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Cystine Deprivation Triggers Programmed Necrosis in VHL-Deficient Renal Cell Carcinomas.
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Oncogenic transformation may reprogram tumor metabolism and render cancer cells addicted to extracellular nutrients. Deprivation of these nutrients may therefore represent a therapeutic opportunity, but predicting which nutrients cancer cells become addicted remains difficult. Here, we performed a
Plasma L-cystine/L-glutamate imbalance increases tumor necrosis factor-alpha from CD14+ circulating monocytes in patients with advanced cirrhosis.
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OBJECTIVE
The innate immune cells can not normally respond to the pathogen in patients with decompensated cirrhosis. Previous studies reported that antigen-presenting cells take up L-Cystine (L-Cys) and secrete substantial amounts of L-Glutamate (L-Glu) via the transport system Xc- (4F2hc+xCT), and
Relation between selenium traces in L-cystine and protection against dietary liver necrosis.
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The cystine and methionine contents of liver protein in acute hepatic necrosis.
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Tumor necrosis factor-alpha and its second messenger, ceramide, stimulate apoptosis in cultured ovarian follicles.
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In the mammalian ovary, only a small fraction of follicles fully mature and ovulate, while most of them die via apoptosis. Multiple factors promoting follicle survival have been identified, but intraovarian mediators of apoptosis are poorly known. Tumor necrosis factor-alpha (TNF alpha) is a
The role of glutathione in L-2-chloropropionic acid induced cerebellar granule cell necrosis in the rat.
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The role of glutathione (GSH) in the neurotoxicity produced following a single oral dose of 750 mg/kg L-2-chloropropionic acid (L-CPA) has been investigated in rats. L-CPA-induced neurotoxicity was characterised by up to 80-90% loss in cerebellar granule cells and cerebellar oedema leading to
Sulfur-containing amino acids that increase renal glutathione protect the kidney against papillary necrosis induced by 2-bromoethylamine.
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Papillary necrosis was observed in the kidneys of rats, 72 h after receiving a single injection of bromoethylamine (BEA). This effect was associated with renal glutathione (GSH) depletion 1 h after the administration of BEA. Stimulation of renal GSH synthesis by pretreatment of the animals either
Structural homology of the central conserved region of the attachment protein G of respiratory syncytial virus with the fourth subdomain of 55-kDa tumor necrosis factor receptor.
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The attachment protein G of respiratory syncytial virus (RSV) has a modular architecture. The ectodomain of the protein comprises a small folded conserved region which is bounded by two mucin-like regions. In this study, a sequence and structural homology is described between this central conserved
CIRRHOSIS OF THE LIVER CAUSED BY EXCESS DIETARY CYSTINE.
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1. Cystine fed to young albino rats as 10 per cent of the diet resulted in: (a) Portal hemorrhagic necrosis, resembling eclampsia, within 3 or 4 days. (b) A high mortality rate. (c) Fatty infiltration of hepatic cells in all rats surviving the initial acute lesion. (d) Cirrhosis of the liver in rats
THE EFFECT OF VARIOUS DIETS ON THE LIVER DAMAGE CAUSED BY EXCESS CYSTINE.
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1. The effect of 9 different diets on the liver lesions resulting from excess dietary cystine has been studied in 130 rats. 2. The incidence and severity of each of the following liver lesions were varied by changes in the composition of diets containing 5 or 10 per cent cystine: (a) Hemorrhage was
LIVER DAMAGE AND URINARY EXCRETION OF SULFATE IN RATS FED l-CYSTINE, dl-METHIONINE, AND CYSTEIC ACID.
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1. Rats fed l-cystine at excessive levels excrete large amounts of sulfate sulfur in the urine and develop liver necrosis and cirrhosis. 2. Rats fed dl-methionine at excessive levels excrete large amounts of sulfate sulfur, but do not develop liver necrosis and cirrhosis. 3. Rats fed cysteic acid at
OBSERVATIONS ON THE CONDITIONS OF DIETARY HEPATIC INJURY (NECROSIS, CIRRHOSIS) IN RATS.
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Experimental dietary hepatic injury (diffuse or focal necrosis and cirrhosis in rats, with or without ascites and pleural and pericardial effusion) is determined by the dietary factors instrumental also in the production of fat infiltration of the liver and thus opposed to the lipotropic activity of
Effects of sulfur amino acids, L: -methionine, L: -cystine and L: -cysteine on lipoprotein lipase and hormone-sensitive lipase in differentiated mouse 3T3-L1 adipocytes.
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Rats subcutaneously implanted with AH109A hepatoma cells show hyperlipidemia with high concentrations of serum triglyceride and nonesterified fatty acid, suppression of lipoprotein lipase (LPL), and elevation of hormone-sensitive lipase (HSL) activities during the growth of the hepatoma.
Effect of different amino acidic pretreatments that protect the kidney against papillary necrosis induced by bromoethylamine on differential distribution of renal nonprotein sulfhydryls.
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Content of nonprotein sulfhydryls (NPSH) was found to be higher in rat renal cortex than in external medulla and papilla. Administration of bromoethylamine (BEA), at a dose that produces extensive papillary necrosis and minor effects in the other renal segments, induced a significant reduction in
Induction of cystine transport activity in mouse peritoneal macrophages by bacterial lipopolysaccharide.
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The transport of cystine has been investigated in mouse peritoneal macrophages cultured in vitro. The transport activity for cystine was very low in freshly isolated macrophages but was potently induced during culture in the presence of bacterial lipopolysaccharide (LPS) at concentrations as low as
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