Department of Medical Biochemistry, Center of Excellence for Cardiovacular Research of the Slovak Academy of Sciences, Jessenius Faculty of Medicine, Comenius University, Martin, Slovakia.
Eur J Med Res. 2009 Dec 7;14 Suppl 4(Suppl 4):116-20. doi: 10.1186/2047-783x-14-s4-116.
Oxygen therapy is used for the treatment of various diseases, but prolonged exposure to high concentrations of O(2) is also associated with formation of free radicals and oxidative damage.
In the present study we compared alpha-ketoglutarate dehydrogenase (KGDH) activity and mitochondrial oxidative damage in the hearts of guinea pigs after long-term (17 and 60 h) oxygenation with 100% normobaric O(2) and with partially negatively (O(2 neg)) or positively (O(2 posit)) ionized oxygen.
Inhalation of O(2) led to significant loss in KGDH activity and thiol group content and accumulation of bityrosines. Inhalation of O(2 neg) was accompanied by more pronounced KGDH inhibition, possibly due to additional formation of protein-lipid conjugates. In contrast, O(2 posit) prevented loss in KGDH activity and diminished mitochondrial oxidative damage.
These findings suggest that oxygen treatment is associated with impairment of heart energy metabolism and support the view that inhalation of O(2 posit) optimizes the beneficial effects of oxygen therapy.
氧气疗法用于治疗各种疾病，但长时间暴露在高浓度的氧气中也会导致自由基的形成和氧化损伤。
本研究比较了豚鼠在长时间（17 和 60 小时）吸入 100%常压氧气以及部分负（O2neg）或正（O2posit）离子化氧气后，α-酮戊二酸脱氢酶（KGDH）活性和心脏线粒体氧化损伤的变化。
吸入氧气导致 KGDH 活性和巯基含量下降，以及双酪氨酸的积累。吸入 O2neg 会导致更明显的 KGDH 抑制，这可能是由于额外形成了蛋白质-脂质共轭物。相比之下，O2posit 可以防止 KGDH 活性的丧失，并减少线粒体氧化损伤。
这些发现表明，氧气治疗与心脏能量代谢的损害有关，并支持吸入 O2posit 可优化氧气治疗有益效果的观点。
