Free radical processes in combined chronic inhalation effect of xenobiotics on the rat

The chronic combined inhalation influence of nitric oxides (II, IV), amorphic hydrophobic silicon dioxide, lead and radon on the free radical processes intensively was investigated. The dienic conjugates, lipid hydroperoxides and MDA concentration in the liver and kidney of the white mongrel male-rats was defined. It has been shown that lipid peroxidation process displaies sensitivity toward complex exposure of the most wide-spreader xenobiotics. It was expressed in the content decreasing of there products at the first step of our experience as a result of the action of the adaptive and compensative mechanisms directed to the suppression of the peroxidation processes. As a result of the antioxidant system powers exhaustion it was found the content rising of the lipid peroxidation products at the last step of our experience. It has been proposed to use the total content index of the lipid peroxidation products as a criteria of the organism resistant ion toward action of the exogenic factors of various origin.     

Structure of the morphogenetic movements of gastrulation in Anura. II. The elementary morphogenetic processes]

The clinostate rotation causes a wide range of gastrulation abnormalities in the Anura. A special investigation has shown that all gastrulation variants may be represented as various spatial-temporal compositions of the same morphogenetic processes isolated by means of formal experimental procedure. These processes are structurally stable rearrangements of tissue morphology and are spread in the tissue as a wave embracing more and more cells. The change of one local morphology for another may proceed either in the form of "shock wave", a moving distinct border between the cells already switched and not yet switched to the new automorphous movement, or in the form of "deployment" when the transition from one local morphology to another is continuously deployed in space.     

Free radical processes in aging, neurodegenerative diseases and other pathological states

Literature data on the role of oxidative stress in aging have been summarized. There are certain links between parameters of free radical processes (intensity of generation of reactive oxygen species in mitochondria, oxidative modification of mitochondrial DNA, activity of desaturases, involved into biosynthesis of polyunsaturated C₂₀ and C₂₂ fatty acids) with life span. The review highlights the role of oxidative stress as on of pathogenic factors of numerous diseases including various neurodegenerative disorders. Special attention is paid to oxidative modification of proteins as one of early and reliable markers of tissue injury in free radical pathology. Oxidative destruction of proteins plays a major role in etiology of such neurodegenerative diseases as Alzheimer’s and Parkinson’s diseases. Oxidative stress and the stress related protein aggregation are considered as the pathogenic link in the development of familiar amyotrophic lateral sclerosis. Oxidative modification of proteins is associated with the development of cataract. The age-and pathology-related increases in the content of oxidized proteins in tissues is assessed as an early and specific parameter of oxidative stress.     

Free radical paradoxes

Unlike bigger and more advanced animals, Caenorhabditis elegans does not generate NO, yet it was recently found that NO produced by chemical or biological sources exerts profound effects in that animal, leading to increased life span and thermotolerance. The biological source was Bacillus subtilis, a natural food for C. elegans. Yet once in the cell, NO might react with superoxide, leading to the production of the potentially toxic peroxynitrite. In this paper, a number of paradoxes that are involved in that situation are discussed. It is also argued that their solution might lead to a sizeable advancement of our knowledge of what constitutes oxidative stress and what role oxidative stress plays in the development of pathological processes and aging.     

自由基稳衡性动态

虽然自由基具有很活泼的化学性质 ,但在需氧生物的进化中却一直保持着自由基稳衡性动态的特征 ,体现于某些生物程序 ,包括 :在生理情况下履行其生理作用 ;维持其产生与清除于接近平衡 ;余剩的自由基引发生物大分子的损伤及其损伤可被修复。营养素及其代谢物和“必需”抗氧化剂对自由基稳衡态的正常维持起着关键性作用。谷胱甘肽及其它生物物质的稳衡性动态与自由基稳衡性动态有着协调的相互关系。在各种生活条件下 ,不同年龄的健康人体内自由基稳衡性动态应维持良好 ,以预防衰老前氧化应激与氧化损伤的发生     

Free radical reduction in the human epidermis

The human epidermis presents the first line of defense against invading free radicals. Therefore, the surface of the skin must be equipped to deal with both the penetration of ultra-violet light as well as the neutralization of reactive photochemical products such as superoxide anion radical, hydrogen peroxide and especially hydroxyl radicals. Consequently, the human epidermis contains a variety of anti-oxidants to reduce oxygen radicals and hydrogen peroxide. The photochemical production of hydroxyl radicals, from both extracellular and intracellular hydrogen peroxide, is of special significance to the integrity of cells in the human epidermis. Recently, both biochemical and clinical studies on the healthy human population, and on patients with pigmentation disorders, suggested a connection between free radical defense by plasma membrane associated thioredoxin reductase and melanin biosynthesis. This research provided the first evidence for a direct relationship between free radical concentration and pigmentation. Furthermore, this system has been shown to be regulated by both extracellular and intracellular calcium concentrations. Clinical studies show depigmentation disorders vitiligo and tyrosinase positive albinism (Hermansky-Pudlak syndrome) appear to have defective calcium uptake systems influencing both free radical defense and melanin biosynthesis.     

Free radical peroxidation of liver mitochondrial and microsomal phospholipids in rat postnatal development]

Activities of both non-enzymic (ascorbate-dependent) and enzymic NADPH-dependent) peroxidation of microsomal and mitochondrial phospholipids are found to be increased in rat liver during postnatal development. It is suggested, that microsomal NADPH-dependent phospholipid dioxygenase forming a chemical modification of membrane polyenic acyls, can be a factor regulating the activities of membrane-linked enzymes under normal physiological processes.     

