Lung Oxidative Damage by Hypoxia

Figure 2

Inhibitors for ROS generation and antioxidants used to study the pulmonary oxidative damage by hypoxia. NOX inhibitors: diphenyleneiodonium (DPI) [39, 71–73, 91, 207]; peroxisome proliferator-activated receptor (PPARγ) [79]; 4-(2-Aminoethyl) benzenesulfonyl fluoride (AEBSF) [74]; apocynin [42, 207]. NOS inhibitors: N^G-monomethyl-L-arginine (L-NMMA): inhibitor of the three isoforms [31]; N-(3-(aminomethyl)benzyl) acetamidine (1400 W) and S-methylisothiourea sulfate (SMT): inhibitors of iNOS [31, 59]; L-NG-nitroarginine (L-NNA): inhibitor of eNOS and nNOS [59, 182]. Mitochondrial inhibitors: complex I: rotenone [38, 40]; diphenyleneiodonium (DPI) [39, 71–73, 91], 1-methyl-4-phenylpyridinium (MPP⁺) [75]. Complex II: 3-nitropropionic acid thenoyltrifluoroacetone: (3-NPA) [208]. Complex III: antimycin A [38, 40, 208]; myxothiazol [40, 42]. Complex IV: cyanide [40]. Enzymatic antioxidants: Catalase [40, 45, 51, 91, 209]; SOD [37, 49, 91]; Ec-SOD [90]; glutathione peroxidase [49]. Nonenzymatic antioxidants: N-acetylcysteine (NAC) [89, 209]; vitamin E [4]; flavonoids [186]; nitro blue tetrazolium (NBT) [30–32]; pyrrolidine dithiocarbamate (PDTC) [42, 209]; U74389G [91]. XO/XD inhibitors: allopurinol [89]; tungsten [85]. Others: clodronate, acts by decreasing the number of macrophages.