Formation of free radicals in mitochondria plays a key role in the development of apoptosis, which includes formation of superoxide by the respiratory chain, formation of radicals by cytochrome c-cardiolipin complex in the presence of hydrogen peroxide or lipids, and chain lipid peroxidation resulting in cytochrome c release from mitochondria and initiation of the apoptotic cascade. In this work the effect of taxifolin (dihydroquercetin) and some other antioxidants on these three radical-producing reactions was studied. Peroxidase activity of the complex of cytochrome c with dioleyl cardiolipin estimated by chemiluminescence with luminol decreased by 50% with quercetin, taxifolin, rutin, Trolox, and ionol at concentrations 0.7, 0.7, 0.8, 3, and 10 microM, respectively. The lipid radical production detected by coumarin C-525-activated chemiluminescence decreased under the action of rutin and taxifolin in a dose-dependent manner, so that a 50% inhibition of chemiluminescence was observed at the antioxidant concentrations of 3.7 and 10 microM, respectively. Thus, these two radical-producing reactions responsible for apoptosis onset are inhibited by antioxidants at rather low concentrations. Experiments performed on liver slices and mash showed that taxifolin, quercetin, naringenin, and Trolox have low inhibitory effect on the lucigenin-dependent chemiluminescence in the tissue only at concentrations higher than 100 microM.
The primary chemical mechanism of the beneficial medical/biological action of negative air ions necessary for life was studied. Air ion deficiency is the cause of many illnesses and treatment with air ion inhalation is effective in many cases. However, its application is limited by the absence of knowledge of the primary mechanism of its action. The superoxide anion O 2 was detected in the flow of negative air ions generated by an electroeffluvial air ionizer. Earlier, the appearance of hydrogen peroxide in solutions treated with air ions was shown. The presence of these reactive oxygen species in ultralow and low concentrations (10 12-10 6 M) suggested that the primary mechanism for the beneficial medical/biological action of negative air ions is moderate activation of free radical peroxidative oxidation within a physiological range that is lower than in tissues under pathology. It was shown in patients that treatment with inhalation of negative air ions did not induce pathological changes in superoxide dismutase activity and, under simultaneous administration of a food antioxidant, led to its mild increase. The latter, along with some previous results, supports the proposed mechanism. In addition, taking the proposed mechanism into consideration, air ion doses for treatment can be selected on an individual basis and should depend on the redox state of the patient. This should achieve better results for medical treatment with ionized air.
1‐Hydroxyadamantan (Ia) bzw. Z‐Hydroxy‐adamantan (Ib) reagieren mit Phosphortrichlorid in Gegenwart von Triethylamin zu den Adamantyl‐dichlorphosphiten (IIa) und (IIb).
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