Effects of hyperbaric oxygenation on activation of immunocompetent cells and lipid peroxidation under immunization by heterologous erythrocytes]

On the basis of rats' experiments under conditions of HBO a close relationship was established between the intensity of immune processes and peroxide oxidation of lipids (POL). The study enabled to show a connection between immunoreactivity stimulation in spleen cells and certain levels of POL intensity and anti-oxidation protection as well. There were assessed diverse HBO effects on intact and immune organism and hyperbaric dependence of immunodepression on POL's intensification.     

Regional lipid peroxidation and protein oxidation in rat brain after hyperbaric oxygen exposure

Reactive oxygen species may participate in development of neurological toxicity resulting from hyperbaric oxygen exposure. To explore the possibility that increased reactive O₂ metabolite generation may result in oxidative modification of lipids and proteins, rats were exposed to five atmospheres (gauge pressure) of O₂ until development of an electroencephalographic seizure. Lipid peroxidation (as thiobarbituric acid-reactive substances) and protein oxidation (as 2,4-dinitrophenyl-hydrazones) were measured in five brain regions. Oxidized and reduced glutathione were also determined because of their role in regulating lipid peroxidation. Lipid peroxidation was confined to the frontal cortex and hippocampus, while protein oxidation (in both cytoplasmic and membranous fractions) and increased oxidized glutathione was evident throughout the brain. These results support a role for formation of reactive O₂ metabolites from hyperbaric O₂ exposure and suggest that protein oxidation, especially in soluble proteins, may be one of the most sensitive measures.     

Status of the main functional systems in humans after long-term exposure to hyperbaric medium]

The exposure of divers to hyperbaric conditions under pressure of 4.6 MPa induced development of astheno-neurotic disorders with cardiovascular component against a background of pronounced fatigue. A decrease of the pulmonary ventilation function in the form of bronchial obstruction syndrome was observed as well. On the 10-15th day of the postdiving period asthenia phenomena extinguished and the pulmonary function tended to restoration. On the 30th day of postdiving period all the functional systems were normalized. The professional activity of divers for many years gives rise to the formation of adaptive reaction (increase of vital capacity of lungs and maximal ventilation of lungs), on the one hand, and to pathological disorders, such as arterial hypertension and bronchial obstruction syndrome, on the other hand.     

Nitrogen metabolism in humans during long-term exposure to hyperbaric conditions]

Results from studies of nitrogenous exchange in a man during long exposure to the hyperbaric conditions (4.1, 4.6, 5.1 MPa, that corresponds to 400, 450 and 500 m) have shown that catabolism of proteins in man under conditions of high pressure of gas and aquatic environments is intensified due to the primarily intensive muscular work. The experimental ration which has been corrected from test to test by the results of studies practically completely satisfies the increasing demands of the organism in proteins, that is evidenced for by the stable content of total protein and its fractions in blood.     

Analysis of lipid peroxidation mechanisms in human spermatozoa

The mechanisms by which ferrous ion promoters induce malondialdehyde generation by human spermatozoa have been investigated in order to provide a rational basis for the quantification and interpretation of lipid peroxidation assays. Incubation of human spermatozoa with a ferrous ion promoter in the presence of thiobarbituric acid (TBA) led to the generation of the bone fide malondialdehyde-TBA adduct. The importance of iron in the stimulation of lipid peroxidation was emphasized by the ability of Desferal* and EDTA to suppress malondialdehyde generation. Paradoxically, when the concentration of EDTA relative to iron was equimolar or greater, the suppression of malondialdehyde formation was accompanied by the generation of hydroxyl radicals. These results suggested that the addition of promoter did not effect the first-chain initiation of lipid peroxidation but favored an alternative mechanism involving the catalytic decomposition of pre-existing lipid peroxides. This conclusion was reinforced by the inability of reagents that would limit the formation (superoxide dismutase and/or catalase) or availability (mannitol, formate) of hydroxyl radicals, to influence malondialdehyde generation. While hydroxyl radicals were not directly involved in Fe²⁺-promoted malondialdehyde generation, the existence of significant correlations between reactive oxygen species production and the outcome of the TBA assay, suggested that Fenton chemistry might be important in the initiation of peroxidative damage. It is proposed that the impeded propagation of peroxidation initiated by Fenton or Haber Weiss reactions would lead to the accumulation of lipid peroxides in the spermatozoa and it is these peroxides that are induced to decompose during the Fe²⁺-promoted TBA assay, stimulating a lipoperoxidative chain reaction and malondialdehyde formation. © 1993 Wiley-Liss, Inc.     

