Tianjin Medical Journal ›› 2019, Vol. 47 ›› Issue (9): 917-923.doi: 10.11958/20190637

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Differential oxidative stress reactions in sulfur mustard-induced acute pulmonary injury with equal toxicity dose in rats via different routes

HU Xiao-xuan1, YU Dan2, XIE Jian-wei2, XU De-feng3△, ZHONG Yu-xu2△   

  1. 1 Ningxia Medical University Shanghai Gongli Hospital Postgraduate Training Base, Shanghai 200135, China; 2 State Key Laboratory of Toxicology and Medical Countermeasures, Beijing Institute of Pharmacology and Toxicology; 3 Department of Respiratory, Shanghai Gongli Hospital
  • Received:2019-03-08 Revised:2019-08-03 Published:2019-09-15 Online:2019-09-18
  • Contact: Xiao-Xuan HU E-mail:hxxdr6927@163.com

Abstract: Objective To compare oxidative stress responses of two acute pulmonary injury models induced by a toxicity dose (1LD50) of mustard gas (SM) in rats through intraperitoneal and tracheal pathways. Methods Male Sprague Dawley rats were selected and randomly divided into the intraperitoneal SM group, the intraperitoneal propylene glycol group, the tracheal SM group, the tracheal propylene glycol group and normal group. The serum enzyme levels and proteins related expressions in alveolar septum were measured by ELISA and immunohistochemistry methods. Results Serum levels of superoxide dismutase, catalase and glutathion peroxidase at different time points were increased in the intraperitoneal SM group compared with those of tracheal SM group (P<0.05). In the alveolar septum, the positive cells of CuZn-superoxide dismutase, Mn-superoxide dismutase, paraoxonase-1 and apolipoprotein-1 expression were increased in the intraperitoneal SM group compared with those of tracheal SM group (P<0.05). Conclusion At a dose of SM (1LD50), there are differences in the oxidative stress responses at the molecular level in two rat models of acute pulmonary injury. The results suggest that the oxidative stress responses reduced by equal toxicity dose (1LD50) of SM in rats are related to the toxic pathway, and which provides an important theoretical basis for the application of antioxidants.

Key words: acute pulmonary injury, mustard gas, oxidative stress, disease models, animal, equal toxic dose