Original contributionOxidant-mediated ciliary dysfunction in human respiratory epithelium
References (45)
Host-defense mechanisms responsible for lung injury
J. Allerg. Clin. Immunol.
(1986)Oxidants from phagocytes: Agents of defence and destruction
Blood
(1984)Reactive oxidant species and airway inflammation
Free Radic. Biol. Med.
(1990)- et al.
Oxidant-mediated ciliary dysfunction. Possible role in airway disease
Chest
(1986) - et al.
Non-invasive sampling of nasal cilia for the measurement of beat frequency and ultrastructure
Lancet
(1980) - et al.
Lucigenin-dependent chemiluminescence as a new assay for NADPH-oxidase activity in particulate fractions of human polymorphonuclear leukocytes
J. Immunol. Meth.
(1984) A peroxidase-independent method for the quantitation of extracellular hydrogen peroxide generated by activated phagocytes in vitro
J. Immunol. Meth.
(1992)- et al.
Ellman's reagent: 5.5-dithiobis (2-nitrobenzoic acid)—A reexamination
Analyt. Biochem.
(1979) - et al.
Quantitative and temporal characterization of the extracellular H2O2 pool generated by human neutrophils
J. Biol. Chem.
(1984) - et al.
Leukocyte-induced tissue injury
Haematol/Oncol. Clin. North Am.
(1988)
Mechanisms of oxidant-mediated cell injury
J. Biol. Chem.
The effect of Streptococcus pneumoniae pheumolysin on human respiratory epithelium in vitro
Microb. Pathogen.
In vivo damage of rat lungs by oxygen metabolites
J. Clin. Invest.
Oxidant injury of lung parencymal cells
J. Clin. Invest.
Acute and progressive lung injury secondary to toxic oxygen products from leukocytes
Chest
Proteases and oxidants in experimental pulmonary inflammatory injury
J. Clin. Invest.
Tissue injury in inflammation. Oxidants, proteinases and cationic proteins
J. Clin. Invest.
Tissue destruction by neutrophils
N. Engl. J. Med.
Role of oxygen-derived free radicals and metabolites in leukocyte-dependent inflammatory reactions
Am. J. Physiol.
Oxidant-mediated epithelial cell injury in idiopathic pulmonary fibrosis
J. Clin. Invest.
The mechanism of chondrocyte hydrogen peroxide damage. Depletion of intracellular ATP due to suppression of glycolysis caused by oxidation of glyceraldehyde-3-phosphate dehydrogenase
J. Rheumatol.
Effects of exogenous free radicals on electromechanical function and metabolism in isolated rabbit and guinea pig ventricle
J. Clin. Invest.
Cited by (61)
Loss of cAMP-dependent stimulation of isolated cilia motility by alcohol exposure is oxidant-dependent
2019, AlcoholCitation Excerpt :Our new data suggest that this may not be limited to nitrosation per se, but linked to a reversible oxidation. Additionally, several reports in many ciliated models have demonstrated that cilia motility is sensitive to the increased presence of oxidants such as H2O2 (Feldman et al., 2002, 1994; Hirst, Rutman, & O'Callaghan, 2009; Honda et al., 2014; Kobayashi et al., 1992; Yoshitsugu et al., 1995). Wakabayashi and King previously reported the flagellate model organism, Chlamydomonas reinhardtii, demonstrates selective sensitivity to oxidation, exhibiting positive phototaxis and altered dynein ATPase activity after exposure to oxidant treatment, likely due to formation of disulfide bonds with the outer dynein arms (Wakabayashi & King, 2006).
Redox regulation of motile cilia in airway disease
2019, Redox BiologyCitation Excerpt :Interestingly, slowing by X/XO further declines upon preincubation with SOD. Surprisingly, in the presence of CAT, X/XO stimulates CBF and with the combination of SOD + CAT CBF is similar to conditions in the absence of X/XO [83,84]. As SOD generates H2O2 and this further slows cilia, these data suggest that H2O2 slows cilia since CAT selectively consumes H2O2 and there is no slowing with the presence of CAT.
Alterations in oviductal cilia morphology and reduced expression of axonemal dynein in diabetic NOD mice
2016, Tissue and CellCitation Excerpt :Growing evidence indicates that oxidative stress is increased in diabetes due to the overproduction of ROS and decreased efficiency of antioxidant defenses (Ahmed, 2005), and recent research suggests that this may have an impact on reproductive function in female diabetics (Amaral et al., 2008). In addition, studies showing a destructive effect of oxidants on ependymal (Hirst et al., 2009) and respiratory (Feldman et al., 1994) cilia indicate that similar processes may occur in oviductal cilia due to the increased oxidative stress known to be present in diabetes. Alternatively, destruction of oviductal cilia may occur as a result of cilia-specific autoantibodies present in the oviduct.
Pathogenesis of Chronic Obstructive Pulmonary Disease
2007, Clinics in Chest MedicineCitation Excerpt :Oxidants are also involved in the signaling pathways for EGF, which has an important role in mucus production [113]. Hydrogen peroxide and superoxide have also been shown to cause increased mucus secretion [247] and significant impairment of ciliary function after short-term exposure in low concentrations [248]. These effects may have important implications in the pathogenesis of chronic bronchitic element in COPD.
Respiratory Defenses in Health and Disease
2007, Veterinary Clinics of North America - Small Animal PracticeCitation Excerpt :Malfunction of the cilia can result from acquired damage or a congenital defect. Inhaled toxins, such as those found in smoke, are damaging to respiratory cilia, as are oxidants (including those elaborated from inflammatory cells) [26,27]. Cilia can also be damaged by toxins elaborated from infectious agents.
Oxidation, inflammation and structural modifications
2007, Archivos de Bronconeumologia