Dietary supplementation with a high dose of daidzein enhances the antioxidant capacity in swine muscle but experts pro-oxidant function in liver and fat tissues

Background： Although isoflavones are natural dietary antioxidants, they may have toxicological effects. This study aimed to evaluate the redox system in tissues of finishing pigs by supplementation with high dose of daidzein（640 mg/kg）.Results： The supplementation of high dose of daidzein for 64 d increased the activity of superoxide dismutase and total antioxidant capacity in longissimus muscle but down-regulated the expression of reactive oxygen species（ROS）-producing enzyme NADPH oxidase-2 and cyclooxygenase-2. In contrast, high-level supplementation with daidzein exerted pro-oxidant changes in back fat, abdominal fat, liver, and plasma, as reflected by increased contents of malondialdehyde, a lipid peroxidation product, in these tissues. Furthermore, daidzein supplementation resulted in higher expression of ROS-producing enzymes, including NADPH oxidase-1 and cyclooxygenase-1in liver, 5-lipoxygenase（5-LOX） in backfat and NADPH oxidase-2 both in abdominal fat and backfat. The supplementation of daidzein did not affect meat quality parameters in longissimus muscle, including marbling score,eye muscle areas, intramuscular fat, shear force, drip loss, p H and meat color.Conclusions： This experiment suggests that dietary supplementation of finishing pigs with daidzein at a high dose level improves redox status in muscle but exerts pro-oxidant effect in liver and fat tissues.

Syringic acid induces cancer cell death in the presence of Cu(Ⅱ)ions via pro-oxidant activity

Objective:To investigate the effects of syringic acid on HEK 293 and HepG2 cells in the absence and presence of exogenous Cu(Ⅱ)and Fe(Ⅱ)ions.Methods:The antiproliferative effects of syringic acid on HEK 293 and HepG2 cells in the absence and presence of exogenous Cu(Ⅱ)and Fe(Ⅱ)ions were examined by MTT assay.Additionally,colony-forming,reactive oxidative species(ROS)generation,apoptosis induction,autophagy,mitochondrial membrane potential,and mitochondrial mass were investigated.Results:At 24 and 72 h,no significant differences were observed in the viability of HepG2 cells between the control and syringic acid+Fe(Ⅱ)groups.However,exposure of HepG2 cells to syringic acid+Cu(Ⅱ)for 72 h reduced the cell viability significantly.Furthermore,ROS formation,induction of apoptosis,and autophagic vacuoles were significantly increased in HepG2 cells without marked changes in mitochondrial membrane potential and mitochondrial mass.Moreover,syringic acid+Cu(Ⅱ)reduced the plating efficiency and surviving fraction significantly.Conclusions:The combination of syringic acid with Cu(Ⅱ)was toxic to cancer cells and showed pro-oxidant activity.In addition,this combination induced autophagy in cancer cells with less cytotoxic effects on normal cells,which is a potential candidate for the development of novel therapeutics towards cancer.

Pro-Oxidant Antioxidant Balance in Inflammatory Bowel Disease

Background: Inflammatory bowel disease (IBD) is associated with increased morbidity and incident of colon cancer;however its etiology is still unclear. Currently, one of the most probable pathogenesis patterns is increased permeability of bowel membrane and it seems that oxidative stress plays an important role in this pathway. This study was done to assess the pro-oxidant antioxidant balance (PAB) in these patients. Materials: This was a cross sectional study of 2 groups including 50 patients with diagnosed IBD and 50 healthy controls. Patients were selected purposively from those referring to adult gastroenterology clinic in 2013. SPSS (ver11.5) has been. A P value < 0.05 was regarded as statistically significant. Results: Mean PAB in patients and controls group was 119.98 ± 38.98 HK unite and 52.67 ± 22.80 HK unite, respectively, (P value < 0.001). PAB mean in ulcerative colitis patients was 120.60 ± 33.90 HK unite and in CD patients was 118.20 ± 45.99 HK unite, and showed no significant difference (P value = 0.85). PAB and MDA could detect healthy subjects from IBD patients with sensitivity more that 90% and specificity more than 84%. Conclusion: PAB shifted to pro-oxidants in IBD patients;moreover this shift was unrelated to disease type. These tests could use as screening test.

Research Progress of Mechanism of Action of Resveratrol

Resveratrol is a kind of polyphenolic compound that widely exists in plants and has extensive physiological pharmacological function and is very useful for human health. For the mechanism of action and function of RV, people are doing a variety of groundbreaking researches. Results show that the molecular mechanism of RV is embodied in aspects such as oxidative stress and diseases of neuropathy, anti-oxygenation and pro-oxidant effect and RV target molecule, etc. This article mainly summarized the mechanism of action of resveratrol in these aspects.

