Bergapten mediated inflammatory and apoptosis through AMPK/eNOS/AKT signaling pathway of isoproterenol-induced myocardial infarction in Wistar rats.

Bergapten (BeG) is explored for its anti-inflammatory and antioxidant properties. Myocardial infarction (MI) is reported to be one of the leading cardiovascular diseases characterized by mitochondrial dysfunction and apoptosis. The main purpose of this study is to assess the cardiopreventive effects of BeG (50 mg/kg) in isoproterenol (ISO)-induced MI in Wistar rats. The increased infarct size after ISO induction was reduced simultaneously on treatment with BeG. Similarly, augmented levels of cardiac biomarkers, namely cardiac troponin T, creatine kinase (CK), cardiac troponin I, and CK-MB were also suppressed by BeG. The increased rate of lipid hydroperoxides and thiobarbituric acid reactive substances owing to the oxidative stress caused by free radical generation in ISO-induced rats were also inhibited by BeG. Antioxidants reduce oxidative stress by scavenging free radicals. ISO induction reduces these antioxidant enzymes glutathione peroxidase, catalase, superoxide dismutase, and glutathione, and levels causing oxidative cardiac damage to the heart tissue. BeG supplementation improved these enzymes synthesis preventing potential damage to the myocardium. Inflammation caused by ISO pretreatment increased the secretion of proinflammatory cytokines in ISO-induced rats. Pretreatment with BeG suppressed these inflammatory cytokines to a normal level in ISO + BeG-treated rats. The histopathological examination of the morphological characteristics showed that the intensity of cardiac damage caused by ISO induction was less in BeG pretreated rats with less inflammatory cells and no necrosis. BeG also showed promising results in the molecular alteration of AMP-activated protein kinase/endothelial nitric oxide synthase/protein kinase B signaling molecules. These observations emphasize the cardioprotective effects of BeG and its potential use as a drug in the near future.

Dietary Antioxidant Capacity Promotes a Protective Effect against Exacerbated Oxidative Stress in Women Undergoing Adjuvant Treatment for Breast Cancer in a Prospective Study.

Breast cancer (Bca) is the most common type of cancer among women worldwide, and oxidative stress caused by adjuvant treatment may be decreased by antioxidant intake. The aim of this study is to investigate the associations between Dietary antioxidant Capacity (DaC) and oxidation and antioxidant biomarkers in women undergoing adjuvant treatment (AT) for Bca. This prospective study had a sample of 70 women (52.2 ± 10.7 y). DaC (mmol/g) was calculated using nutritional data obtained from a Food Frequency Questionnaire, and blood was collected to measure the oxidation and antioxidant biomarkers at baseline (T0), and after AT (T1). Carbonylated protein levels were inversely associated with DaC at T1 (p = 0.004); women showed an increased risk of having increment on lipid hydroperoxides and thiobarbituric acid reactive substances (TBARS), and decrement on ferric reducing antioxidant power (FRAP) and reduced glutathione after AT, in response to lowered DaC (p < 0.05). Carbonylated proteins, TBARS and FRAP levels remained stable between the periods for women at the 3rd DaC tertile at T1, differentiating them from those at the 1st tertile, who showed negative changes in these biomarkers (p < 0.04). DaC may be beneficial for women undergoing AT for Bca, since it promoted a reduction in oxidative stress.

Ameliorative effect of ferruginol on isoprenaline hydrochloride-induced myocardial infarction in rats.

