Tissue Responses to Hyperoxia

Webster, Nigel R.; Toothill, C.; Cowen, P. N.

doi:10.1093/bja/59.6.760

Cited by 22 publications

(6 citation statements)

References 12 publications

(4 reference statements)

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“…This finding may be interpreted in different ways. For instance, it could be a response to hyperoxia-induced haemolytic reactions, as exposure of rats to 80% hyperoxia for 11 days has been reported to increase haemolysis and decrease haemoglobin concentration [38]. Otherwise, it could be intriguing to hypothesize a direct effect of hyperoxia on haemopoietic stem cells.…”

Section: Discussionmentioning

confidence: 99%

Postnatal Hyperoxia Exposure Differentially Affects Hepatocytes and Liver Haemopoietic Cells in Newborn Rats

et al. 2014

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Premature newborns are frequently exposed to hyperoxic conditions and experimental data indicate modulation of liver metabolism by hyperoxia in the first postnatal period. Conversely, nothing is known about possible modulation of growth factors and signaling molecules involved in other hyperoxic responses and no data are available about the effects of hyperoxia in postnatal liver haematopoiesis. The aim of the study was to analyse the effects of hyperoxia in the liver tissue (hepatocytes and haemopoietic cells) and to investigate possible changes in the expression of Vascular Endothelial Growth Factor (VEGF), Matrix Metalloproteinase 9 (MMP-9), Hypoxia-Inducible Factor-1α (HIF-1α), endothelial Nitric Oxide Synthase (eNOS), and Nuclear Factor-kB (NF-kB). Experimental design of the study involved exposure of newborn rats to room air (controls), 60% O2 (moderate hyperoxia), or 95% O2 (severe hyperoxia) for the first two postnatal weeks. Immunohistochemical and Western blot analyses were performed. Severe hyperoxia increased hepatocyte apoptosis and MMP-9 expression and decreased VEGF expression. Reduced content in reticular fibers was found in moderate and severe hyperoxia. Some other changes were specifically produced in hepatocytes by moderate hyperoxia, i.e., upregulation of HIF-1α and downregulation of eNOS and NF-kB. Postnatal severe hyperoxia exposure increased liver haemopoiesis and upregulated the expression of VEGF (both moderate and severe hyperoxia) and eNOS (severe hyperoxia) in haemopoietic cells. In conclusion, our study showed different effects of hyperoxia on hepatocytes and haemopoietic cells and differential involvement of the above factors. The involvement of VEGF and eNOS in the liver haemopoietic response to hyperoxia may be hypothesized.

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Section: Discussionmentioning

confidence: 99%

Postnatal Hyperoxia Exposure Differentially Affects Hepatocytes and Liver Haemopoietic Cells in Newborn Rats

et al. 2014

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“…Hyperoxia has frequently been reported to increase SOD activity in animal tissues after prolonged exposure (Kimball et al 1976; Housset and Junod 1982; Freeman et al 1986; Webster et al 1987; Taylor and Bray 1991; also see Allen and Balin 1989 for review). Increases in Cu/Zn SOD activity have Taylor and Bray 1991 also been reported in some types of human cell culture, such as human umbilical vein endothelial cells exposed to hyperoxia (Jornot and Junod 1992); however, neither form of SOD responded to variations in oxygen tension in the early passage WI-38 cultures examined.…”

Section: Discussionmentioning

confidence: 99%

Effects of oxygen, growth state, and senescence on the antioxidant responses of WI-38 fibroblasts

Balin

Reimer

Reenstra

et al. 2010

AGE

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Mitotically active, growth-arrested cells and proliferatively senescent cultures of human fetal lung fibroblasts (WI-38) were exposed to six different oxygen tensions for various lengths of time and then analyzed to determine the responses of their antioxidant defense system. Glutathione (GSH) concentration increased as a function of ambient oxygen tension in early passage cultures; the effect was larger in exponentially growing cultures than in those in a state of contact-inhibited growth arrest, but was absent in senescent cells. Conversely, the activity of glutathione disulfide reductase was greater in growth-arrested cultures than in mitotically active cells irrespective of oxygen tension. Glucose-6-phosphate dehydrogenase was lowest in log-phase cells exposed to different oxygen tensions for 24 h and in senescent cells. Both hypoxia and hyperoxia depressed selenium-dependent glutathione peroxidase activity in early passage cultures, while the activity of the enzyme progressively declined with increasing oxygen in senescent cells. The GSH S-transferase activity was unresponsive to changes in ambient oxygen tension in either young or senescent cultures. Manganese-containing superoxide dismutase (MnSOD) activity was unaffected by oxygen tension, but was elevated in young confluent cultures as compared with cultures in log-phase growth. MnSOD activity was significantly higher in senescent cultures than in early passage cultures and was also responsive to increased oxygen tension in senescent cultures. Copper–zinc-containing superoxide dismutases activity was not affected by oxygen tension or the passage of time, but it declined in senescent cultures.

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“…Except possibly in skin (e.g., wound healing), high O 2 induces oxidant injury in almost every organ, especially in the lung, retina, heart and brain [1], [2], [3]. Prolonged exposure to high oxygen generates excessive reactive oxygen species, induces cell death and oxidative stress responses, affects immune response and DNA integrity and modulates cell growth [4], [5], [6], [7], [8].…”

Section: Introductionmentioning

confidence: 99%

Experimental Selection for Drosophila Survival in Extremely High O2 Environments

et al. 2010

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Although oxidative stress is deleterious to mammals, the mechanisms underlying oxidant susceptibility or tolerance remain to be elucidated. In this study, through a long-term laboratory selection over many generations, we generated a Drosophila melanogaster strain that can live and reproduce in very high O2 environments (90% O2), a lethal condition to naïve flies. We demonstrated that tolerance to hyperoxia was heritable in these flies and that these hyperoxia-selected flies exhibited phenotypic differences from naïve flies, such as a larger body size and increased weight by 20%. Gene expression profiling revealed that 227 genes were significantly altered in expression and two third of these genes were down-regulated. Using a mutant screen strategy, we studied the role of some altered genes (up- or down-regulated in the microarrays) by testing the survival of available corresponding P-element or UAS construct lines under hyperoxic conditions. We report that down-regulation of several candidate genes including Tropomyosin 1, Glycerol 3 phosphate dehydrogenase, CG33129, and UGP as well as up-regulation of Diptericin and Attacin conferred tolerance to severe hyperoxia. In conclusion, we identified several genes that were not only altered in hyperoxia-selected flies but we also prove that these play an important role in hyperoxia survival. Thus our study provides a molecular basis for understanding the mechanisms of hyperoxia tolerance.

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Tissue Responses to Hyperoxia

Cited by 22 publications

References 12 publications

Postnatal Hyperoxia Exposure Differentially Affects Hepatocytes and Liver Haemopoietic Cells in Newborn Rats

Postnatal Hyperoxia Exposure Differentially Affects Hepatocytes and Liver Haemopoietic Cells in Newborn Rats

Effects of oxygen, growth state, and senescence on the antioxidant responses of WI-38 fibroblasts

Experimental Selection for Drosophila Survival in Extremely High O2 Environments

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