Free radical theory of autoimmunity

Background  

Despite great advances in clinical oncology, the molecular mechanisms underlying the failure of chemotherapeutic intervention in treating lymphoproliferative and related disorders are not well understood.     

Free radical mechanisms in enzyme reactions

Free radicals are formed in prosthetic groups or amino acid residues of certain enzymes. These free radicals are closely related to the activation process in enzyme catalysis, but their formation does not always result in the formation of substrate free radicals as a product of the enzyme reactions. The role of free radicals in enzyme catalysis is discussed.     

Free radical scavengers in myocardial ischemia

Reperfusion of ischemic myocardium is recognized as potentially beneficial because mortality is directly related to infarct size, and the latter is related to the severity and duration of ischemia. However, reperfusion is associated with extension of the injury that is additive to that produced by ischemia alone. The phenomenon of reperfusion injury is caused in large part by oxygen-derived free radicals from both extracellular and intracellular sources. The loci of oxygen-free radical formation include: myocardial sources (mitochondria), vascular endothelial sources (xanthine oxidase and other oxidases), or the inflammatory cellular infiltrate (neutrophils). Experimental studies have shown that free radical scavengers and agents that prevent free radical production can reduce myocardial infarct size in dogs subjected to temporary regional ischemia followed by reperfusion. Superoxide dismutase and catalase, which catalyze the breakdown of superoxide anion and hydrogen peroxide, respectively, limit experimental myocardial infarct size. The free radical scavenging agent N-(2-mercaptopropionyl)glycine (MPG) is reported to be effective in limiting infarct size. The ischemic-reperfused myocardium derives significant protection when experimental animals are pretreated with the xanthine oxidase inhibitor allopurinol. Neutrophils also serve as a significant source of oxygen-derived free radicals at the site of tissue injury. A number of agents have been shown to directly inhibit neutrophil-derived oxygen free radical formation and neutrophil accumulation within the reperfused myocardium. These agents include ibuprofen, nafazatrom, BW755C, prostacyclin, and iloprost. Thus, free radical scavengers and agents that prevent free radical formation can provide significant protection to the ischemic-reperfused myocardium.     

Free radical chemistry in biological systems

Mitochondria are an active source of the free radical superoxide (O2-) and nitric oxide (NO), whose production accounts for about 2% and 0.5% respectively, of mitochondrial O2 uptake under physiological conditions. Superoxide is produced by the auto-oxidation of the semiquinones of ubiquinol and the NADH dehydrogenase flavin and NO by the enzymatic action of the nitric oxide synthase of the inner mitochondrial membrane (mtNOS). Nitric oxide reversibly inhibits cytochrome oxidase activity in competition with O2. The balance between NO production and its utilization results in a NO intramitochondrial steady-state concentration of 20-50 nM, which regulates mitochondrial O2 uptake and energy supply. The regulation of cellular respiration and energy production by NO and its ability to switch the pathway of cell death from apoptosis to necrosis in physiological and pathological conditions could take place primarily through the inhibition of mitochondrial ATP production. Nitric oxide reacts with O2- in a termination reaction in the mitochondrial matrix, yielding peroxynitrite (ONOO-), which is a strong oxidizing and nitrating species. This reaction accounts for approximately 85% of the rate of mitochondrial NO utilization in aerobic conditions. Mitochondrial aging by oxyradical- and peroxynitrite-induced damage would occur through selective mtDNA damage and protein inactivation, leading to dysfunctional mitochondria unable to keep membrane potential and ATP synthesis.     

Cell cycles in the early embryogenesis of the peled]

The dynamics of cell cycles in early embryogenesis of the peled has been studied using various methofs: determination of mitotic and mitotic phase index, of cell doubling time and of coefficient of asynchrony. The desynchronization of divisions begins at the V division after the longitudinal furrow has passed and is completed after the beginning of the cell cycle lengthening. The animal-vegetative gradient in the distribution of mitotic phases is observed at the early stages of desynchronization. The lengthening of cell cycle begins in interphase of the XI-XII cleavage and markedly accelerates from the interphase of the XII-XIII cleavage on. The methods of analysis of the cell cycles in early embryogenesis and possible factors influencing the dynamics of desynchronization are discussed.     

Rhythmic processes in early embryogenesis timed by cell division

he data on rhythmic processes in early embryogenesis coinciding with cell divisions are considered. Possible mechanisms which determine the rhythm frequency and are its motive power are discussed, as well as the role of individual rhythmic processes in the regulation of consecutive cell cycle events. A suggestion is put forward that these rhythmic processes are transformed during subsequent development in circum-hour rhythms of some biochemical, physiological and biophysical processes discovered in the cells and organs of adult organism.     

Free radical metabolites of L-cysteine oxidation

The oxidation of L-cysteine by horseradish peroxidase in the presence of oxygen forms a thiyl free radical as demonstrated with the spin-trapping ESR technique. Reactions of this thiyl free radical result in oxygen consumption, which is inhibited by the spin trap 5,5'-dimethyl-1-pyrroline-N-oxide. Cysteine sulfinic acid, a cysteine metabolite, is a poorer substrate for horseradish peroxidase than cysteine and is oxidized to form both sulfur-centered and carbon-centered free radicals.