Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Duchenne muscular dystrophy muscles undergo increased oxidative stress and altered calcium homeostasis, which contribute to myofiber loss by trigging both necrosis and apoptosis. Here, we asked whether treatment with free radical scavengers could improve the dystrophic pattern of mdx muscles. Five-week-old mdx mice were treated for 2 weeks with alpha-lipoic acid/l-carnitine. This treatment decreased the plasmatic creatine kinase level, the antioxidant enzyme activity, and lipid peroxidation products in mdx diaphragm. Free radical scavengers also modulated the phosphorylation/activity of some component of the mitogen-activated protein kinase (MAPK) cascades: p38 MAPK, the extracellular signal-related kinase, and the Jun kinase. beta-Dystroglycan (beta-DG), a multifunctional adaptor or scaffold capable of interacting with components of the extracellular signal-related kinase-MAP kinase cascade, was also affected after treatment. In the mdx muscles, beta-DG (43 kd) was cleaved by matrix metalloproteinases into a 30-kd form (beta-DG30). We show that the proinflammatory protein nuclear factor-kappaB activator decreased after the treatment, leading to a significant reduction of matrix metalloproteinase activity in the mdx diaphragm. Our data highlight the implication of oxidative stress and cell signaling defects in dystrophin-deficient muscle via the MAP kinase cascade-beta-DG interaction and nuclear factor-kappaB-mediated inflammation process.
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PMID:Modulation of p38 mitogen-activated protein kinase cascade and metalloproteinase activity in diaphragm muscle in response to free radical scavenger administration in dystrophin-deficient Mdx mice. 1725 31

Reaumuria soongorica (Pall.) Maxim. is a short woody shrub widely found in semi-arid areas of China, and can survive severe environmental stresses. To understand its potential signaling transduction pathway in stress tolerance, we investigated the participation of mitogen-activated protein kinases (MAPKs) as possible mediators of abiotic stresses. A novel MAP kinase cDNA (RsMPK2) that encodes a 374 amino acid protein was isolated from R. soongorica. RsMPK2 belongs to the C1 subgroup, which is still functionally uncharacterized compared to groups A and B; and contains all 11 of the conserved MAPK subdomains and the TEY phosphorylation motif. RsMPK2 is expressed in vegetative (root, stem, leaf and callus) and reproductive (flower) organs. The transcripts of RsMPK2 were rapidly accumulated at high levels when R. soongorica was subjected to dehydration, salinity conditions and treatment with abscisic acid or hydrogen peroxide. Growth analysis of Escherichia coli (srl::Tn10) cells transformed with pPROEXHT-RsMPK2 showed that the expression products of RsMPK2 do not act as an osmoprotectant. But, the inhibition of RsMPK2 expression by the inhibitor U0126 induced a decrease of antioxidant enzyme activity under stresses, indicating that RsMPK2 is involved in the regulation of the antioxidant defense system in the response to stress signaling.
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PMID:Molecular characterization of RsMPK2, a C1 subgroup mitogen-activated protein kinase in the desert plant Reaumuria soongorica. 2083 58

Gelsemine is an important toxic substance extracted from Gelsemium elegans, which has a lot of biological functions in cells and organisms, but its toxicity has been rarely reported in Tetrahymena thermophila. In this study, we used the protozoan T. thermophila as an experimental model to investigate the potential toxicity-induced mechanism of gelsemine in the unicellular eukaryote. Our results clearly showed gelsemine inhibited T. thermophila growth in a dose-dependent manner. This exposure also resulted in oxidative stress on T. thermophila cells and antioxidant enzyme levels were significantly altered at high gelsemine levels (p < 0.05). Gelsemine produced a slight apoptotic effect at the highest (0.8 mg/mL) gelsemine level used here (p < 0.05). Furthermore, the toxin-induced DNA damage in a dose-dependent manner. The ultrastructural analysis also revealed mitophagic vacuoles at 0.4 and 0.8 mg/mL levels of gelsemine exposure. Moreover, expressions of oxidative stress-related and MAP kinase genes were significantly changed after exposure to 0.8 mg/mL level of gelsemine (p < 0.05). Altogether, our results clearly show that gelsemine from G. elegans can inhibit the growth via inducing oxidative stress and DNA damage in T. thermophila cells.
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PMID:Effects of gelsemine on oxidative stress and DNA damage responses of Tetrahymena thermophila. 3058 79