Hydrogen peroxide induces oxidative DNA damage in rat type II pulmonary epithelial cells

Meehan, William J.; Spencer, Jeremy P.E.; Rannels, D. E.; Welch, Danny R.; Knobbe, Edward T.; Ostrander, Gary K.

doi:10.1002/(sici)1098-2280(1999)33:4<273::aid-em3>3.0.co;2-t

Cited by 11 publications

(5 citation statements)

References 36 publications

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“…In addition, H 2 O 2 is a major component of ROS produced intracellularly during a number of physiological and pathological processes, and causes oxidative damage (25,26). For this reason, H 2 O 2 has often been used as an experimental model to investigate the mechanisms of cell injury induced by oxidative stress (27)(28)(29). In the present study, when HepG2 cells pre-treated with FBG were challenged with H 2 O 2 , ROS formation decreased.…”

Section: Discussionmentioning

confidence: 66%

Detoxifying effect of fermented black ginseng on H2O2-induced oxidative stress in HepG2 cells

Bak

Jeong

Kim

2014

International Journal of Molecular Medicine

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Abstract. Fermented black ginseng (FBG) is prepared by repeated steaming and drying processes with fresh ginseng followed by fermentation with Saccharomyces cerevisiae. It has recently been shown to have several bioactivities. FBG contains crude saponin (1,440 µg/ml), ginsenoside Rg2 (2.86 µg/ml), ginsenoside Rg3 (24.52 µg/ml), ginsenoside Rh1 (12.64 µg/ml), ginsenoside Rh2 (0.63 µg/ml) and ginsenoside Rf (1.32 µg/ml). The present study investigated the antioxidant defense properties of FBG against hydrogen peroxide (H 2 O 2 )-mediated oxidative stress in HepG2 human hepatocellular carcinoma cells. The increased production of reactive oxygen species (ROS) induced by H 2 O 2 was attenuated in a dose-dependent manner when the cells were pre-treated with FBG (10-50 µg/ml). FBG induced both the expression and activity of antioxidant enzymes, such as superoxide dismutase, catalase and glutathione peroxidase in the H 2 O 2 -treated HepG2 cells. The inhibitory effects of FBG on the phosphorylation of upstream mitogen-activated protein kinases (MAPKs), such as c-Jun N-terminal kinase, extracellular signal-regulated kinase and p38 were also observed. Overall, our results demonstrate that FBG protects HepG2 cells from oxidative stress through the induction of antioxidant enzyme activity and the inhibition of MAPK pathways.

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Section: Discussionmentioning

confidence: 66%

Detoxifying effect of fermented black ginseng on H2O2-induced oxidative stress in HepG2 cells

Bak

Jeong

Kim

2014

International Journal of Molecular Medicine

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“…Hydrogen peroxide (H 2 O 2 ), a reactive oxygen species, is an established polymorphonuclear leukocyte-derived mediator of epithelial injury. In alveolar epithelial cells, H 2 O 2 effects are manyfold and include an initial depletion of intracellular ATP, a sustained inhibition of alveolar epithelial type II cell (ATII) surfactant synthesis, loss of epithelial barrier properties, DNA damage, and cell lysis at high dosage (5)(6)(7)(8)(9).…”

mentioning

confidence: 99%

Apical, But Not Basolateral, Endotoxin Preincubation Protects Alveolar Epithelial Cells Against Hydrogen Peroxide-Induced Loss of Barrier Function: The Role of Nitric Oxide Synthesis

