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Query: UMLS:C0242706 (hyperoxia)
 5,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanisms that lead to mitochondrial damage under oxidative stress conditions were examined in primary and cultured cells as well as in the nematode Caenorhabditis elegans (C. elegans) treated simultaneously with electron transport inhibitors and oxygen gas. Oxygen loading enhanced the damage of PC 12 cells by thenoyltrifluoroacetone (TTFA, a complex II inhibitor), but did not by rotenone (a complex I inhibitor), antimycin (a complex III inhibitor), and sodium azide (a complex IV inhibitor). In primary hepatocytes, the enhancement was observed with the addition of sodium azide and rotenone, but not by TTFA or antimycin. In the nematode, only rotenone and TTFA enhanced the sensitivity under hyperoxia. These results demonstrate that highly specific inhibitors of electron transport can induce oxygen hypersensitivity in cell levels such as PC 12 cells and primary hepatocytes, and animal level of C. elegans. In addition the cell damage is different dependent on cell type and organism.
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PMID:Enhancement of oxidative damage to cultured cells and Caenorhabditis elegans by mitochondrial electron transport inhibitors. 1156 21

Oxidative damage shortens the life span of the nematode Caenorhabditis elegans (C. elegans), even in an age-1 mutant that is characterized by a long life and oxygen resistance. We found that daily short-term exposure (3 h) to hyperoxia further extended the life span of age-1, a phenomenon known as an adaptive response. age-1 also showed resistance to paraquat and heat. Acute hyperoxic treatment did not extend the life spans of wild type, daf-16 or mev-1. daf-16 mutant had a slightly shorter life span compared to wild type and was sensitive to heat and paraquat. The daf-16 phenotype resembles that of mev-1 showing a short life and oxygen sensitivity. We measured mRNA levels of superoxide dismutase genes (sod-1 through 4), catalase genes (clt-1 and ctl-2), known to encode anti-oxidant enzymes, and found they were elevated in age-1 young adults. On the other hand, in daf-16 and mev-1, the expression of sod-1, sod-2 and sod-3 genes was lower rather than in wild type. Conversely, ctl-1 and ctl-2 genes expression was significantly elevated in daf-16 and mev-1. This suggests that DAF-16, a forkhead/winged-helix transcription factor, whose expression is suppressed by AGE-1, phosphoinositide 3-kinase (PI3-kinase), regulates anti-oxidant genes as well as energy metabolism under atmospheric conditions. However, the level of gene expression of SOD and catalase was not elevated by short-term exposure to 90% oxygen in wild type, mev-1, daf-16 and even age-1. This suggests that SOD and catalase do not play a role in the adaptive response against oxidative stress under hyperoxia, at least under these experimental conditions.
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PMID:Adaptive responses to oxidative damage in three mutants of Caenorhabditis elegans (age-1, mev-1 and daf-16) that affect life span. 1247 Aug 95

The hormetic effect, which extends the lifespan by various stressors, has been confirmed in Caenorhabditis elegans (C. elegans). We have previously reported that oxidative stress resistance in a long-lived mutant age-1 is associated with the hormesis. In the age-1 allele, which activates an insulin/insulin-like growth factor-1 (Ins/IGF-1) signaling pathway, the superoxide dismutase (SOD) and catalase activities increased during normal aging. We now demonstrate changes in the mitochondrial superoxide radical (*O(2)(-)) levels of the hormetic conditioned age-related strains. The *O(2)(-) levels in age-1 strain significantly decreased after intermittent hyperoxia exposure. On the other hand, this phenomenon was not observed in a daf-16 null mutant. This hormesis-dependent reduction of the *O(2)(-) levels was observed even if the mitochondrial Mn-SOD was experimentally reduced. Therefore, it is indicated that the hormesis is mediated by events that suppress the mitochondrial *O(2)(-) production. Moreover, some SOD gene expressions in the hormetic conditioned age-1 mutant were induced over steady state mRNA levels. These data suggest that oxidative stress-inducible hormesis is associated with a reduction of the mitochondrial *O(2)(-) production by activation of the antioxidant system via the Ins/IGF-1 signaling pathway.
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PMID:Hyperoxia exposure induced hormesis decreases mitochondrial superoxide radical levels via Ins/IGF-1 signaling pathway in a long-lived age-1 mutant of Caenorhabditis elegans. 1828 59

Oxygen levels are unequal in different living geographical locations of human and related to normal physiology of health. The reduction of oxygen level in the body can lead to a variety of diseases, such as stroke caused by cerebral ischemia and hypoxia. In the recent years, many studies have elucidated the molecular and cellular mechanisms of organism response to different oxygen concentrations by using the nematode Caenorhabditis elegans (C. elegans) as model organism. C. elegans can escape hypoxia or hyperoxia and adapt to the ambient oxygen environments, and there are different response and regulation mechanisms in different degrees of hypoxia environment. In this paper, recent advances in the reaction of nematodes to different oxygen concentrations and the underlying mechanism were reviewed.
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PMID:[Progress in the mechanisms of response to different oxygen concentrations in Caenorhabditis elegans]. 3257 38