Decreased Cu,Zn-SOD activity in asthmatic airway epithelium: correction by inhaled corticosteroid in vivo

Raeve, H. R. De; Thunnissen, F.B.J.M.; Kaneko, F. Takao; Guo, Fuhua H.; Lewis, Marc J.; Kavuru, Mani S.; Secic, Michelle; Thomassen, Mary Jane; Erzurum, Serpil C.

doi:10.1152/ajplung.1997.272.1.l148

Cited by 100 publications

(133 citation statements)

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“…De Raeve HR et al have reported a decreased Zn-SOD activity airway and Zinc serum in children with lower respiratory tract infection. 11,12 Further Meeks-Gardner J et al have shown a positive Zinc supplementation in these patients.…”

Section: Discussionmentioning

confidence: 93%

Estimation of Zinc Levels in Children With Lower Respiratory Tract Infections: A Prospective Observational Study from India

Hussain¹,

Saldanha²,

Sharma³

et al. 2016

Pediatr Neonatal Nurs Open J

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Aims: To assess the serum zinc levels in children aged 2 months to 5 years admitted with Lower Respiratory Tract Infections and to study the association between low zinc levels and other known risk factors LRTI. Material and Method: This prospective, observational study enrolled 200 children in age group of 2 months to 5 years admitted with acute LRTI. Serum Zinc level were measured and its association was seen with other risk factors of LRTI. Results: Mean serum zinc level of study population was 57.9±29.2 microgram/dL. There was significant difference in zinc level depending on severity of pneumonia, nutritional status, anemia, clinical vitamin A deficiency, breast feed infants and birth weight (p<0.05). Conclusion: Low serum level of zinc were seen in severe pneumonia cases. Serum zinc levels were found to be lower in risk factors of LRTI like poor nutritional status, anemia, vitamin A deficiency, low birth weight and formula fed patients. Zinc supplementation is required in LRTI patients especially those with the above mentioned risk factors.

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Section: Discussionmentioning

confidence: 93%

Estimation of Zinc Levels in Children With Lower Respiratory Tract Infections: A Prospective Observational Study from India

Hussain¹,

Saldanha²,

Sharma³

et al. 2016

Pediatr Neonatal Nurs Open J

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“…Hence, oxidative inactivation of CuZn SOD may also contribute to the loss of total SOD activity noted in asthma. 17,18 The loss of SOD activity likely reflects the increased oxidative and nitrative stress in the asthmatic airway, and may serve as a marker of asthma severity. In support of SOD as a surrogate marker of oxidant stress and asthma severity, Smith and colleagues 18 showed a correlation between the degree of airway reactivity to methacholine and SOD activity levels.…”

Section: Discussionmentioning

confidence: 99%

“…12,17 Furthermore, other reports have shown that loss of SOD can initiate apoptosis in some cell types, 29 therefore we hypothesized that diminished SOD in airway epithelial cells might be a central event mediating airway epithelial cell apoptosis. To address whether inactivation of SOD and/or increasing reactive oxygen species play a role in airway apoptosis, we treated BET1A cells with pyrogallol, a superoxide-producing agent, 2-ME, a SOD activity inhibitor or hydrogen peroxide, in a dose-and time-dependent manner.…”

Section: Effects Of Oxidative Stress On Airway Epithelial Cellsmentioning

confidence: 98%

“…17 The brush sample was immediately placed into sterile media, RPMI 1640 (Life Technologies, Inc., Rockville, MD) and an aliquot taken for cytology and cell differential determination.…”

Section: Isolation Of Bronchial Epithelial Cellsmentioning

confidence: 99%

“…16 -18 Activity of superoxide dismutase (SOD) is lower in asthmatic lungs as compared to healthy controls, and decreases further during an asthmatic attack. 16,17 Inhibition of SOD activity in malignant cells leads to free radical mediated damage to mitochondrial membranes, release of cytochrome c, and entry of cells into apoptosis. 19 In this context, we hypothesized that the loss of airway epithelial cells in asthma is because of apoptosis triggered by SOD modification and inactivation, which is specifically related to the inflammatory environment of the asthmatic airway.…”

mentioning

confidence: 99%

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Superoxide Dismutase Inactivation in Pathophysiology of Asthmatic Airway Remodeling and Reactivity

Comhair

Ghosh

et al. 2005

The American Journal of Pathology

173

149

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Airway hyperresponsiveness and remodeling are defining features of asthma. We hypothesized that impaired superoxide dismutase (SOD) antioxidant defense is a primary event in the pathophysiology of hyperresponsiveness and remodeling that induces apoptosis and shedding of airway epithelial cells. Mechanisms leading to apoptosis were studied in vivo and in vitro. Asthmatic lungs had increased apoptotic epithelial cells compared to controls as determined by terminal dUTP nick-end labeling-positive cells. Apoptosis was confirmed by the finding that caspase-9 and -3 and poly (ADP-ribose) polymerase were cleaved. On the basis that SOD inactivation triggers cell death and low SOD levels occur in asthma, we tested whether SOD inactivation plays a role in airway epithelial cell death. SOD inhibition increased cell death and cleavage/activation of caspases in bronchial epithelial cells in vitro. Asthma is commonly diagnosed using physiological measures, but alterations in airway structure are the defining features of asthma. Damage to airway epithelium, eosinophil infiltration, smooth muscle hyperplasia, thickening and aberrant collagen, and protein composition of the basement membrane are well established elements of the asthmatic airway. 1,2 The injury to the bronchial epithelium in asthma is marked by loss of columnar epithelial cells. Extensive loss of cells and denuded basement membrane with few basal cells remaining on the airway surface are noted in severe asthma, but shedding of airway epithelium is present even in clinically mild asthma. 2,3 Physical loss of epithelial lining cells is considered one proximate cause of the airway hyperresponsiveness to inhaled mediators, and has been speculated to contribute to asthmatic airway remodeling, in particular abnormal collagen synthesis. Evidence from organ culture systems supports the concept of an epithelial-mesenchymal unit in which loss of epithelium leads to mucosal myofibroblast and fibroblast proliferation, and collagen deposition. 2,4 -6 Thus, if the epithelial injury and loss could be understood and prevented in asthma, the clinical symptoms of airway hyperresponsiveness and long-term progressive sequelae in the airways, which contribute to fixed airflow limitation, might be prevented.Several reports have proposed that loss of epithelial cells is because of apoptosis based on immunostaining for the proteins that regulate apoptosis, or by detection of DNA strand breaks by immunostaining with the terminal dUTP nick-end labeling (TUNEL) assay. 7-11 However, not all reports have confirmed increased TUNEL positivity in airways. 9 Furthermore, if airway epithelial cells are undergoing increased cell death, it is unclear whether this is because of an inherent cell defect or a response to the asthmatic airway environment. Although nonspecific events related to increased levels of reactive oxygen and

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Anti‐inflammatory, antioxidant, and immunomodulatory effects of curcumin in ovalbumin‐sensitized rat

Shakeri

Boskabady

2017

BioFactors

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Decreased Cu,Zn-SOD activity in asthmatic airway epithelium: correction by inhaled corticosteroid in vivo

Cited by 100 publications

References 0 publications

Estimation of Zinc Levels in Children With Lower Respiratory Tract Infections: A Prospective Observational Study from India

Estimation of Zinc Levels in Children With Lower Respiratory Tract Infections: A Prospective Observational Study from India

Superoxide Dismutase Inactivation in Pathophysiology of Asthmatic Airway Remodeling and Reactivity

Anti‐inflammatory, antioxidant, and immunomodulatory effects of curcumin in ovalbumin‐sensitized rat

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