Plant catechols prevent lipid peroxidation in human plasma and erythrocytes

The antioxidant activity of several plant catechol derivatives was tested in buffer, plasma, and human erythrocytes. In buffer, chlorogenic acid (CGA), caffeic acid (CA), and dihydrocaffeic acid (DCA) reduced ferric iron equally well in the ferric reducing antioxidant power (FRAP) assay. Low concentrations of the polyphenols enhanced the ability of plasma to reduce ferric iron by about 10%. In plasma, lipid hydroperoxide and F₂-isoprostane formation induced by a water-soluble free radical initiator were reduced by CGA at concentrations as low as 20 M. During incubation at 37°C, human erythrocytes took up DCA, but not CGA, and intracellular DCA enhanced the ability of erythrocytes to reduce extracellular ferricyanide. When intact erythrocytes were exposed to oxidant stress generated by liposomes containing small amounts of lipid hydroperoxides, extracellular CGA at a concentration of 5 M decreased both lipid peroxidation in the liposomes, and spared -tocopherol in erythrocyte membranes. These results suggest that the catechol structure of these compounds convey the antioxidant effect in plasma and in erythrocytes.     

Reparative processes in cardiac muscle following exposure to hyperbaric oxygenation

In 150 rabbits by means of histoautoradiographic, histochemical and certain histological methods, reparative processes in the cardiac muscle have been studied at experimental myocardial infarction and its combination with atherosclerosis under various regimes of hyperbaric oxygenation (HBO). It has been demonstrated that HBO (pO2--2 kgs/cm2, saturation time--45 min, 3-7 sessions) positively affects the proliferative processes in the ischemic zone, contributes to better preservation of the periinfarction parts of the myocardium and enhances maturation of the scar. If HBO is used in another regime (pO2--1 kgs/cm2, saturation time--30 min, 1-7 sessions), its positive effect on the regenerative processes in the ischemic zone is preserved, while its toxic effect on distant cardiac zones decreases considerably.     

Oxygen radicals stimulate intracellular proteolysis and lipid peroxidation by independent mechanisms in erythrocytes

Exposure of red blood cells to oxygen radicals can induce hemoglobin damage and stimulate protein degradation, lipid peroxidation, and hemolysis. To determine if these events are linked, rabbit erythrocytes were incubated at 37 degrees C with various oxygen radical-generating systems and antioxidants. Protein degradation, measured by the production of free alanine, increased more than 11-fold in response to xanthine (X) + xanthine oxidase (XO). A similar increase in proteolysis occurred when the cells were incubated with acetaldehyde plus XO, with ascorbic acid plus iron (Asc + Fe), or with hydrogen peroxide (H2O2) alone. Upon addition of XO, increased proteolysis was evident within 5 min and was linear for up to 5 h. In contrast, lipid peroxidation, as shown by the production of malonyldialdehyde, conjugated dienes, or lipid hydroperoxides was observed only after 2 h of incubation with X + XO, acetaldehyde + XO, or H2O2. Ascorbate plus Fe2+ induced both protein degradation and lipid peroxidation; however, the addition of various antioxidants (urate, xanthine, glucose, or butylated hydroxytoluene) decreased lipid peroxidation without affecting proteolysis. Thus, these processes seem to occur by distinct mechanisms. Furthermore, at low concentrations of XO, protein degradation was clearly increased in the absence of detectable lipid peroxidation products. Hemolysis occurred only in a small number of cells (9%) and followed the appearance of lipid peroxidation products. Thus, an important response of red cells to oxygen radicals is rapid degradation of damaged cell proteins. Increased proteolysis seems to occur independently of membrane damage and to be a more sensitive indicator of cell exposure to oxygen radicals than is lipid peroxidation.     

