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Scientists around the world concur that maintaining proper levels of redox signaling, which often will mistakenly interpret as oxidative and nitrosative stress. So, identifying the roots of such condition allowed us to design a strategy of nutritional intervention. Utilizing this approach, we performed a randomized, controlled, long-term study of the effect of a multifunctional nutritional supplement on redox signaling and health markers in 48 healthy and pre-metabolic syndrome volunteers. The measurement of extended cellular metabolic index based on cellular and mitochondrial dependent ROS formation and respiratory activity was performed using electron spin resonance spectrometer NOXYSCAN. Spin probe 1-hydroxy-3-methoxycarbonyl-2.2.5.5-tetramethylpyrrolidine (CMH) and oxygen label NOX-14.1 were used. Health parameters (blood pressure, heart rate, lipid and glucose profile, bioavailability of circulating NO was analyzed at control day, after 6 and 12 weeks of twice daily supplementation. Long-term supplementation resulted in significant inhibition of metabolic activity (20.7% cellular and 42.6% mitochondrial). We also observed significant inhibition of extracellular NADPH oxidase dependent generation of superoxide, nearly complete inhibition of extracellular H2O2 formation as well as a 2.5 times increase in bioavailable NO. Evaluated health parameters were improved on healthy people with even greater effects on those with metabolic syndrome: significant improvements in lipid profiles (TC, LDL, HDL, VLDL and TG), glucose metabolism (glucose, insulin, HbA1c, HOMA, postprandial hyperglycemia), inflammatory resistance as well as expression of redox sensitive proteins as NRF2, eNOS, SOD1, HO1 were shown. For the first time, we demonstrate the effects of a multifunctional nutritional supplement containing minerals, vitamins, antioxidant and anti-inflammatory phytonutrients on cellular redox signaling in pre-metabolic syndrome volunteers. We observed strong correlation of extended cellular metabolic index with the more than 25 markers and the indicators of “optimal health” as lipid-, glucose-, inflammatory profile, expression of redox sensitive proteins and other functional cardiovascular parameters. [ABSTRACT FROM AUTHOR]

The research community is generally agreed that maintenance of healthy levels of free radicals and related oxidants are important for good health. However, utilization of the “redox stress hypothesis” can provide us with concrete nutritional targets in order to better support and maintain “optimal health.” Following this hypothesis, we performed a single-dose study on the effects of dietary supplement Spectra5 TM on oxidative and nitrosative stress markers as well as metabolic, inflammatory and cardiovascular parameters in human participants (n=8). The measurements of ex vivo intra- and extracellular formation of reactive oxygen species (ROS, O 2 – , H 2 O 2 , OH) in whole blood, respiratory activity of blood cells, as well as mitochondrial-dependent ROS formation, and respiratory activity were performed using EPR spectrometer NOXYSCAN, spin probe CMH, and oxygen label NOX-15.1, respectively. Furthermore, we investigated the ability of supplement to modulate ex vivo cellular inflammatory responses induced by stimulation with exogenous TNF-α and also followed changes in bioavailable NO concentrations. In this study, we demonstrated that administration of single dose Spectra5 TM resulted in statistically significant long-term, time depended inhibition of mitochondrial and cellular ROS generation by as much as 13% as well as 2.5-times inhibition in extracellular NADPH system-dependent generation of O 2 – , and nearly complete inhibition of extracellular H 2 O 2 formation. This was reflected in more significant inhibition of ex-vivo cellular inflammatory response and also increases in bioavailable NO concentration. In this study we have measured synergetic, biological effects of a natural supplement on changes in oxidative and nitrosative stress as well as cellular metabolic activity. The unique design and activity of the plant-based natural supplement, in combination with the validated “Extended Vitality Test”, demonstrates the efficiency to use the dietary supplements by utilizing the “redox stress hypothesis”. [ABSTRACT FROM AUTHOR]

Scientists around the world concur that maintaining proper levels of oxidative and nitrosative stress is necessary to maintain “optimal health.” So, identifying thee roots of such stress allowed us to design a strategy of nutritional intervention. Utilizing this approach, we performed a controlled, long-term study of the effect of a complex nutritional supplement system on multiple oxidative stress and health markers in healthy and metabolic syndrome volunteers (n=48). The measurement of cellular and mitochondrial dependent ROS formation and respiratory activity was performed using “Vitality & Extended Vitality Tests” (Fink B. et al., FSN-2014). More than 25 health parameters (blood pressure, heart rate, lipid and glucose profile, bioavailability of circulating NO was analyzed at control day, after 6 and 12 weeks of twice daily supplementation. Long-term supplementation resulted in significant inhibition of ROS generation (20.7% cellular and 42.6% mitochondrial). We also observed significant inhibition of extracellular NADPH oxidase dependent generation of superoxide, nearly complete inhibition of extracellular H 2 O 2 formation as well as a 2.5 times increase in bioavailable NO. Evaluated health parameters were improved on healthy people with even greater effects on those with metabolic syndrome: significant improvements in lipid profiles (TC, LDL, HDL, VLDL and TG), glucose metabolism (glucose, insulin, HbA1c, HOMA, postprandial hyperglycemia) were shown. For the first time, we were able to demonstrate the biological effects of long-term administration of a multifunctional supplement containing minerals, vitamins and antioxidant and anti-inflammatory phytonutrients. We were able to observe the changes of inflammatory, oxidative and nitrosative stress markers the indicators of “optimal health” in correlation to more than 25 laboratories, metabolic, inflammatory and cardiovascular parameters. [ABSTRACT FROM AUTHOR]

