ethyl ester/necrosis

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Induction of apoptosis and necrosis in human peripheral blood mononuclear cells by fatty acid ethyl esters.

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BACKGROUND Fatty acid ethyl esters (FAEE), nonoxidative products of ethanol metabolism, are formed by the esterification of fatty acids and ethanol. Alcoholic subjects have high levels of FAEE in the circulation as well as in organs and tissues, especially those most often damaged by ethanol abuse.

Glutamine and glutaminolysis are required for efficient replication of infectious spleen and kidney necrosis virus in Chinese perch brain cells.

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Viruses rely on host cellular metabolism for energy and macromolecule synthesis during their replication. Infectious spleen and kidney necrosis virus (ISKNV) causes significant economic losses in the Chinese perch (Siniperca chuatsi) industry worldwide. However, little is known about the

Protective role of intracellular glutathione against nitric oxide-induced necrosis in rat gastric mucosal cells.

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BACKGROUND Nitric oxide synthase activity is increased in the stomach in association with Helicobacter pylori infection and portal hypertension, but the mechanism by which nitric oxide contributes to mucosal damage remains unclear. OBJECTIVE To examine whether nitric oxide injures gastric mucosal

Influence of eicosapentaenoic acid, an omega-3 fatty acid, on ultraviolet-B generation of prostaglandin-E2 and proinflammatory cytokines interleukin-1 beta, tumor necrosis factor-alpha, interleukin-6 and interleukin-8 in human skin in vivo.

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Dietary omega-3 polyunsaturated fatty acids (omega-3 PUFA) reduce sunburn, an acute inflammatory response, in humans. We assessed whether this may be mediated by reduced ultraviolet-B (UV-B) induction of proinflammatory mediators tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1 beta,

Selective involvement of superoxide anion, but not downstream compounds hydrogen peroxide and peroxynitrite, in tumor necrosis factor-alpha-induced apoptosis of rat mesangial cells.

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Tumor necrosis factor-alpha (TNF-alpha) induces reactive oxygen species (ROS) that serve as second messengers for intracellular signaling. Currently, precise roles of individual ROS in the actions of TNF-alpha remain to be elucidated. In this report, we investigated the roles of superoxide anion

Highly purified eicosapentaenoic acid ethyl ester prevents development of steatosis and hepatic fibrosis in rats.

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OBJECTIVE Pathogenesis of nonalcoholic steatohepatitis (NASH) is considered to be involved in fat accumulation, oxidative stress, inflammation, and fibrosis in liver, but no drug therapy has been established as yet. Eicosapentaenoic acid (EPA) is an agent used clinically to treat

Selective glutathione depletion of mitochondria by ethanol sensitizes hepatocytes to tumor necrosis factor.

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OBJECTIVE Tumor necrosis factor (TNF)-alpha induces cell injury by generating oxidative stress from mitochondria. The purpose of this study was to determine the effect of ethanol on the sensitization of hepatocytes to TNF-alpha. METHODS Cultured hepatocytes from ethanol-fed (ethanol hepatocytes) or

Accelerated recovery of mitochondrial membrane potential by GSK-3β inactivation affords cardiomyocytes protection from oxidant-induced necrosis.

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Loss of mitochondrial membrane potential (ΔΨm) is known to be closely linked to cell death by various insults. However, whether acceleration of the ΔΨm recovery process prevents cell necrosis remains unclear. Here we examined the hypothesis that facilitated recovery of ΔΨm contributes to

TRO40303 Ameliorates Alcohol-Induced Pancreatitis Through Reduction of Fatty Acid Ethyl Ester-Induced Mitochondrial Injury and Necrotic Cell Death.

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Mitochondrial permeability transition pore inhibition is a promising approach to treat acute pancreatitis (AP). We sought to determine (i) the effects of the mitochondrial permeability transition pore inhibitor 3,5-seco-4-nor-cholestan-5-one oxime-3-ol (TRO40303) on murine and human pancreatic

L-arginine and arginine ethyl ester enhance proliferation of endothelial cells and preadipocytes - how an arginine ethyl ester-releasing biomaterial could support endothelial cell growth in tissue engineering.

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Adipose tissue engineering is a promising solution for the reconstruction of soft tissue defects. An insufficient neovascularisation within the scaffolds that leads to necrosis and tissue loss is still a major shortcoming of current tissue engineering attempts. Biomaterials, which release angiogenic

Fatty Acid Ethyl Esters Are Less Toxic Than Their Parent Fatty Acids Generated during Acute Pancreatitis.

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Although ethanol causes acute pancreatitis (AP) and lipolytic fatty acid (FA) generation worsens AP, the contribution of ethanol metabolites of FAs, ie, FA ethyl esters (FAEEs), to AP outcomes is unclear. Previously, pancreata of dying alcoholics and pancreatic necrosis in severe AP, respectively,

Selective cytotoxicity of indomethacin and indomethacin ethyl ester-loaded nanocapsules against glioma cell lines: an in vitro study.

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Gliomas are the most common and devastating tumors of the central nervous system. Several studies have suggested that nonsteroidal anti-inflammatory drugs (NSAIDs) are promising anticancer agents. Biodegradable nanoparticulate systems have received considerable attention as potential drug delivery

Glutathione elevation by gamma-glutamyl cysteine ethyl ester as a potential therapeutic strategy for preventing oxidative stress in brain mediated by in vivo administration of adriamycin: Implication for chemobrain.

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Oxidative stress in heart and brain by the cancer chemotherapeutic drug adriamycin (ADR), used for treating solid tumors, is well established. Long-term treatment with ADR in breast cancer patients has led to symptoms of cardiomyopathy. Less well recognized, but increasingly well documented, is

Fatty acid ethyl ester synthase inhibition ameliorates ethanol-induced Ca2+-dependent mitochondrial dysfunction and acute pancreatitis.

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OBJECTIVE Non-oxidative metabolism of ethanol (NOME) produces fatty acid ethyl esters (FAEEs) via carboxylester lipase (CEL) and other enzyme action implicated in mitochondrial injury and acute pancreatitis (AP). This study investigated the relative importance of oxidative and non-oxidative pathways

Differential inflammatory status in rats susceptible or resistant to diet-induced obesity: effects of EPA ethyl ester treatment.

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BACKGROUND Obesity has been associated with a chronic low degree inflammatory response, characterized by an increase of inflammatory adipocytokines like tumoral necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) as well as the synthesis of acute phase reactants such as haptoglobin. OBJECTIVE To

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