Suppression of humoral antibody synthesis on exposure to hyperbaric oxygenation

The influence of hyperbaric oxygenation (HBO) on the immune response in mice, immunized intraperitoneally with sheep red blood cells, was studied. HBO was shown to reduce hemagglutinin and hemolysin titres in peripheral blood as well as to decrease the amount of antibody-forming cells in the spleen. The most pronounced immunodepressant HBO effect is seen when hyperbaric oxygenation is carried out under toxic conditions before immunization of the animals with low antigen doses. Relationship is shown between the immunodepressant HBO effect and reduced leucocyte and lymphocyte counts in peripheral blood of the animals.     

Cytogenetic after-effects of fractionated and prolonged exposure to hyperbaric oxygenation

The effect of hyperbaric oxygenation was investigated in bone marrow cells of rats, at prolongated and fractionated regimes usually employed in medicine. As a result of this study, it was pointed out that fractionated treatment of animals at I ata I h during 5 and 10 days affects the rats cytogenetically and causes several chromosomal damages. Prolongated treatment with high pressure oxygen was of a less mutagenic activity. The data obtained suggest nondirect action of this mutagen on the genetic apparatus.     

Erythropoietic activity of human blood following exposure to hyperbaric hyperoxygenation]

Before exposure of man to hyperoxia the blood plasma posessed erythropoietic activity, but 18 to 20 hours after exposure to compressed air condition in the high pressure chamber corresponding to the depth of 100 metres there proved to be a marked fall of the erythropoietic activity. No statistically significant shifts were revealed in the peripheral blood indices by that time.     

Acetylcholinesterase activation and enhanced lipid peroxidation after long-term exposure to low levels of aluminum on different mouse brain regions

Aluminum (Al), oxidative stress and impaired cholinergic functions have all been related to Alzheimer's disease (AD). The present study evaluates the effect of aluminum on acetylcholinesterase (AChE) and lipid peroxidation in the mouse brain. Mice were loaded by gavage with Al 0.1 mmol/kg/day 5 days per week during 12 weeks. The mice were divided into four groups: (1) control; (2) 10 mg/mL of citrate solution; (3) 0.1 mmol/kg of Al solution; (4) 0.1 mmol/kg of Al plus 10 mg/mL of citrate solution. AChE activity was determined in the hippocampus, striatum, cortex, hypothalamus and cerebellum and lipid peroxidation was determined in the hippocampus, striatum and cortex. An increase of AChE activity was observed in the fourth group (Al + Ci) in the hippocampus (36%), striatum (54%), cortex (44%) and hypothalamus (22%) (p<0.01). The third group (Al) presented a decrease of AChE activity in the hypothalamus (20%) and an enhancement in the striatum (27%). Lipid peroxidation, measured by TBARS (thiobarbituric acid reactive substances), was elevated in the hippocampus and cerebral cortex when compared with the control (p < 0.01). The effect of aluminum on AChE activity may be due to a direct neurotoxic effect of the metal or perhaps a disarrangement of the plasmatic membrane caused by increased lipid peroxidation.     

Effects of prolonged hyperbarism on lipid peroxidation and structural-functional state of erythrocytes]

Prolonged helium-oxygen hyperbaric (pressure 3,6 MPa) increased diene conjugate and Schiff's base level in plasma and erythrocyte membranes of mice. In those conditions SOD and glucose 6-phosphate dehydrogenase activities were inhibited in erythrocytes. Lipid bilayer microviscosity and cholesterol content of erythrocyte membranes were increased.     

Effects of long-term exposure to low levels of organophosphorous pesticides and their mixture on altered antioxidative defense mechanisms and lipid peroxidation in rat liver

Organophosphorous pesticides, commonly used in agriculture for achieving better quality products, are toxic substances that have harmful effects on human health. Recent research on pesticides, especially pesticide mixtures, has shown that they are one of the key environmental health issues. The aim of the present study was to investigate whether dichlorvos, acephate, dimethoate and phorate, either used separately or in combination, can induce oxidative damage in rat livers. The levels of superoxide dismutase, glutathione peroxidase, catalase and lipid peroxidation products (malondialdehyde) were used as criteria. Low, middle and high doses of pesticides in drinking water were continuously administered orally to rats ad libitum for 24 weeks. Results show that the antioxidative defense mechanisms and lipid peroxidation in the rat livers display different responses, depending on the pesticide treatments and doses. The parameters for acephate, dichlorvos, phorate and dimethoate in the low-dose group, and the corresponding low-dose co-treated group were not altered. The oxidative damage in rat livers showed different responses with increasing pesticide dose according to the different pesticide treatments. The combination group of dichlorvos, acephate, dimethoate and phorate displayed different responses compared with the single pesticide-treated group. However, these responses did not constitute the sum of the response produced by each pesticide in the liver.     

