The unregulated oxidative modification of biological molecules has been implicated in the pathogenesis of various diseases, and the beneficial effects of antioxidants against detrimental oxidation have received much attention. Among the multiple oxidants, peroxyl radical and peroxynitrite play an important role as chain-carrying species in lipid peroxidation and one of the major oxidants produced in vivo, respectively. This study was performed to elucidate the prominent features of these two oxidants by comparing their reactivity and selectivity and also the effects of antioxidants against plasma lipid oxidation induced by the two oxidants. It was shown that despite peroxyl radical and peroxynitrite gave similar pattern of lipid peroxidation products of plasma, and these two oxidants exert different selectivity and reactivity towards probes and antioxidants. The capacity of antioxidants to scavenge peroxynitrite and peroxyl radical decreased in the order BSA > glutathione > α-tocopherol ∼ bilirubin ∼ α - tocotrienol > γ-tocotrienol ∼ γ - tocopherol > uric acid and α-tocopherol ∼ α - tocotrienol > bilirubin > γ-tocotrienol ∼ γ - tocopherol > BSA > glutathione > uric acid, respectively. α-Tocopherol localised within plasma lipoproteins was six times less effective than trolox in aqueous phase for scavenging peroxynitrite and the derived oxidants, despite the same chemical reactivity of the two chromanols. BSA was relatively more effective as antioxidant against peroxynitrite than peroxyl radical, whereas TEMPO did not act as efficient antioxidant against both oxidants. It was suggested that thiols act as more potent antioxidant against peroxynitrite than phenolic antioxidants, while phenolic antioxidants are potent inhibitor of lipid peroxidation induced by free radicals including those derived from peroxynitrite. Abbreviations: AAPH: 2,2'-azobis(2-amidinopropane) dihydrochloride; C11-BODIPY: 4,4-difluoro-5-(4-phenyl-1,3-butadienyl)-4-bora-3a,4a-diaza-s-indacene-3-undecanoic acid; BSA: bovine serum albumin; DPPP: diphenyl-1-pyrenylphosphine; H(p)ODE: hydro(pero)xyoctadecadienoates; PGR: pyrogallol red; PUFA: polyunsaturated fatty acid; SIN-1: 3-morpholinosydnonimine; TEMPO: 2,2-6,6 tetramethylpiperidine-1-oxyl; Trolox: 2-carboxy-2,5,7,8-tetramethyl-6-hydroxychroman.

中文翻译：

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过氧亚硝酸盐和过氧自由基引起的血浆脂质氧化及其抗氧化剂抑制作用的比较研究。

生物分子的未经调节的氧化修饰已涉及多种疾病的发病机理，并且抗氧化剂对抗有害氧化的有益作用已引起广泛关注。在多种氧化剂中，过氧自由基和过氧亚硝酸盐作为脂质过氧化中的链状携带物质和体内产生的主要氧化剂之一，起着重要的作用。通过比较这两种氧化剂的反应性和选择性以及抗氧化剂对这两种氧化剂诱导的血浆脂质氧化的作用，来阐明这两种氧化剂的显着特征。结果表明，尽管过氧自由基和过氧亚硝酸盐具有相似的血浆脂质过氧化产物模式，这两种氧化剂对探针和抗氧化剂的选择性和反应性不同。抗氧化剂清除过氧亚硝酸盐和过氧自由基的能力按BSA>谷胱甘肽>α-生育酚〜胆红素〜α-生育三烯酚>γ-生育三烯酚〜γ-生育酚>尿酸和α-生育酚〜α-生育三烯酚>胆红素>胆碱-生育三烯酚〜γ-生育酚> BSA>谷胱甘肽>尿酸。尽管两种色酚具有相同的化学反应性，但定位在血浆脂蛋白中的α-生育酚在水相中清除过氧亚硝酸盐和衍生氧化剂的效率比trolox低六倍。BSA作为抗过氧亚硝酸盐的抗氧化剂比过氧自由基相对更有效，而TEMPO不能作为对两种氧化剂的有效抗氧化剂。有人提出，硫醇对过氧亚硝酸盐的作用强于酚类抗氧剂，而酚类抗氧剂是由自由基（包括过氧亚硝酸盐衍生的自由基）诱导的脂质过氧化的有效抑制剂。缩写：AAPH：2，2′-偶氮二（2-ami基丙烷）二盐酸盐；C11-BODIPY：4,4-二氟-5-（4-苯基-1,3-丁二烯基）-4-硼3a，4a-二氮杂-s-茚并三-3-十一酸; BSA：牛血清白蛋白；DPPP：二苯基-1-吡啶膦；H（p）ODE：氢（过）羟基十八碳二烯酸酯；PGR：邻苯三酚红；PUFA：多不饱和脂肪酸；SIN-1：3-吗啉代亚胺；TEMPO：2,2-6,6四甲基哌啶-1-氧基；Trolox：2-羧基-2,5,7,8-四甲基-6-羟基苯并二氢吡喃。酚类抗氧化剂可有效抑制自由基（包括过氧亚硝酸盐衍生的自由基）引起的脂质过氧化。缩写：AAPH：2，2′-偶氮二（2-ami基丙烷）二盐酸盐；C11-BODIPY：4,4-二氟-5-（4-苯基-1,3-丁二烯基）-4-硼3a，4a-二氮杂-s-茚并三-3-十一酸; BSA：牛血清白蛋白；DPPP：二苯基-1-吡啶膦；H（p）ODE：氢（过）羟基十八碳二烯酸酯；PGR：邻苯三酚红；PUFA：多不饱和脂肪酸；SIN-1：3-吗啉代亚胺；TEMPO：2,2-6,6四甲基哌啶-1-氧基；Trolox：2-羧基-2,5,7,8-四甲基-6-羟基苯并二氢吡喃。酚类抗氧化剂可有效抑制自由基（包括过氧亚硝酸盐衍生的自由基）引起的脂质过氧化。缩写：AAPH：2，2′-偶氮二（2-ami基丙烷）二盐酸盐；C11-BODIPY：4,4-二氟-5-（4-苯基-1,3-丁二烯基）-4-硼3a，4a-二氮杂-s-茚并三-3-十一酸; BSA：牛血清白蛋白；DPPP：二苯基-1-吡啶膦；H（p）ODE：氢（过）羟基十八碳二烯酸酯；PGR：邻苯三酚红；PUFA：多不饱和脂肪酸；SIN-1：3-吗啉代亚胺；TEMPO：2,2-6,6四甲基哌啶-1-氧基；Trolox：2-羧基-2,5,7,8-四甲基-6-羟基苯并二氢吡喃。4a-二氮杂-s-茚并三-3-十一酸; BSA：牛血清白蛋白；DPPP：二苯基-1-吡啶膦；H（p）ODE：氢（过）羟基十八碳二烯酸酯；PGR：邻苯三酚红；PUFA：多不饱和脂肪酸；SIN-1：3-吗啉代亚胺；TEMPO：2,2-6,6四甲基哌啶-1-氧基；Trolox：2-羧基-2,5,7,8-四甲基-6-羟基苯并二氢吡喃。4a-二氮杂-s-茚并三-3-十一酸; BSA：牛血清白蛋白；DPPP：二苯基-1-吡啶膦；H（p）ODE：氢（过）羟基十八碳二烯酸酯；PGR：邻苯三酚红；PUFA：多不饱和脂肪酸；SIN-1：3-吗啉代亚胺；TEMPO：2,2-6,6四甲基哌啶-1-氧基 Trolox：2-羧基-2,5,7,8-四甲基-6-羟基苯并二氢吡喃。