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Recent interest has focused on maintenance of healthy levels of redox signalling 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 labelled here as S7 (SPECTRA7), related to how it affected the cellular metabolic index (CMI) in healthy human participants (n = 8). We demonstrated using the electron spin resonance/electron paramagnetic resonance spectrometer NOXYSCAN that the administration S7 resulted in statistically significant, long-term, dose-dependent inhibition of mitochondrial and cellular reactive oxygen species generation by as much as 9.2 or 17.7% as well as 12.0 or 14.8% inhibition in extracellular nicotinamide-dinucleotide-phosphate oxidase system-dependent generation of O 2 •- , and 9.5 or 44.5% inhibition of extracellular H 2 formation. This was reflected with dose-dependent 13.4 or 17.6% inhibition of tumour necrosis factor 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 affect cellular redox signalling, 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 signalling. This opens the door to future research into the use of S7 for modulation of inflammatory markers, for sports endurance or recovery applications.2 formation. This was reflected with dose-dependent 13.4 or 17.6% inhibition of tumour necrosis factor 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 affect cellular redox signalling, 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 signalling. This opens the door to future research into the use of S7 for modulation of inflammatory markers, for sports endurance or recovery applications.

The main purpose of this study was to investigate the acute local and systemic effects of low-load resistance exercise (30% 1RM) with partial vascular occlusion on exercise-induced free radical production and to compare these effects with other established training methods. Fifteen young and healthy males (25 ± 3 years) performed the following four sessions in a counterbalanced order on separate days: low-load resistance exercise (LI: 30% 1RM), low-load resistance exercise with blood flow restriction (LIBR: 30% 1RM), high-load resistance exercise (HI: 80% 1RM) and an additional session without exercise but blood flow restriction only (BR). Blood samples were obtained 15 min prior to and immediately after exercise sessions from the right index finger and first toe. To analyze concentrations of reactive oxygen species (ROS), electron paramagnetic resonance (EPR) spectroscopy was used. Additionally, mitochondrial ROS production was measured by adding inhibitors of electron transport chain complex III. There was an increased systemic ROS generation after the LIBR session from 0.837 ± 0.093 to 0.911 ± 0.099 µmol/l/min. However, no local or systemic time × condition interaction was detected for ROS production. Regarding mitochondrial ROS production, results were not different between the conditions. Although the low-load resistance exercise session with partial vascular occlusion elicited systemic increases of ROS production, no significant changes were seen on a local level. We assume that this ROS concentration might not be high enough to induce cellular damage but is rather involved in muscle remodulation. However, this needs to be confirmed by future research. [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 crossover, double-blind, placebo-controlled, single-dose study on the effects of SPECTRA™, a dietary supplement, on oxidative stress markers (OSM) in human participants ( n = 22). The measurement of OSM (ex vivo intra- and extracellular formation of reactive oxygen species (ROS, O2−, H2O2, OH−) in whole blood, respiratory activity of blood cells, as well as mitochondrial-dependent ROS formation, and respiratory activity), was performed using EPR spectrometer nOxyscan, spin probe CMH, and oxygen label NOX-15.1, respectively. Furthermore, we investigated the ability of SPECTRA™ to modulate ex vivo cellular inflammatory responses induced by stimulation with exogenous TNF- α and also followed changes in bioavailable NO concentrations. In this clinical study, we demonstrated that administration of SPECTRA™ resulted in statistically significant long-term inhibition of mitochondrial and cellular ROS generation by as much as 17% as well as 3.5-times inhibition in extracellular NADPH system-dependent generation of O2−, and nearly complete inhibition of extracellular H2O2 formation. This was reflected in more than two times inhibition of ex vivo cellular inflammatory response and also increases in bioavailable NO concentration. For the first time, we have measured synergetic, biological effects of a natural supplement on changes in OSM and cellular metabolic activity. The unique design and activity of the plant-based natural supplement, in combination with the newly developed and extended Vitality test, demonstrates the potential of using dietary supplements to modulate OSM and also opens the door to future research into the use of natural supplements for supporting optimal health. [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]