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Role of Sulfur Dioxide in Acute Lung Injury Following Limb Ischemia/Reperfusion in Rats
Author(s) -
Huang XinLi,
Liu Yang,
Zhou JunLin,
Qin YongChao,
Ren XiaoBao,
Zhou XiaoHong,
Cao Hua
Publication year - 2013
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.21492
Subject(s) - lung , ischemia , endogeny , chemistry , inflammation , saline , pathogenesis , sulfur dioxide , myeloperoxidase , reperfusion injury , medicine , cysteine , endocrinology , biochemistry , pharmacology , enzyme , inorganic chemistry
Sulfur dioxide (SO 2 ) is naturally synthesized by glutamate‐oxaloacetate transaminase (GOT) from l ‐cysteine in mammalian cells. We aim to investigate the role of SO 2 in inflammation in acute lung injury (ALI) following limb ischemia/reperfusion (I/R). Male Wistar rats were subjected to limb I/R and were injected with saline, GOT inhibitor hydroxamate (HDX, 0.47 mmol/kg), or the SO 2 donor Na 2 SO 3 /NaHSO 3 (0.54 mmol/kg/0.18 mmol/kg). Compared with the sham operation, the plasma SO 2 levels were significantly decreased by limb I/R treatment. In addition, SO 2 concentration and GOT activity in the lung tissue were also reduced in ALI. The occurrence of ALI following limb I/R can be prevented by Na 2 SO 3 /NaHSO 3 treatment, whereas it can be significantly aggravated by HDX. The plasma IL‐1β, IL‐6, and IL‐10 levels were consistent with myeloperoxidase activity and inflammation in lung tissue. In conclusion, our data suggest that downregulation of endogenous SO 2 production might be involved in pathogenesis of ALI following limb I/R in rats. © 2013 Wiley Periodicals, Inc. J BiochemMol Toxicol 27:389‐397, 2013; View this article online at wileyonlinelibrary.com . DOI 10.1002/jbt.21492