s adenosylmethionine/hypoxie

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GADD45β induction by S-adenosylmethionine inhibits hepatocellular carcinoma cell proliferation during acute ischemia-hypoxia.

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Growth arrest DNA damage-inducible gene 45β (GADD45β), which influences cell growth, apoptosis and cellular response to DNA damage, is downregulated in hepatocellular carcinoma (HCC). S-adenosylmethionine (SAMe) serves as an essential methyl donor in multiple metabolic pathways and is a polyamine

The methyl donor S-adenosylmethionine prevents liver hypoxia and dysregulation of mitochondrial bioenergetic function in a rat model of alcohol-induced fatty liver disease.

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Mitochondrial dysfunction and bioenergetic stress play an important role in the etiology of alcoholic liver disease. Previous studies from our laboratory show that the primary methyl donor S-Adenosylmethionine (SAM) minimizes alcohol-induced disruptions in several mitochondrial functions in the

Impact of S-adenosylmethionine decarboxylase 1 on pulmonary vascular remodeling.

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BACKGROUND Pulmonary hypertension (PH) is a life-threatening disease characterized by vascular remodeling and increased pulmonary vascular resistance. Chronic alveolar hypoxia in animals is often used to decipher pathways being regulated in PH. Here, we aimed to investigate whether chronic

Mild neonatal hypoxia exacerbates the effects of vitamin-deficient diet on homocysteine metabolism in rats.

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Elevated plasma homocysteine has been linked to pregnancy complications and developmental diseases. Whereas hyperhomocysteinemia is frequently observed in populations at risk of malnutrition, hypoxia may alter the remethylation of homocysteine in hepatocytes. We aimed to investigate the combined

Influence of preconditioning-like hypoxia on the liver of developing methyl-deficient rats.

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Deficiency in nutritional determinants of homocysteine (HCY) metabolism, such as vitamin B(12) and folate, during pregnancy is known to influence HCY levels in the progeny, which in turn may exert adverse effects during development, including liver defects. Since short hypoxia has been shown to

Epigenetic signature of chronic cerebral hypoperfusion and beneficial effects of S-adenosylmethionine in rats.

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Chronic cerebral hypoperfusion is associated with cognitive decline in aging and age-related neurodegenerative disease. Epigenetic mechanisms are involved in the maintenance of long-term hypoxia-adapted cellular phenotypes. In the present study, the epigenetic signatures such as DNA methylation and

Epigenetic Features Induced by Ischemia-Hypoxia in Cultured Rat Astrocytes.

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Epigenetic mechanisms are involved in the maintenance of long-term hypoxia-adapted cellular functions. Astrocytes as the dividing neuroglia cell in the nervous tissue can be activated under hypoxia condition. In the present study, the epigenetic characteristics such as DNA methylation and histone

S-adenosylhomocysteine metabolism in different cell lines: effect of hypoxia and cell density.

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OBJECTIVE The methylation potential (MP) is defined as the ratio of S-adenosylmethionine (AdoMet) to S-adenosylhomocysteine (AdoHcy). It was shown recently that hypoxia increases AdoMet/AdoHcy ratio in HepG2 cells (Hermes et al., Exp Cell Res 294: 325-334, 2004). In the present study, we compared

[Effects of exogenous gamma-aminobutyric acid on polyamine metabolism of melon seedlings under hypoxia stress].

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Taking melon cultivar 'Xiyu No. 1 ' as test material, a hydroponic experiment was conducted to investigate the effects of exogenous gamma-aminobutyric acid (GABA) on the seedlings polyamine metabolism under hypoxia stress. Compared with the control in normoxic treatment, the seedlings under hypoxia

Polyamine biosynthesis and degradation are modulated by exogenous gamma-aminobutyric acid in root-zone hypoxia-stressed melon roots.

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We detected physiological change and gene expression related to PA metabolism in melon roots under controlled and hypoxic conditions with or without 5 mM GABA. Roots with hypoxia treatment showed a significant increase in glutamate decarboxylase (GAD) activity and endogenous GABA concentration.

Expression and localization of S-adenosylhomocysteine-hydrolase in the rat kidney following carbon monoxide induced hypoxia.

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OBJECTIVE Tissue hypoxia induces a variety of functional changes including enhanced transcriptional activity associated with high transmethylation activity (e.g. mRNA cap methylation) in the nucleus. It is well known that the kidney responds to hypoxia with enhanced transcription of erythropoietin

Regulation of ornithine decarboxylase by hypoxia in pulmonary artery smooth muscle cells.

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The polyamines are a family of low-molecular-weight organic cations that play essential intracellular regulatory roles in cell growth and differentiation. Elevations in cellular polyamine contents necessary for most physiological and pathological events in the lung appear to be driven by increase de

Proteomic analysis reveals response of differential wheat (Triticum aestivum L.) genotypes to oxygen deficiency stress.

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Waterlogging is one of the main abiotic stresses that limit wheat production. Quantitative proteomics analysis has been applied in the study of crop abiotic stress as an effective way in recent years (e.g. salt stress, drought stress, heat stress and waterlogging stress). However, only

Hypoxia induces genomic DNA demethylation through the activation of HIF-1α and transcriptional upregulation of MAT2A in hepatoma cells.

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Hypoxia-inducible factor 1 (HIF-1) emerges as a crucial player in tumor progression. However, its role in hepatocellular carcinoma (HCC), especially its relation with global DNA methylation patterns in HCC under hypoxic tumor microenvironment is not completely understood. Methionine

Oxygen dependence of glutathione synthesis in hepatocytes.

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The O2 dependence of glutathione (GSH) synthesis was studied in freshly isolated hepatocytes of white male rats. The rate of synthesis with methionine as the sulfur-containing amino acid precursor was decreased at hypoxic O2 concentrations and was half-maximal at 5 microM O2. ATP-dependent formation

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