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menadione/lafyèv

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Preferential killing of glucose-depleted HeLa cells by menadione and hyperthermia.

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Energy deprivation of cancer cells increases sensitivity to killing by hyperthermia. Recent cell culture studies suggest that certain naphthoquinones, especially menadione (vitamin K3), have anti-tumour activity by interfering with the energy metabolism of cells, resulting in the inhibition of

Protocatechuic acid protects against menadione-induced liver damage by up-regulating nuclear erythroid-related factor 2.

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Menadione (Vitamin K3) is an over-the-counter (OTC) drug used in the treatment of abdominal cramps, colitis, diarrhea, hay fever, hemorrahage, hypoprothrombinemia, and joint pains. In this study, we evaluated the protective influence of protocatechuic acid on menadione-induced

Induction of a 23 kDa stress protein by oxidative and sulfhydryl-reactive agents in mouse peritoneal macrophages.

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The synthesis of 23 kDa protein was enhanced when mouse peritoneal macrophages were exposed to oxidative agents such as hydrogen peroxide and menadione, or to sulfhydryl-reactive agents such as diethylmaleate, cadmium chloride and sodium arsenite. After 11 h exposure to these agents the 23 kDa
We have isolated and conducted preliminary characterization of a cell line derived from the Chinese hamster ovary cell line AA8, which we have designated AG8 and which is highly resistant to the cytotoxic effects of H2O2 (approximately 17-fold when the H2O2 treatment was at 37 degrees; approximately

Murine cells transfected with human Hsp27 cDNA resist TNF-induced cytotoxicity.

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Hyperthermia sensitizes tumor cells to killing by tumor necrosis factor-alpha (TNF). Sensitization is greater in cells exposed to TNF before heating begins than with the reverse sequence, and heat-shock proteins (hsp) have been suggested to protect cells from TNF cytotoxicity. Here we examined the
OBJECTIVE To elucidate the pathophysiology of SCAD deficient patients who have a unique neurological phenotype, among fatty acid oxidation disorders, with early developmental delay, CNS malformations, intractable seizures, myopathy and clinical signs suggesting oxidative stress. METHODS We studied
Hyperthermia and other forms of stress that induce and/or stimulate heat shock or stress protein (hsp) expression enhance the cellular resistance to TNF-alpha. One of the stress proteins, hsp70, has been shown to participate in the molecular mechanisms that regulate this phenomenon. Here we have

Inducible and constitutive HSP70s confer synergistic resistance against metabolic challenges.

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Chaperonic proteins, including inducible HSP70 (HSP70i) and constitutive HSP70 (HSC70), have been implicated as essential players in the cellular adaptive protection. Ensuing studies demonstrated that overexpression of either protein individually protects against thermal and oxidative challenges.

Oxidants differentially regulate the heat shock response.

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Cells, animals, and humans respond to hyperthermia through the synthesis of a family of proteins termed heat shock proteins (HSPs). Because hyperthermic stress may also result in mitochondrial uncoupling and the generation of reactive oxygen species, we wondered whether oxidant stress was sufficient

Multiple cellular effects of leaf extracts from Parinari curatellifolia.

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BACKGROUND Parinari curatellifolia is a prominent plant in folk medicine in Sub-Saharan Africa. The plant decoctions are used to treat various ailments, including the treatment of cancer, pneumonia, fever, microbial infections and anti-inflammation. The aims of the study were to investigate the
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