Invitro impact of a combination of red and infrared LEDs, infrared laser and magnetic field on biomarkers of oxidative stress and hemolysis of erythrocytes sampled from healthy individuals and diabetes patients.

AIMS: Low-intensity infrared laser irradiation with output emissions of the laser and LED for in vitro irradiation of plasma and erythrocyte samples collected from healthy individuals and diabetes mellitus (DM) patients was used in the current study. METHODS: The generated emission was in the range 0.85-0.89 nm with pulse duration near 130 ns and repetition rates of pulses 50, 150, 600, and 1500 Hz, average power 0, 50, or 100 mW, in the range of 1-9 min for different 30 variants of irradiation. The levels of 2-thiobarbituric-acid reactive substances (TBARS), aldehydic and ketonic derivatives of oxidatively modified proteins (OMP), total antioxidant capacity (TAC), acid-induced resistance of erythrocytes, and activities of the main antioxidant enzymes were assessed in erythrocyte and plasma samples after irradiation. RESULTS: The low-intensity infrared laser irradiation and low-intensity light emitted by a red LED decreased the lipid peroxidation levels in the erythrocytes of both healthy individuals and DM patients. A statistically significant decrease in TBARS and OMP levels and an increase in the TAC level were observed at the irradiation energy of 34.39 and 68.79 J/cm2 for samples collected from both healthy individuals and DM patients. The effects of the irradiation were accompanied by a statistically significant decrease in catalase activity of both healthy individuals and DM patients. CONCLUSIONS: In many variants of the laser irradiation and low-intensity light emitted by a red LED used in our study, a decrease in the percent of hemolyzed erythrocytes was observed, suggesting that laser therapy protocols should take into account fluencies, frequencies, and wavelengths of the laser before the beginning of treatment, especially in DM patients.

Effect of water diuresis with hydrogen saturation on the course of acute kidney damage during the separation of oxidation and phosphorylation.

Molecular hydrogen has the ability to penetrate cells, easily reach mitochondria, overcome body barriers, penetrate areas of ischemia, edema and inflammation, improve energy supply by supplying additional electrons and have antioxidant and anti-inflammatory effects by neutralizing highly reactive hydroxyl radical and peroxynitrite. In this experiment, we included 60 nonlinear male rats weighing 0.16-0.18 kg and investigated the effect of a negative redox potential solution -297.3±5.27 mV with a molecular hydrogen saturation of 1.2 ppm on the functional-biochemical processes of the kidneys in tissue hypoxia in moderately resistant rats during the separation of oxidation and phosphorylation with the introduction of 2,4-dinitrophenol at a dose of 3 mg/kg. All studies were performed on moderately stable rats. Experimental, functional, biochemical, enzyme-linked immunosorbent, physicochemical, histoenzymochemical, and statistical research methods were used. Under conditions of renal hypoxia in the separation of oxidation and phosphorylation, the use of a solution of negative redox reabsorption of sodium ions in the distal nephron reduces the manifestations of tubular proteinuria, increases the activity of succinate dehydrogenase in the proximal nephron and reduces the redox potential of urine to negative values. Negative redox potential solution with molecular hydrogen saturation has a protective effect on the kidneys and reduces elevated levels of proinflammatory cytokines of tumor necrosis factor-α, interleukin-1-ß, and interleukin-6 in blood plasma, and causes oxidative modification of proteins in the renal cortex for their hypoxia in the separation of oxidation and phosphorylation.

Selected Atherosclerosis-Related Diseases May Differentially Affect the Relationship between Plasma Advanced Glycation End Products, Receptor sRAGE, and Uric Acid.

Our study aimed to identify the relationship between advanced glycation end products (AGEs), soluble receptor for advanced glycation end products (sRAGE), the AGEs/sRAGE, and uric acid (UA) levels in selected atherosclerosis diseases, i.e., abdominal aortic aneurysms (AAA), aortoiliac occlusive disease (AIOD), and chronic kidney disease (CKD), resulting from apparent differences in oxidative stress intensity. Furthermore, we suggest that increased AGEs levels may stimulate an antioxidant defense system reflected by the UA level. The studied group size consisted of 70 AAA patients, 20 AIOD patients, 50 patients in the pre-dialyzed group (PRE), and 35 patients in the hemodialyzed group (HD). The enzyme-linked immunosorbent assay was used to measure AGEs and sRAGE levels. We found a significantly higher concentration of AGEs in CKD patients as compared to AAA and AIOD patients. Furthermore, the sRAGE level was higher in the CKD patients in comparison to AIOD and AAA patients. UA level was significantly higher in the PRE group compared to AAA patients. In conclusion, the diseases included in this study differ in the anti- and prooxidant defense system, which is reflected in the relations between the AGEs, the sRAGE, the AGEs/sRAGE ratio, as well as the UA levels.

Formation of an antioxidant profile in the sea trout (Salmo trutta m. trutta L.) from the Slupia River.

Using a stage- and sex-based multivariate significance tests on the sea trout Salmo trutta m. trutta L. model, we show dependencies in the balance between lipid peroxidation processes, levels of carbonyl derivatives, and activity of antioxidant enzymes (superoxide dismutase SOD, catalase CAT, glutathione reductase GR, and peroxidase GPx) in the processes of antioxidant profile formation during the fish growing process. The study was aimed at examination of the relationships between the biomarkers of oxidative stress estimated by the total antioxidant status as well as the dependencies between the sex (male, female) and developmental stage of the wild sea trout from the Slupia River and its catchment area rivers. Functioning of the pro/antioxidant balance of the liver tissue reflected the course of the individual developmental stages of the trout and was associated with significant intensification of lipoperoxidation, oxidative modification of proteins, and reduction of the total antioxidant capacity of fish along with age. Formation of a holistic model for the analysis of the involvement of all parameters of antioxidant protection in all stages of development and sex allowed us to obtain the following rank order for the level of lipoperoxidation processes, modified proteins, and antioxidant enzyme complex: CAT > SOD > GPx > GR and TBARS > OMP KD > TAC > OMP AD.

Effects of melatonin on low-dose lipopolysaccharide-induced oxidative stress in mouse liver, muscle, and kidney.

Lipopolysaccharide (LPS) administration in an in vivo experimental mice model causes oxidative damage in the liver, muscle, and kidney. We aimed to determine specific mechanisms underlying melatonin's antioxidant protective role. Assays were carried out in quadruplicate in the control, melatonin (10 mg/kg, 10 days), acute LPS administration (once 150 µg), and LPS + melatonin groups. LPS stimulated lipid peroxidation processes (dienes and malondialdehyde) and antioxidant enzyme concentrations (superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase) were assessed in all investigated tissues. Protein oxidation processes (measured as aldehyde and kenotic carbonyl protein derivatives) were enhanced by LPS in the kidney and liver but not in muscle. Melatonin reversed LPS-induced changes, with the exception of muscle protein oxidation. LPS-induced oxidative stress resulted in augmented early-stage diene conjugated and end-stage malondialdehyde lipid peroxidation processes and affected antioxidant activity in liver, kidney, and muscle tissues. LPS activated protein oxidation processes in the kidney and liver. Melatonin ameliorated oxidative damage in the liver, kidney, and partially in the muscle. Melatonin modulates oxidative stress-induced states. Potential synergism between melatonin and systemic inflammation in terms of oxidative modification of muscle proteins needs to be clarified in further studies.