Bocci V, Valacchi G, Corradeschi F, Aldinucci C, Silvestri S, Paccagnini E, Gerli R
Institute of General Physiology, University of Siena, Italy.
J Biol Regul Homeost Agents. 1998 Jul-Sep;12(3):67-75.
The acceptance of any complementary medical approach is conditioned by the results obtained after the same scientific scrutiny applied in orthodox medicine. Otherwise any claim of efficacy remains in the realm of fiction. In the case of ozone therapy, the mechanisms of action have remained nebulous and in a series of publications we are trying to present the biochemical, immunological and morphological evidence in favour or against ozone therapy. We have now shown that ozone (O3) dissolved in the water of either plasma or serum or physiological saline generates reactive oxygen species (ROS), of which hydrogen peroxide (H2O2) can be unequivocally demonstrated by using specific methods for its detection. Lipids present in plasma preferentially those present in lipoproteins, undergo peroxidation that is somewhat O3-dose dependent and can be observed by the measurement of thiobarbituric acid reactive substances (TBARS). While the generation of H2O2 is crucial in activating both biochemical (hexose monophosphate shunt) and immunological (via the transcription factor NF-kB) mechanisms, the role of lipid oxidation products (LOP) remains to be investigated. We have shown here that there is a small but consistent induction of some cytokines (TNF-alpha, IFN-gamma and IL-2) when human blood is directly exposed to O3 concentrations up to 100 micrograms/ml per g of blood. On the other hand, isolated blood mononuclear cells (PBMC) in tissue culture medium are far more sensitive to the oxidant action of O3 as shown by a progressive reduction of the proliferation index with comparatively far lower O3, concentrations. On the whole, these results support the concept that much of the O3 toxicity is neutralized by the powerful antioxidant system of blood. The minimal hemolysis supports this idea but as far as platelets are concerned, we must mention that they tend to aggregate in heparinized blood, even when it is exposed to an O3 concentration of 40 micrograms/ml. In spite of the lack of side-effects after autohemotherapy, this drawback must be kept in mind and avoided in clinical practice.
任何补充医学方法被接受的前提是，其要经过与正统医学相同的科学审查并取得相应结果。否则，任何关于疗效的说法都只是虚构的。就臭氧疗法而言，其作用机制一直模糊不清，在一系列出版物中，我们试图展示支持或反对臭氧疗法的生化、免疫和形态学证据。我们现已表明，溶解于血浆、血清或生理盐水中的臭氧（O3）会产生活性氧（ROS），其中过氧化氢（H2O2）可通过特定检测方法明确检测到。血浆中的脂质，尤其是脂蛋白中的脂质，会发生过氧化反应，这种反应在一定程度上依赖于O3剂量，可通过测量硫代巴比妥酸反应性物质（TBARS）来观察。虽然H2O2的产生对于激活生化机制（磷酸己糖旁路）和免疫机制（通过转录因子NF-κB）至关重要，但脂质氧化产物（LOP）的作用仍有待研究。我们在此表明，当人体血液直接暴露于每克血液高达100微克/毫升的O3浓度时，会有一些细胞因子（TNF-α、IFN-γ和IL-2）出现轻微但持续的诱导。另一方面，组织培养基中的分离血液单核细胞（PBMC）对O3的氧化作用更为敏感，这表现为在相对低得多的O3浓度下增殖指数逐渐降低。总体而言，这些结果支持这样一种观点，即血液强大的抗氧化系统可中和大部分O3毒性。最小程度的溶血支持了这一观点，但就血小板而言，我们必须提到，即使在暴露于40微克/毫升的O3浓度时，它们在肝素化血液中也容易聚集。尽管自血疗法后没有副作用，但在临床实践中必须牢记并避免这一缺点。
