Endotoxin-induced hydrogen peroxide production in intact pulmonary circulation of rat.

Minamiya, Yoshihiro; Abo, Shichisaburo; Kitamura, Michihiko; Izumi, Keiichi; Kimura, Yoshihiko; Tozawa, Kasumi; Saitô, Satoshi

doi:10.1164/ajrccm.152.1.7599844

Cited by 39 publications

(30 citation statements)

References 18 publications

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“…Also, recent evidence has indicated that superoxide anion production and PMN phagocytic activity are impaired in the presence of LPS [9]. In addition, there has been no direct, convincing evidence for the production of active oxygen radicals from the LPS-treated lungs, although Minamiya et al [13] showed that hydrogen peroxide was produced in the rat pulmonary microcirculation in vivo using fluorescent dye and a computer image analysis system. However, they could not prove that the increased production of active oxygen radicals induced the lung injury since indices of vascular permeability, the wet/dry ratio, and Evans blue dye method remained unchanged.…”

Section: Introductionmentioning

confidence: 99%

The Importance of Polymorphonuclear Leukocytes in Lipopolysaccharide-Induced Superoxide Anion Production and Lung Injury: Ex Vivo Observation in Rat Lungs

Tsuji

Minhaz

Shioya

et al. 1998

Lung

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The purpose of this study is to determine if the polymorphonuclear leukocyte (PMN) is a major causative agent for lipopolysaccharide (LPS)-induced lung injury and responsible for the excess production of superoxide anion in the lung. We measured superoxide anion production from the lung and pulmonary capillary permeability in rats with and without PMN depletion. The superoxide anion production from the lung was measured using a purpose-built ex vivo chemiluminescence apparatus. Pulmonary capillary permeability was evaluated by the Evans blue dye extravasation method. PMN sequestration was determined by counting PMNs in histologic tissue specimens using microscopy. All rats received 3 mg/kg LPS intravenously. Examinations were undertaken at 2, 6, and 12 h after the LPS injection. The PMN-depleted group received cyclophosphamide 4 days before the LPS injection, which resulted in a PMN count of less than 200 cells/microliter. In rats without PMN depletion, Evans blue dye extravasation increased significantly at 12 h after the LPS injection; PMN sequestration increased at 2, 6, and 12 h after the LPS injection; and superoxide anion production increased at 6 h and remained elevated at 12 h after the LPS injection. The increased permeability, PMN sequestration, and superoxide anion production were not seen in the PMN-depleted group. The contribution of the xanthine/xanthine oxidase system and alveolar macrophages to the observed superoxide anion production was negligible. We conclude that, in rats, the PMN is a major causative agent in LPS-induced lung injury and is responsible for the excess production of superoxide anion in the lung.

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Section: Introductionmentioning

confidence: 99%

The Importance of Polymorphonuclear Leukocytes in Lipopolysaccharide-Induced Superoxide Anion Production and Lung Injury: Ex Vivo Observation in Rat Lungs

Tsuji

Minhaz

Shioya

et al. 1998

Lung

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“…LUNG DISEASES, SUCH AS ASTHMA (10), chronic obstructive pulmonary disease (12), endotoxin shock (33), and vascular microembolism (50), or inhalation of oxidant irritants, such as toxic smoke (35), cigarette smoke (35), and ozone (45), may cause increased pulmonary production of reactive oxygen species from endogenous and/or exogenous sources. The major reactive oxygen species are the superoxide anion radical, hydrogen peroxide (H 2 O 2 ), and the hydroxyl radical (⅐ OH) (5).…”

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confidence: 99%

Afferent vagal pathways mediating respiratory reflexes evoked by ROS in the lungs of anesthetized rats