Bacillus sp. SAB E-41-derived extract shows antiaging properties via ctt1-mediated oxidative stress tolerance response in yeast Schizosaccharomyces pombe

Objective: To analyze potential activation of oxidative stress tolerance systems by SAB E-41 bacterial extract in promoting the life span of yeast Schizosaccharomyces pombe. Methods: In vitro analysis was done to assess antioxidant activity of SAB E-41 bacterial extract. Antiaging property of the particular extract was then assayed through spot test and chronological life span assays. Furthermore, sty1 mitogen-activated protein kinase, pap1 transcriptional factor of oxidative stress response and its downstream genes, ctt1 were evaluated via real time PCR. The protein level of ctt1 was then observed via Western Blot analysis. In addition, accumulation of reactive oxygen species and mitochondrial activity were conducted to understand the effect of SAB E-41 upon oxidative stress response systems in vivo. Results: The IC50 values of corresponding extract for antioxidant(DPPH; ABTS) and antiglycation were 402.40, 358.13 and 683.55 μg/mL, respectively. In addition, SAB E-41 extract(750 μg/mL) exhibited antiaging properties, which could be attributed to significant up-regulation of oxidative stress response genes, sty1, pap1 and ctt1. Interestingly, SAB E-41 extract could enhance stress tolerance phenotype of Schizosaccharomyces pombe against H2 O2-induced oxidative stress. These results were supported by increasing mitochondrial activity and reactive oxygen species intracellular levels. Conclusions: SAB E-41 extract could promote yeast life span likely via up-regulation of oxidative stress responses in yeast. Our results suggest that adaptive response via up-regulation of oxidative stress transcriptional factors, and its downstream gene, ctt1, as well as mitochondrial activity contributes in combating oxidative stress thus promoting yeast life span.

The Cyclic Feeding Regime Induces Decaying Age-Dependent Oxidative Stress and Regulates the Cell Chain of the Immunity

We developed an experimental model of a cyclic feeding regime (CFR) that increased a lifespan in rats. The manifestations of oxidative stress and their interrelation with parameters of cell immunity were assessed in rats at CFR. It is shown that changes of body mass, liver mass and indexes of pro/antioxidant system after periods of starving—ad libitum nutrition at CFR diet in old animals were less pronounced than in young animals. The body mass loss of 30% in 14 days was accompanied by oxidative stress. Indexes of phagocytosis did not change, but activity of oxidase system of neutrophil was increased in 2 times. The response of metabolic and physiological systems on repeat starving—ad libitum nutrition cycles differs from the response to the initial cycle of CFR. This is interpreted as a change of adaptation strategy and the effect of metabolic memory, which influences the choice of organism strategy of adaptation for subsequent starving. The dynamics of change of the studied indexes in response to CFR was age-dependent. It was supposed that different answer to CFR in young and old animals is determined by the different amount of carbon and fat depots in young and old animals.

Tunable catalytic activity of gadolinium-doped ceria nanoparticles for pro-oxidation of hydrogen peroxide

We report a study of the roles of gadolinium(lll)(Gd3+)dopants in influencing the catalytic activity of gadolinium-doped ceria nanoparticles towards the pro-oxidation of hydrogen peroxide to hydroxyl radicals.These doped ceria nanoparticles with dopant concentrations of 0.6 wt.%,3 wt.%,and 6 wt.%Gd^3+were synthesized using an ozone-mediated method for tuning their catalytic activities.The Gd dopants were found to foster an increase in the percentage of Ce^3+ions in the doped ceria nanoparticles.Our reaction kinetic study revealed that the relationship between the overall reaction rates and the Gd dopant concentrations in our doped materials followed a volcano-like trend.In contrast,the apparent activation energy values of these Gd-doped ceria nanoparticles were found to be positively associated with the concentrations of Gd dopants.The overall catalytic activity trend was attributed to the interplay between the promotion and degradation effects of the Gd dopants on the properties of doped ceria nanoparticles.

Reactive oxygen species in the progression and treatment of malignant mesothelioma

Malignant mesothelioma(MM)is an aggressive cancer that affects the pleural and peritoneal mesothelial lining of the lungs and abdomen.Survival rates for patients with MM remain extremely low and effective treatments are limited.MM tumors harbor both genotypic and phenotypic features that indicate MM tumor cells are under increased oxidative stress,similar to other aggressive cancers.This increased oxidative stress in MM cells supports aggressive growth while providing a therapeutic vulnerability exploitable by redox-modulating compounds.MM tumor cells also exhibit altered mitochondrial structure and function that contribute to the disease through perturbations in metabolism and reactive oxygen species(ROS)production and metabolism.Targeting the altered redox status in cancer through increasing cellular ROS levels directly or inhibiting cellular antioxidant pathways and disrupting ROS scavenging mechanisms has become an exciting area for therapeutic intervention.This review discusses ROS sources and signaling,mitochondrial structure and function and targeting mitochondria ROS as a therapeutic approach for the treatment of MM.