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Corrigendum to “Antioxidants attenuate Acute Lung injury post Chlorine gas exposure in rats” [Free Radic. Biol. Med. 49 (2010) S202]
Free Radical Biology & Medicine 50 (2011) 216
Contents lists available at ScienceDirect
Free Radical Biology & Medicine j o u r n a l h o m e p a g e : w w w. e l s e v i e r. c o m / l o c a t e / f r e e r a d b i o m e d
Corrigendum
Corrigendum to “Antioxidants attenuate Acute Lung injury post Chlorine gas exposure in rats” [Free Radic. Biol. Med. 49 (2010) S202] Amit Yadav
The abstract “Antioxidants attenuate Acute Lung injury post Chlorine gas exposure in rats” was printed with an incorrect author line. The entire abstract with the corrected author line appears below: Antioxidants attenuate Acute Lung injury post Chlorine gas exposure in rats. Amit K. Yadav, Stephen F. Doran, Ruchita Sharma, Giuseppe L. Squadrito, Michelle V. Fanucchi, Edward M. Postlethwait, Sadis Matalon Departments of Anesthesiology, Medicine and Environmental Health Sciences, Center for Free Radical Biology and Pulmonary Injury and Repair Center, University of Alabama at Birmingham Rationale: Chlorine gas (Cl2) inhalation causes acute lung injury (ALI) resembling Acute Respiratory Distress Syndrome (ARDS). Currently, there are no specific therapies to treat Cl2 induced injury which can also be used in a mass casualty situation. The HOCl is a potent oxidant along with Cl2 gas itself. It depletes the protective Antioxidants which lead to ALI. Cl2 activates various pro-inflammatory enzymes which cause prolonged injury to the lung epithelium even after the exposure is over. Objective: We hypothesized that antioxidants administered after Cl2 exposure will decrease acute lung injury in animals. Methods: Male Sprague-Dawley rats were exposed to Cl 2 (400 ppm) for 30 minutes in environmental chambers and returned to room air within 30 min after exposure, saline or Antioxidant cocktail
DOI of original article: 10.1016/j.freeradbiomed.2010.10.587. E-mail address: [email protected].
doi:10.1016/j.freeradbiomed.2010.11.001
[Ascorbic acid (20 mg/rat) and Deferoxamine Mesylate (15 mg/kg)] were administered by tail vein injection. After 1 hr, the rats received aerosolized antioxidant cocktail [Ascorbic acid (150 mg/ml) and Deferoxamine Mesylate (0.357 mg/ml)] for 1 hour and repeated again at 15 hr time point. The rats were sacrificed at 24 hr or 7 day time point and lung injury was assessed by measuring protein levels into BALF, Ascorbic acid (AA), Reduced and oxidized Glutathione ratio (GSH/GSSG) and uric acid in plasma via HPLC. Histological assessment on H/E slides, AB-PAS staining for mucus, trichrome stain for collagen and caspase 3 on paraffin embedded sections. Results: Rats exhibited significant lung injury post-Cl2 exposure as shown by elevation of protein in the BALF, hyperplastic epithelium on histology, marked mucus production. In addition, no staining of airway epithelia with caspase 3 with widespread epithelial sloughing seen on corresponding histology sections was consistent with necrosis. Administration of antioxidant cocktail decreased ALI as indicated by decreased hyperplasia of the epithelium, decreased mucus production and higher AA values in the lung tissue. These data suggest that antioxidants are therapeutically effective in Cl2-induced pulmonary toxicity, amenable to administration post-Cl2 exposure. Conclusion: We demonstrated that antioxidants provide a novel post-exposure therapeutic strategy to decrease Cl2 toxicity.
Contents lists available at ScienceDirect
Free Radical Biology & Medicine j o u r n a l h o m e p a g e : w w w. e l s e v i e r. c o m / l o c a t e / f r e e r a d b i o m e d
Corrigendum
Corrigendum to “Antioxidants attenuate Acute Lung injury post Chlorine gas exposure in rats” [Free Radic. Biol. Med. 49 (2010) S202] Amit Yadav
The abstract “Antioxidants attenuate Acute Lung injury post Chlorine gas exposure in rats” was printed with an incorrect author line. The entire abstract with the corrected author line appears below: Antioxidants attenuate Acute Lung injury post Chlorine gas exposure in rats. Amit K. Yadav, Stephen F. Doran, Ruchita Sharma, Giuseppe L. Squadrito, Michelle V. Fanucchi, Edward M. Postlethwait, Sadis Matalon Departments of Anesthesiology, Medicine and Environmental Health Sciences, Center for Free Radical Biology and Pulmonary Injury and Repair Center, University of Alabama at Birmingham Rationale: Chlorine gas (Cl2) inhalation causes acute lung injury (ALI) resembling Acute Respiratory Distress Syndrome (ARDS). Currently, there are no specific therapies to treat Cl2 induced injury which can also be used in a mass casualty situation. The HOCl is a potent oxidant along with Cl2 gas itself. It depletes the protective Antioxidants which lead to ALI. Cl2 activates various pro-inflammatory enzymes which cause prolonged injury to the lung epithelium even after the exposure is over. Objective: We hypothesized that antioxidants administered after Cl2 exposure will decrease acute lung injury in animals. Methods: Male Sprague-Dawley rats were exposed to Cl 2 (400 ppm) for 30 minutes in environmental chambers and returned to room air within 30 min after exposure, saline or Antioxidant cocktail
DOI of original article: 10.1016/j.freeradbiomed.2010.10.587. E-mail address: [email protected].
doi:10.1016/j.freeradbiomed.2010.11.001
[Ascorbic acid (20 mg/rat) and Deferoxamine Mesylate (15 mg/kg)] were administered by tail vein injection. After 1 hr, the rats received aerosolized antioxidant cocktail [Ascorbic acid (150 mg/ml) and Deferoxamine Mesylate (0.357 mg/ml)] for 1 hour and repeated again at 15 hr time point. The rats were sacrificed at 24 hr or 7 day time point and lung injury was assessed by measuring protein levels into BALF, Ascorbic acid (AA), Reduced and oxidized Glutathione ratio (GSH/GSSG) and uric acid in plasma via HPLC. Histological assessment on H/E slides, AB-PAS staining for mucus, trichrome stain for collagen and caspase 3 on paraffin embedded sections. Results: Rats exhibited significant lung injury post-Cl2 exposure as shown by elevation of protein in the BALF, hyperplastic epithelium on histology, marked mucus production. In addition, no staining of airway epithelia with caspase 3 with widespread epithelial sloughing seen on corresponding histology sections was consistent with necrosis. Administration of antioxidant cocktail decreased ALI as indicated by decreased hyperplasia of the epithelium, decreased mucus production and higher AA values in the lung tissue. These data suggest that antioxidants are therapeutically effective in Cl2-induced pulmonary toxicity, amenable to administration post-Cl2 exposure. Conclusion: We demonstrated that antioxidants provide a novel post-exposure therapeutic strategy to decrease Cl2 toxicity.