Ruan

Kou

2003

Journal of Applied Physiology

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vagal pathways mediating respiratory reflexes evoked by ROS in the lungs of anesthetized rats. J Appl Physiol 94: 1987, 2003. First published January 10, 2003 10.1152/ japplphysiol.01047.2002We investigated the afferent vagal pathways mediating respiratory reflexes evoked by reactive oxygen species (ROS) in the lungs of anesthetized rats. Spontaneous inhalation of 0.2% aerosolized H 2O2 acutely evoked initial bradypnea followed by delayed tachypnea, which was frequently mixed with delayed augmented inspiration. The initial response was abolished after perivagal capsaicin treatment (PCT), but was prolonged during vagal cooling (VC) to 7°C; PCT and VC are known to differentially block the conduction of unmyelinated C and myelinated fibers, respectively. The delayed responses were eliminated during VC but emerged earlier after PCT. Vagotomy, catalase (an antioxidant for H 2O2), dimethylthiourea (an antioxidant for ⅐ OH), or deferoxamine (an antioxidant for ⅐ OH) largely or totally suppressed these reflexive responses, whereas sham nerve treatment, heat-inactivated catalase, saline vehicle, or iron-saturated deferoxamine failed to do so. These results suggest that 1) the H 2O2-evoked initial and delayed airway reflexes are antagonistic and may result from stimulation of lung C fibers and rapidly adapting receptors, respectively, and 2) the reflex effects of H 2O2 are, in part, due to the action of ⅐ OH on these afferents. vagal sensory receptors; oxygen radicals; reactive oxygen species; hydrogen peroxide LUNG DISEASES, SUCH AS ASTHMA (10), chronic obstructive pulmonary disease (12), endotoxin shock (33), and vascular microembolism (50), or inhalation of oxidant irritants, such as toxic smoke (35), cigarette smoke (35), and ozone (45), may cause increased pulmonary production of reactive oxygen species from endogenous and/or exogenous sources. The major reactive oxygen species are the superoxide anion radical, hydrogen peroxide (H 2 O 2 ), and the hydroxyl radical (⅐ OH) (5). The superoxide anion radical dismutates to form H 2 O 2 , which, in the presence of iron, can further react to form ⅐ OH, a more reactive oxygen radical, via the Fenton reaction (5). Vagal sensory receptors are known to play an important role in detecting the onset of pathophysiological conditions and are responsible for triggering defensive or protective airway reflexes (8, 29, 39).While abundant information suggests the importance of reactive oxygen species in producing pulmonary pathophysiological consequences (4), very few studies have investigated their role and mechanism in eliciting airway reflexes.The concept that reactive oxygen species may stimulate pulmonary sensory receptors and play a vital role in eliciting airway reflexes is considerably new (29). This concept is indirectly supported from findings that vagally mediated airway reflexes evoked by inhaled cigarette smoke (27), inhaled wood smoke (22), or pulmonary air embolism (6) and responses of vagal sensory receptors to the latter two insults (7,24,25) are greatly attenuated b...

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“…Transition metal ions have been suggested to play a role in endotoxin-induced lipid peroxidation [18]. Endotoxin is capable of enhancing the generation of reactive oxygen species [6,7,34], which in turn may release iron from its protein complex. Therefore, increased reactive oxygen species generation resulting from endotoxin treatment may promote iron release from ferritin or other protein complexes.…”

Section: Discussionmentioning

confidence: 99%

Endotoxin increases hepatic susceptibility to lipid peroxidation: A possible role of iron

Ibrahim

Lee

Chow

2004

J Biochem & Molecular Tox

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The purpose of this study was to investigate the possible mechanism by which endotoxin enhances peroxidative damage to membrane lipids. Male B6C3 mice were treated with endotoxin intraperitoneally 0 or 20 mg/kg body weight for 24 h. Freshly prepared liver homogenate was incubated with either 1-5 mM of reduced glutathione (GSH), glucose, H(2)O(2), ascorbic acid (AA), FeSO(4), FeCl(3), EDTA, FeCl(3) plus AA, AA plus EDTA or EDTA plus FeCl(3) in phosphate-buffered saline (PBS), pH 7.0, or PBS, at 37 degrees C for 60 min. The levels of lipid peroxidation products, thiobarbituric acid reactants (TBAR), were significantly higher in the liver of endotoxin-treated mice, and the values were markedly increased following incubation. Compared to PBS, incubation with H(2)O(2), FeCl(3), FeSO(4), and AA, but not glucose, significantly enhanced TBAR formation. The greatest increase of TBAR was found when AA and FeCl(3) were added together. On the other hand, EDTA and GSH inhibited the formation of TBAR during incubation. When added before AA, EDTA completely inhibited the peroxidative effect of AA or FeSO4, and when added subsequent to AA, EDTA partially prevented the adverse effect of AA. The results obtained suggest that ionic iron plays an important role in initiating endotoxin-induced peroxidative damage to membrane lipids, and that AA may be involved in releasing iron from its protein complex and/or maintaining ionic iron in a reduced or catalytic state.

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Endotoxin-induced hydrogen peroxide production in intact pulmonary circulation of rat.

Cited by 39 publications

References 18 publications

The Importance of Polymorphonuclear Leukocytes in Lipopolysaccharide-Induced Superoxide Anion Production and Lung Injury: Ex Vivo Observation in Rat Lungs

The Importance of Polymorphonuclear Leukocytes in Lipopolysaccharide-Induced Superoxide Anion Production and Lung Injury: Ex Vivo Observation in Rat Lungs

Afferent vagal pathways mediating respiratory reflexes evoked by ROS in the lungs of anesthetized rats

Endotoxin increases hepatic susceptibility to lipid peroxidation: A possible role of iron

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