cumene/некроза

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Radioresistant Sf9 insect cells display moderate resistance against cumene hydroperoxide.

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Lepidopteran insect cells serve as excellent model to study stress responses and are known to display resistance against DNA damaging agents including ionizing radiation; however, limited information is available on the effects of membrane damaging agents in these cells. In this study, we

Protective effect of photodegradation product of nifedipine against tumor necrosis factor alpha-induced oxidative stress in human glomerular endothelial cells.

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Recently, increasing evidence suggests that the antihypertensive drug nifedipine acts as a protective agent for endothelial cells, and that the activity is unrelated to its calcium channel blocking. Nitrosonifedipine (NO-NIF) is metabolically and photochemically produced from nifedipine, and NO-NIF

Studies on cumene hydroperoxide-induced lipid peroxidation in the isolated perfused rat heart.

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In the isolated, perfused rat heart, lipid peroxidation, induced by cumene hydroperoxide (Cum OOH), is accompanied by the release of malondialdehyde (MDA). Using a modified perfusion technique resulting in the separate collection of coronary and interstitial effluent, it can be shown that upon Cum

Cumene hydroperoxide induced changes in calcium homeostasis in cultured neonatal rat heart cells.

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OBJECTIVE The relationship between oxidative stress induced cell necrosis and perturbation of intracellular calcium homeostasis was investigated in cultured myocytes. METHODS Cultured neonatal rat heart cells were loaded with fura-2 AM to measure cytosolic free calcium ([Ca2+]i). Probenecid, an

Cumene hydroperoxide debilitates macrophage physiology by inducing oxidative stress: possible protection by alpha-tocopherol.

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Macrophages, the major phagocytes of body, are largely dependent on membrane for their apposite functioning. Cum-OOH, a catalyst used in chemical and pharmaceutical industry, is a peroxidative agent, which may induce oxidative stress in macrophages hampering the integrity of their membrane.

Alkyl hydroperoxide reductase subunit C (AhpC) protects bacterial and human cells against reactive nitrogen intermediates.

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In Salmonella typhimurium, ahpC encodes subunit C of alkyl hydroperoxide reductase, an enzyme that reduces organic peroxides. Here, we asked if ahpC could protect cells from reactive nitrogen intermediates (RNI). Salmonella disrupted in ahpC became hypersusceptible to RNI. ahpC from either

Buthionine sulfoximine reduces the protective capacity of myocytes to withstand peroxide-derived free radical attack.

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Mammalian heart myocytes have a limited capacity to withstand the deleterious effects of free radical generating compounds. To assess the role of the glutathione redox cycle relative to this capacity, rat heart cell cultures were subjected for 90 min to 80 mumol/l cumene hydroperoxide (CHPO) without

Role of lipid peroxidation in gastric mucosal lesions induced by HCl, NaOH, or ischemia.

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We investigated whether lipid peroxidation is an important biochemical mechanism in acute gastric mucosal injury induced by acid, base, or postischemic reperfusion. Lipid peroxidation products, i.e., the concentration of conjugated dienes (absorbance at 242 nm), products absorbing at 270 nm, and

Comparative inhalation toxicity of ethyltoluene isomers in rats and mice.

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The C9 alkylbenzenes, composed mostly of ethyltoluenes and trimethylbenzenes, comprise 75-90% of the naphtha fraction of crude oil. Occupational and environmental exposure to C9 alkylbenzenes occur via inhalation. We conducted short-term inhalation studies on the ethyltoluene isomers (2-, 3- or 4-)

Oxidative stress-induced perturbations of calcium homeostasis and cell death in cultured myocytes: role of extracellular calcium.

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The role of extracellular calcium in the process of oxidative stress-induced calcium overload and cell death was investigated in cultured neonatal rat myocytes. Oxidative stress was induced by addition of cumene hydroperoxide (CHPO), a toxic organic hydroperoxide, in combination with varying

Peroxides and macrophages in the toxicity of fine particulate matter in rats.

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Epidemiologists have observed a positive association between human morbidity and mortality and the atmospheric concentrations of fine particulate matter (PM), but the mechanisms underlying the toxic effects of PM have not been elucidated. Various components of ambient PM have been implicated in

In vitro and in vivo characterization of alkyl hydroperoxide reductase mutant strains of Helicobacter hepaticus.

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Mutant strains in the tsaA gene encoding alkyl hydroperoxide reductase were more sensitive to O(2) and to oxidizing agents (paraquat, cumene hydroperoxide and t-butylhydroperoxide) than the wild type, but were markedly more resistant to hydrogen peroxide. The mutant strains resistance phenotype

ohr, Encoding an organic hydroperoxide reductase, is an in vivo-induced gene in Actinobacillus pleuropneumoniae.

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Actinobacillus pleuropneumoniae is the causative agent of porcine pleuropneumonia, a disease characterized by pulmonary necrosis and hemorrhage caused in part by neutrophil degranulation. In an effort to understand the pathogenesis of this disease, we have developed an in vivo expression technology

Combined effects of cadmium and nickel on testicular xenobiotic metabolizing enzymes in rats.

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When male rats were given a single dose of cadmium (Cd) (3.58 mg CdCl2 x H2O/kg, i.p.) 72 hr prior to sacrifice, the testicular 7-ethoxyresorufin O-deethylase (EROD) and glutathione S-transferase (GST) activities toward the substrates 1-chloro-2,4-dinitrobenzene (CDNB), 1,2-dichloro-4-nitrobenzene

Antioxidative and protective properties of extracts from leaves of the artichoke (Cynara scolymus L.) against hydroperoxide-induced oxidative stress in cultured rat hepatocytes.

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Primary rat hepatocyte cultures exposed to tert-butylhydroperoxide (t-BHP) or cumene hydroperoxide were used to assess the antioxidative and protective potential of water-soluble extracts of artichoke leaves. Both hydroperoxides stimulated the production of malondialdehyde (MDA), particularly when

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