Mitochondrial damage is implicated in the progression of cardiac disease. Considerable evidence suggests that proinflammatory cytokines induce oxidative stress and contribute to cardiac dysfunction. This study was conducted to determine whether a TNF-induced increase in superoxide (O2˙-) contributes to mitochondrial damage in the left ventricle (LV) by impairing respiratory complex I activity. We employed an electron paramagnetic resonance (EPR) method to measure O2˙- and oxygen consumption in mitochondrial respiratory complexes, using an oxygen label. Adult male Sprague–Dawley rats were divided into four groups: control, TNF treatment (ip), TNF+ apocynin (APO; 200 μmol/kg bw, orally), and TNF+ Tempol (Temp; 300 μmol/kg bw, orally). TNF was injected daily for 5 days. Rats were sacrificed, LV tissue was collected, and mitochondria were isolated for EPR studies. Total LV ROS production was significantly higher in TNF animals than in controls; APO or Temp treatment ameliorated TNF-induced LV ROS production. Total mitochondrial ROS production was significantly higher in the TNF and TNF+ APO groups than in the control and TNF+ Temp groups. These findings suggest that TNF alters the cellular redox state, reduces the expression of four complex I subunits by increasing mitochondrial O2˙- production and depleting ATP synthesis, and decreases oxygen consumption, thereby resulting in mitochondrial damage and leading to LV dysfunction. [Copyright &y& Elsevier]

The excessive formation of reactive oxygen and nitrogen species (RONS) in tissue has been implicated in the development of various diseases. In this study we adopted ex vivo low temperature EPR spectroscopy combined with spin trapping technique to measure local RONS levels in frozen tissue samples. CP-H (1-hydroxy-3-carboxy-pyrrolidine), a new nontoxic spin probe, was used to analyze RONS in vivo. In addition, nitrosyl complexes of hemoglobin were determined to trace nitric oxide released into blood. By this technique we found that RONS formation in tissue of control animals increased in the following order: liver < heart < brain < cerebellum < lung < muscle < blood < ileum < kidney < duodenum < jejunum. We also found that endotoxin challenge, which represents the most common model of septic shock, increased the formation of RONS in rat liver, heart, lung, and blood, but decreased RONS formation in jejunum. We did not find changes in RONS levels in other parts of gut, brain, skeletal muscles, and kidney. Scavenging of RONS by CP-H was accompanied by an increase in blood pressure, indicating that LPS-induced vasodilatation may be due to RONS, but not due to nitric oxide. Experiments with tissue homogenates incubated in vitro with CP-H showed that ONOO− and O2•−, as well as other not identified RONS, are detectable by CP-H in tissue. In summary, low-temperature EPR combined with CP-H infusion allowed detection of local RONS formation in tissues. Increased formation of RONS in response to endotoxin challenge is organ specific. [Copyright &y& Elsevier]

Recent interest has focused on maintenance of healthy levels of redox signaling and the related oxidants; these parameters are crucial for providing us with concrete nutritional targets that may help us to better understand and maintain “optimal health”. Following the above hypothesis we performed a pilot double blind, crossover, placebo controlled, single dose study to measure the dose dependent effects of a proprietary plant-based dietary supplement labeled here as S7 (SPECTRA7), related to how it affected the cellular metabolic index (CMI) in healthy human participants (n = 8). We demonstrated using the EPR spectrometer NOXYSCAN that the administration S7 resulted in statistically significant, long-term, dose dependent inhibition of mitochondrial and cellular ROS generation by as much as 9.2 or 17.7 % as well as 12.0 or 14.8% inhibition in extracellular NADPH system-dependent generation of O 2 •‒ and 9.5 or 44.5% inhibition of extracellular H 2 O 2 formation. This was reflected with dose dependent 13.4 or 17.6% inhibition of TNF-alpha induced cellular inflammatory resistance and also 1.7 or 2.3-times increases of bioavailable NO concentration. In this pilot study we demonstrated the ability of a natural supplement to effect cellular redox signaling, which is considered by many researchers as oxidative stress. The design and activity of this proprietary plant-based material, in combination with the newly developed “CMI” test, demonstrates the potential of using dietary supplements to modulate redox signaling. This opens the door to future research into the use of S7 for modulation of inflammatory markers, for sports endurance or recovery applications. [ABSTRACT FROM AUTHOR]