Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017638 (glioma)
 30,880 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The potential cytoprotective effects of estrogen in the brain are of special interest in aging, neurodegenerative diseases, exposure to toxins, and trauma. Estrogen effects on neurons have been widely explored, but less is known about estrogen effects on glia. Glial cells are primary targets of ammonia toxicity, which arises from liver disease or failure (such as from cirrhosis in alcoholics), urea cycle disorders, or inborn errors of metabolism. We examined the ability of estrogen to protect glial cells from ammonium chloride toxicity using an in vitro model system. C6-glioma cells in later passage have many astrocytic characteristics and provided a convenient and well established model system for this work. When C6-glioma cells were exposed to 15 mM ammonium chloride, we observed major cell death (only 32% cell survival relative to control) within 72 h. Pretreatment with 17beta-estradiol (10 microM) significantly protected C6-glioma cells from ammonia toxicity (99% cell survival relative to control). In addition to enhancing the viability of C6-glioma cells against ammonia challenge, estrogen pretreatment was also found to protect mitochondrial function as assayed using the MTT reduction assay. Mitochondrial function was reduced to 39% of control levels in ammonia-challenged cultures and was mostly protected by estrogen (72% of control levels). The findings are potentially relevant for the development of therapeutic strategies to protect glial cells against ammonia toxicity resulting from hepatic failure or other causes.
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PMID:Cytoprotective effect of estrogen on ammonium chloride-treated C6-glioma cells. 1520 65

Alcoholism is a serious health problem. Alcohol-dependent subjects have many health-related problems, such as severe cognitive impairments, alcoholic liver disease and coronary heart disease, resulting from ethanol-induced cell injury or cell death. Understanding the mechanisms underlying the cell death may provide clues for novel treatment strategies to prevent alcohol-induced cell damage. Prolonged ethanol consumption causes apoptotic activity in a host of cell types - more obviously affecting the liver, heart and surprisingly affecting the brain. This study uses four cell lines: neuronal cell line (SH-SY5Y), glia cell line (U-118 MG), liver cell line (E47) and heart cell line (the rat H9c2), and addresses that alcohol does, in fact, cause cell death in these four cell types, whether ethanol induced cell death is through apoptotic pathway, and whether an monoamine oxidase (MAO) inhibitor (e.g. deprenyl) protects cells from the effects of alcohol. We have found that ethanol exposure lowers cell proliferation in all cell types, but affects brain cell lines (neuron and glioma) the most, while ethanol and deprenyl exposure in unison increases cell viability largely in brain cells, and then in liver cells. Our results suggest that MAO mediated apoptosis may contribute to ethanolinduced cell death. Individuals suffering from alcoholism or alcohol abuse may be treated with deprenyl to alleviate the apoptotic activity resulting from alcohol consumption and protect the body's cells from alcohol-induced death. In summary, this study demonstrates the effects of deprenyl as an anti-apoptotic agent against the detrimental effects of alcohol.
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PMID:The effects of antidepressant drug on ethanol-induced cell death. 2250 99