts are effective and convenient animal models for simulation of human senile nuclear cataracts. These models are widely used to study the effects of various stresses on eye lenses and to screen anticataract drugs. However, there have been no comprehensive toxicological evaluations of

Shikonin attenuates acetaminophen-induced acute liver injury via inhibition of oxidative stress and inflammation.

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Acetaminophen (APAP) overdose causes acute liver injury and leads to fatal liver damage. However, the therapies are quite limited. Shikonin is a natural product with antioxidant and anti-inflammatory activities. In the present study, the hepatoprotective effects and the underlying mechanisms of

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