Lipid peroxidation in experimental myocardial infarct: the action of hyperbaric oxygenation

Rats with experimental myocardial infarction demonstrated decrease in the activity of superoxide dismutase and catalase and increase in the content of lipid peroxidation (LPO) products and Schiff bases both in and outside the area of necrosis. The combined ischemic damage and hyperbaric oxygenation resulted in the over additive effect of accumulation of LPO products in and outside the area of infarction. The data suggest that it is desirable to use antioxidants during hyperbaric oxygenation.     

The impact of long-term past exposure to elemental mercury on antioxidative capacity and lipid peroxidation in mercury miners

Limited information is available on the effects of chronic mercury exposure in relation to the risk of cardiovascular disease (CVD). It is known from in vitro and in vivo studies that Hg can promote lipid peroxidation through promotion of free radical generation, and interaction with antioxidative enzymes and reduction of bioavailable selenium. The objective of the study was to test the hypothesis that long-term past occupational exposure to elemental Hg (Hg⁰) can modify antioxidative capacity and promote lipid peroxidation in miners.

The study population comprised 54 mercury miners and 58 workers as the control group. The miners were examined in the post-exposure period. We evaluated their previous exposure to Hg⁰, the putative appearance of certain nonspecific symptoms and signs of micromercurialism, as well as the main behavioural and biological risk factors for CVD, and determined: 1) Hg and Se levels in blood and urine, 2) antioxidative enzymes, Cu/Zn superoxide dismutase (CuZn-SOD), catalase (CAT), and selenoenzyme glutathione peroxidase (GSH-Px) activity in erythrocytes as indirect indices of free radical activity, 3) pineal hormone melationin (MEL) in blood and urine, and 4) lipid hydroperoxides (LOOHs) and malondialdehyde (MDA) as lipid peroxidation products.

The mercury miners were intermittently exposed to Hg⁰ for periods of 7 to 31 years. The total number of exposure periods varied from 13 to 119. The cumulative U-Hg peak level varied from 794-11,365 μg/L. The current blood and urine Hg concentrations were practically on the same level in miners and controls. Miners showed some neurotoxic and nephrotoxic sequels of micromercurialism. No significant differences in behavioural and biological risk factors for CVD were found between miners and controls. A weak correlation (r = 0.36, p < 0.01) between systolic blood pressure and average past exposure U-Hg level was found. The mean P-Se in miners (71.4 μg/L) was significantly lower (p < 0.05) than in the controls (77.3 μg/L), while the mean U-Se tended to be higher (p < 0.05) in miners (16.5 μg/g creatinine) than in the controls (14.0 μg/g creatinine). Among antioxidative enzyme activities, only CAT in erythrocytes was significantly higher (p < 0.01) in miners (3.14 MU/g Hb) than in the controls (2.65 MU/g Hb). The mean concentration of B-MEL in miners (44.3 ng/L) was significantly higher (p < 0.01) than in the controls (14.9 ng/L). The mean value of U-MEL sulphate (31.8 μg/L) in miners was significantly lower (p < 0.01) than in the control group (46.9 μg/L). Among the observed lipid peroxidative products, the mean concentration of U-MDA was statistically higher (p < 0.01) in miners (0.21 μmol/mmol creatinine) than in the controls (0.17 μmol/mmol creatinine).

In the group of miners with high mercury accumulation and the presence of some nonspecific symptoms and signs of micromercurialism, the results of our study partly support the assumption that long-term occupational exposure to Hg⁰ enhances the formation of free radicals even several years after termination of occupational exposure. Therefore, long-term occupational exposure to Hg⁰ could be one of the risk factors for increased lipid peroxidation and increased mortality due to ischaemic heart disease (ICH) found among the mercury miners of the Idrija Mine.     

