Free Radicals in Inner Ear Immune Responses; Immunohistochemical Study of Myeloperoxidase

Kinoshita, Toshiyuki; Tomiyama, Shunichi

doi:10.3950/jibiinkoka.97.1608

Cited by 3 publications

(2 citation statements)

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“…Immunohistochemical analysis of neutrophil infiltration was performed with antibodies against myeloperoxidase (MPO) [29]. MPO-positive cells were rarely observed in morphologically normal mucosa, but frequently seen in active inflammatory areas (Fig.2A).…”

Section: Resultsmentioning

confidence: 99%

Soluble Epoxide Hydrolase Gene Deficiency or Inhibition Attenuates Chronic Active Inflammatory Bowel Disease in IL-10(−/−) Mice

et al. 2012

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Background Soluble epoxide hydrolase (sEH) metabolizes anti-inflammatory epoxyeicosatrienoic acids (EETs) into their much less active dihydroxy derivatives dihydroxyeicosatrienoic acids (DHETs). Thus, targeting sEH would be important for inflammation. Aims To determine whether knockout or inhibition of sEH would attenuate the development of inflammatory bowel disease (IBD) in a mouse model of IBD in IL-10(−/−) mice. Methods Either the small molecule sEH inhibitor trans/-4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid (t-AUCB) or sEH knockout mice were used in combination with IL-10(−/−) mice. t-AUCB was administered to mice in drinking fluid. Extensive histopathologic, immunochemical and biochemical analyses were performed to evaluate effect of sEH inhibition or deficiency on chronic active inflammation and related mechanism in the bowel. Results Compared to IL-10 (−/−) mice, sEH inhibition or sEH deficiency in IL-10(−/−) mice resulted in significantly lower incidence of active ulcer formation and transmural inflammation, along with a significant decrease in myeloperoxidase-labeled neutrophil infiltration in the inflamed bowel. The levels of IFN-γ, TNF-α, and MCP-1, as well VCAM-1 and NF-kB/IKK-α signals were significantly decreased as compared to control animals. Moreover, an eicosanoid profile analysis revealed a significant increase in the ratio of EETs/DHET and EpOME/DiOME, and a slightly down-regulation of inflammatory mediators LTB4 and 5-HETE. Conclusion These results indicate that sEH gene deficiency or inhibition reduces inflammatory activities in the IL-10 (−/−) mouse model of IBD, and that sEH inhibitor could be a highly potential in the treatment of IBD.

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Section: Resultsmentioning

confidence: 99%

Soluble Epoxide Hydrolase Gene Deficiency or Inhibition Attenuates Chronic Active Inflammatory Bowel Disease in IL-10(−/−) Mice

et al. 2012

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“…Twenty-five years later, we are now learning that noise-induced and drug-induced hearing loss could share a common damaging agent, specifically toxic free-oxygen radicals (FOR) and other reactive oxygen species (ROS). The direct evidence for free-radical generation and damage in the cochlea is sparse, 2,16,29,30 but free-radical damage is a reasonable hypothesis that is supported both by in vitro studies of FOR in cochlear cultures treat-ed with cisplatin 18,24,25 and by indirect evidence showing the protective effects of antioxidant enzymes. 7,11,26,27 High levels of noise are likely to create damaging free radicals by at least two pathways.…”

Section: Introductionmentioning

confidence: 99%

The Role of Antioxidants in Protection from Impulse Noise

Henderson

McFadden

Liu

et al. 1999

Annals of the New York Academy of Sciences

111

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The hearing loss from exposure to noise and ototoxic drugs share a number of audiological and pathological similarities. Recent research has shown that reactive oxygen species (ROS) may be a common factor in both noise- and drug-induced hearing loss. This review describes three experiments that point to ROS as a causative factor in both noise- and drug-induced hearing loss and antioxidants as a protective agent. In the first experiment, the ears of chinchillas were treated with R-N6-phenylisopropyladenoisine (R-PIA) and exposed to 150-dB impulse noise. The treated ears developed substantially less permanent hearing loss (PTS) and hair cell loss than the untreated ears. One interpretation of this experiment is that R-PIA increases the availability of glutathione (GSH). In the second experiment, the role of GSH was specifically examined. The ears of chinchillas were treated with glutathione monoethylester (GEE), a pro-GSH drug that has been shown to readily cross cell membranes and increase GSH levels. The GEE-treated ears had significantly less PTS and hair-cell loss than the nontreated ear. Previous research has shown that moderate levels of noise exposure can increase a subject's resistance to noise, and also increase the availability of antioxidant enzymes in the cochlea. In the third experiment, chinchillas were given a series of "toughening" exposures (i.e., 6 h of a 0.5-kHz OB noise at 95 dB for 10 days). After the series of "toughening" exposures, the subjects were treated with carboplatin, a drug that causes massive inner-hair-cell lesions in the chinchilla. The animals receiving the 10-day toughening exposure developed less PTS and hair-cell loss than the control animals.

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Immunoreactivity for myeloperoxidase (MPO) in the vestibule after the injection of bacterial lipopolysaccharide into the middle ear

2002

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Free Radicals in Inner Ear Immune Responses; Immunohistochemical Study of Myeloperoxidase

Abstract: Previously, we reported that immune reactions in the endolymphatic sac of guinea pigs caused spontaneous nystagmus, a suppressed caloric response, and fluctuating hearing loss.In order to evaluate immune injury to the sensory organs of the inner ear, we conducted an immunohisto-

Cited by 3 publications

References 12 publications

Soluble Epoxide Hydrolase Gene Deficiency or Inhibition Attenuates Chronic Active Inflammatory Bowel Disease in IL-10(−/−) Mice

Soluble Epoxide Hydrolase Gene Deficiency or Inhibition Attenuates Chronic Active Inflammatory Bowel Disease in IL-10(−/−) Mice

The Role of Antioxidants in Protection from Impulse Noise

Immunoreactivity for myeloperoxidase (MPO) in the vestibule after the injection of bacterial lipopolysaccharide into the middle ear

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