PDF(Pubmed)
Abstract：
Our hypothesis that controlled ozone applications interfere with the redox balance of a biological organism (first published in 1998 with a preclinical trial on protecting the liver from CCl4 intoxication) has been verified over the past two decades in reactive oxygen species (ROS)-induced mitochondrial pathologies, such as rheumatoid arthritis, osteoarthritis, aging processes and type 2 diabetes, and in the prevention of intoxications. Low-dose ozone acts as a redox bioregulator: the restoration of the disturbed redox balance is comprehensible in a number of preclinical and clinical studies by a remarkable increase in the antioxidant repair markers, here mainly shown as a glutathione increase and a reduction in oxidative stress markers, mainly malondialdehyde. The mechanism of action is shown, and relevant data are displayed, evaluated and comprehensively discussed: the repair side of the equilibrium increases by 21% up to 140% compared to the non-ozone-treated groups and depending on the indication, the stress markers are simultaneously reduced, and the redox system regains its balance.
摘要：
我们的假设，即受控的臭氧应用会干扰生物体的氧化还原平衡（首次发表于1998年，一项关于保护肝脏免受CCl4中毒的临床前试验）在过去的二十年中在活性氧（ROS）诱导的线粒体病理中得到了证实。比如类风湿性关节炎，骨关节炎,衰老过程和2型糖尿病，以及预防中毒。低剂量臭氧充当氧化还原生物调节剂：通过抗氧化剂修复标志物的显着增加，在许多临床前和临床研究中可以理解受干扰的氧化还原平衡的恢复。这里主要表现为谷胱甘肽的增加和氧化应激标志物的减少，主要是丙二醛。显示了作用机制，并显示相关数据，评估和全面讨论：与非臭氧处理组相比，平衡的修复方面增加了21％至140％，并且取决于适应症，压力标记同时减少，氧化还原系统恢复平衡.