Short-time UVA exposure to human keratinocytes instigated polyunsaturated fatty acid without inducing lipid peroxidation

Short-term exposure to ultraviolet A (UVA) radiation can directly injure our skin through inflammatory response and indirectly through oxidative stress, triggering polyunsaturated fatty acid (PUFA) peroxidation in skin cell membrane and formation of DNA adduct, 8-hydroxy-2′-deoxyguanosine (8-OHdG). It is known that UVA exposure leads to photoaging, immunosuppression and skin cancer. However, the changes in PUFA and its oxidized metabolites, and cell cycle after short UVA exposure, are debatable. In this study, human keratinocytes (HaCaT) were exposed to low dose (5?J/cm²) and high dose (20 J/cm²) of UVA and assessed immediately, 8?h, 12?h, and 24?h post-treatment. Both doses showed a transient suppression in S-phase after 8?h of UVA exposure, and G₂/M phase arrest after 12-h UVA exposure in the cell cycle but subsequently returned to normal cycle. Also, no observable DNA damage took place, where 8-OHdG levels were below par after 24-h UVA exposure. A dose of 20 J/cm² UVA stimulated significant amount of arachidonic acid, n-3 docosapentaenoic acid, and docosahexaenoic acid (DHA) but lowered adrenic acid and eicospentaenoic acid after 24-h exposure. Among the 43 oxidized PUFA products determined, enzyme-dependent oxidized PUFAs, namely, 14-hydroxy-DHA (HDoHE) level reduced, and 8- and 13-HDoHE levels elevated significantly in a linear trend with post-treatment time. Out of the nonenzymatic oxidized PUFAs, a significant linear trend with post-treatment time was shown on the reduction of 5-F_2t-Isoprostane (IsoP), 15-F_2t-IsoP, Isofurans, 5-F_3t-IsoP, Neurofurans, and 20-HDoHE. Our observations indicate oxidative stress through short UVA exposure on human keratinocytes did not have detrimental consequences.     

Increased lipid peroxidation in the erythrocytes of kidney stone formers

The level of lipid peroxidation was significantly increased in erythrocytes and erythrocyte membrane in patients with stone disease. Increased activities of catalase and acetylcholinesterase in the erythrocyte membrane were observed, while hemolysate displayed no significant change in superoxide dismutase activity. The amount of phospholipids in the RBC membrane of patients was significantly increased. Peroxidation was stimulated by oxalate in vitro and was further enhanced in the presence of ferrous ion. The changes in lipid peroxidation and antioxidant enzymes are suggestive of chemical alteration of the RBC membrane during urolithiasis.     

Status of the spinal inhibitory reactions in humans subjected to hyperbaric oxygenation]

The state of human spinal inhibition responses under normo- and hyperbaric pressure (6.5 ata) was comparatively studied. The paired stimulation method has been used to estimate resetting of tested monosynaptic reflex in the 20-900 ms interval of paired stimulation at rest or against the background of supraspinal modulation of spinal reflective processes (Jendrassik manoeuvre, voluntary plantar flexion) were studied. The depression of inhibition reactions under hyperbaric pressure identical to that during the supraspinal modulation under normobaric conditions is shown. It is supposed that these influences on spinal reflection processes are caused by the same neuronal mechanism.     

Responses of antioxidants and lipid peroxidation in mussels to oxidative damage exposure

• 1.1. The aim of this work was to evaluate the relationships between free radical scavengers and lipid peroxidation in the common mussel Mytilus edulis.
• 2.2. Mussels were exposed to compounds known for their ability to produce free radicals (carbon tetrachloride, CCl₄) and reactive oxygen species via redox cycling (menadione), and the effects on digestive gland, gills and remaining tissues were studied.
• 3.3. Lipid peroxidation parameters and the status of free radical scavengers (glutathione, vitamins A, E and C) were affected more by exposure to menadione than to CCl₄.
• 4.4. The observed changes in the free radical scavengers content are indicative of a role in detoxication of damaging reactive species.