Rose

Guthmann

Tenenbaum

et al. 2002

The Journal of Immunology

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The influence of LPS preincubation on hydrogen peroxide (H2O2)-induced loss of epithelial barrier function was investigated in rat alveolar epithelial type II cells (ATII). Both apical and basolateral H2O2 administration caused a manyfold increase in transepithelial [3H]mannitol passage. Apical but not basolateral preincubation of ATII with LPS did not influence control barrier properties but fully abrogated the H2O2-induced leakage response. The effect of apical LPS was CD14 dependent and was accompanied by a strong up-regulation of NO synthase II mRNA and protein and NO release. Inhibition of NO by NG-monomethyl-l-arginine suppressed the LPS effect, whereas it was reproduced by exogenous application of gaseous NO or NO donor agents. Manipulation of the glutathione homeostasis (buthionine-(S,R)-sulfoximine) and the cGMP pathway (1H-(1,2,4)oxadiazolo[4,3-α]quinoxaline-1-one; zaprinast) did not interfere with the protective effect of LPS. Superoxide (O⨪2) generation by ATII cells was reduced by exogenous NO and LPS preincubation. O⨪2 scavenging with exogenous superoxide dismutase, the intracellular superoxide dismutase analog Mn(III)tetrakis(4-benzoic acid) porphyrin, and the superoxide scavenger nitroblue tetrazolium and, in particular, hydroxyl radical scavenging with hydroxyl radical scavenger 1,3-dimethyl-thiourea inhibited the H2O2-induced epithelial leakage response. In conclusion, apical but not basolateral LPS preincubation of ATII cells provides strong protection against H2O2-induced transepithelial leakage, attributable to an up-regulation of epithelial NO synthesis. It is suggested that the LPS-induced NO formation is effective via interaction with reactive oxygen species, including superoxide and hydroxyl radicals. The polarized epithelial response to LPS may be part of the lung innate immune system, activated by inhaled endotoxin or under conditions of pneumonia.

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“…This is similar to the photosensitizing activity of the short-wavelength UVA found in the present study and raises the question of whether the latter points to an increased risk of melanoma from the photosensitization of o-PABA. At present the evidence for hydroxyl radicals being mutagenic is limited (27,28). The significance of the present results will therefore require further evaluation such as measurement of outcomes more closely related to carcinogenesis.…”

Section: Discussionmentioning

confidence: 80%

Photosensitization of the Sunscreen Octyl p-Dimethylaminobenzoate by UVA in Human Melanocytes but not in Keratinocytes¶

Xu¹,

Green²,

Parisi³

et al. 2007

Photochemistry and Photobiology

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Sunscreens penetrate human epidermis and modify the biology of proliferating cells. This study addressed the question whether the UV response of cultured human cells is affected by direct treatment with nontoxic levels of sunscreens. Cell survival following exposure to UVC or unfiltered UVB was not altered by preincubation with 25 g/mL of octyl p-dimethylaminobenzoate (o-PABA), 2-ethylhexyl p-methoxycinnamate (EHMC) or oxybenzone. However, UVA or UVB filtered to reproduce the solar UV spectrum penetrating to the basal layer of the epidermis, highly sensitized cells to killing by o-PABA but not by its hydrolysis product, 4-dimethylaminobenzoic acid. Sensitization was found in all cell types tested, except normal keratinocytes, and could be prevented by certain antioxidants particularly pyruvate and the hydroxyl radical scavenger mannitol. o-PABA and EHMC applied without UV reduced the adherence of cells. The results indicate that sunscreens may increase cell mobility and the combination of o-PABA with solar UV may selectively damage melanocytes in the skin.

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Hydrogen peroxide induces oxidative DNA damage in rat type II pulmonary epithelial cells

Cited by 11 publications

References 36 publications

Detoxifying effect of fermented black ginseng on H2O2-induced oxidative stress in HepG2 cells

Detoxifying effect of fermented black ginseng on H2O2-induced oxidative stress in HepG2 cells

Apical, But Not Basolateral, Endotoxin Preincubation Protects Alveolar Epithelial Cells Against Hydrogen Peroxide-Induced Loss of Barrier Function: The Role of Nitric Oxide Synthesis

Photosensitization of the Sunscreen Octyl p-Dimethylaminobenzoate by UVA in Human Melanocytes but not in Keratinocytes¶

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