Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypoxic preconditioning is protective against oxidant-related damage in various organs, such as the heart. We previously showed that rats exposed to hypoxia also exhibit resistance to lethal pulmonary oxygen toxicity. The underlying mechanism and whether similar preconditioning is applicable to cellular models is unknown. In the present study, it was found that hypoxic pre-exposure induces a significant protective effect against hyperoxia-induced cell death in human lung microvascular endothelial cells (HLMVECs) and epithelial type II-like A549 cells. This effect of hypoxia is mediated by the phosphatidylinositol 3-kinase (PI3-K) signaling pathway because the presence of the PI3-K inhibitors, LY294002 and wortmannin, during pre-exposure to hypoxia completely blocks subsequent protection. Further, the hypoxia-dependent protection from hyperoxia was found to be associated with a 2-fold increase in PI3-K activity in hypoxia. Transient overexpression of a catalytically active class IA PI3-K p110alpha isoform also enhanced survival of A549 cells 2-fold compared with the empty vector control. These results indicate that hypoxia-induced activation of PI3-K is an important event in the acquisition of resistance against subsequent hyperoxic toxicity.
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PMID:Hypoxia protects human lung microvascular endothelial and epithelial-like cells against oxygen toxicity: role of phosphatidylinositol 3-kinase. 1254 Apr 85

Life span could be modified by genetic or environmental perturbations in Caenorhabditis elegans. Here we show that two extensions of life span are associated with oxidative stress resistance and upregulation of the gene expression of antioxidant enzymes. First, mutations in age-1 gene (PI3 kinase homologue) that confer life span extension, display oxidative stress resistance and increase in the gene expression of sod-3, one of two Mn-superoxide dismutases (SOD) and ctl-1, cytosolic catalase. In this study, these traits appear to be regulated by the following genetic pathway: daf-2 (insulin receptor family)-> daf-18 (PTEN homologue)-> age-1-> daf-16 (Fork head transcription factor family), similar to the genetic pathway for the life span extension. Second, we show that short-term exposure to hyperoxia extends life span slightly but significantly. This treatment increases oxidative stress resistance and the gene expression of three types of SOD isoforms. These results suggest that both of these two life span extensions are closely related with increase in the antioxidant defense function.
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PMID:Life span extensions associated with upregulation of gene expression of antioxidant enzymes in Caenorhabdms elegans; studies of mutation in the AGE-1, PI3 kinase homologue and short-term exposure to hyperoxia. 2360 83

Life span could be modified by genetic or environmental perturbations in Caenorhabditis elegans. Here we show that two extensions of life span are associated with oxidative stress resistance and upregulation of the gene expression of antioxidant enzymes. First, mutations in age-1 gene (PI3 kinase homologue)that confer life span extension, display oxidative stress resistance and increase in the gene expression of sod-3, one of two Mn-superoxide dismutases (SOD) and ctl-1, cytosolic catalase. In this study, these traits appear to be regulated by the following genetic pathway: daf-2 (insulin receptor family)-> daf-18 (PTEN homologue)-> age-1-> daf-16 (Fork head transcription factor family), similar to the genetic pathway for the life span extension. Second, we show that short-term exposure to hyperoxia extends life span slightly but significantly. This treatment increases oxidative stress resistance and the gene expression of three types of SOD isoforms. These results suggest that both of these two life span extensions are closely related with increase in the antioxidant defense function.
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PMID:Life span extensions associated with upregulation of gene expression of antioxidant enzymes in Caenorhabditis elegans; studies of mutation in the age-1, PI3 kinase homologue and short-term exposure to hyperoxia. 2360 87