Cardiovascular-related diseases continue to be a leading cause of death globally. Among ischemic-induced cardiac diseases, myocardial infarction (MI) is reported to be of an alarming value. Despite numerous improvements in the medical intrusions, still this armamentarium fails to be effective in managing the illness without setbacks. Ferruginol (FGL) is a major polyphenols and terpenoids with numerous pharmacological activities including antioxidant and anti-inflammatory. Following, this work was aimed to explore the cardio protective effect of FGL (50 mg/kg) in isoprenaline hydrochloride (ISO)-induced MI in experimental rats. After treatment with FGL in ISO-induced MI in rats, noticeable changes were observed in the experimental rats. Injection of ISO to rats resulted in the augmented cardiac weight, serum cardiac markers (creatine kinase, creatine kinase-MB, cardiac troponin T, and Cardiac troponin I), lipid peroxidation end products (thiobarbituric acid-reactive substance and lipid hydroperoxides), reduced endogenous antioxidants (superoxide dismutase, catalase, glutathione peroxidase, and glutathione), reduced ATPase activity, and escalated pro-inflammatory cytokines (interleukin-6, tumor necrosis factor-α, and nuclear factor-κB) levels. Interestingly, the FGL supplementation to the ISO-treated rats revealed the diminished heart weight, reduced cardiac markers, and lipid peroxidation. FGL also possessed the improved antioxidants status and diminished pro-inflammatory mediator levels. The outcomes of histological analysis also evidenced the cardio protective role of FGL. Treatment with FGL reduced the cardiac damage biomarkers maintained to near normal levels in ISO-induced rats. These study findings disclose the prospective capability of FGL in the treatment of MI in the future.

Botanical sulfane sulfur donors inhibit ferroptotic cell death caused by the depletion of cysteine.

Inhibitors against cystine-glutamate antiporter, including erastin, elicit ferroptotic cell death. The erastin-induced ferroptotic cell death appears to be caused by cysteine as well as glutathione depletion. Cysteine is an essential substrate for sulfane sulfur producing systems in cells, generating persulfides that function as intracellular antioxidants and intermediates in iron-sulfur cluster production. Therefore, we examined whether botanical sulfane sulfur donors such as diallyl trisulfide (DATS) and dimethyl trisulfide (DMTS) prevent ferroptotic cell death in HT1080 cells treated with erastin. As a result, DMTS (20 µM) and DATS (10 µM) rescued the erastin-treated HT1080 cells by 69.6% and 91.6%, respectively. Furthermore, DMTS-containing squeeze of cabbage (2.0 g/L) and DATS-containing squeeze of garlic (0.07 g/L) rescued the erastin-treated HT1080 cells by 76.5% and almost 100%, respectively. In conclusion, the ingestion of trisulfides may bring about increased resistance to ferroptotic cell death in vivo.

Cinnamomum cassia ameliorates Ni-NPs-induced liver and kidney damage in male Sprague Dawley rats.

Nickel nanoparticles (Ni-NPs) have been widely used in various industries related to electronics, ceramics, textiles, and nanomedicine. Ambient and occupational exposure to Ni-NPs may bring about potential detrimental effects on animals and humans. Thus, there is a growing effort to identify compounds that can ameliorate NPs-associated pathophysiologies. The present study examined Cinnamomum cassia (C. cassia) bark extracts (CMBE) for its ameliorative activity against Ni-NPs-induced pathophysiological and histopathological alterations in male Sprague Dawley rats. The biochemical analyses revealed that dosing rats with Ni-NPs at 10 mg/kg/body weight (b.w.) significantly altered the normal structural and biochemical adaptations in the liver and kidney. Conversely, supplementations with CMBE at different doses (225, 200, and 175 mg/kg/b.w. of rat) ameliorated the altered blood biochemistry and reduced the biomarkers of liver and kidney function considerably (p < 0.05) in a dose-dependent manner. However, the best results were at 225 mg/kg/b.w. of rat. The study provided preliminary information about the protective effect of C. cassia against Ni-NPs indicated liver and kidney damages. Future investigations are needed to explore C. cassia mechanism of action and isolation of single constituents of C. cassia to assess their pharmaceutical importance accordingly.

Natural antioxidants in emulsions O/W.

This study compared the capacity of propolis extract (PE) and thyme waste extract (TWE) to prevent the oxidation of oil in water (O/W) emulsion, as well as their impact on emulsion apparent viscosity (AV) in the presence of wheat germ and almond oils as lipid phase. For this, central composite design (CCD) and principal component analysis (PCA) were performed. Oxidation process was monitored by evaluating the formation of primary and secondary lipid oxidation products, at the same time the AV behavior was determined evaluating consistency index and flow behavior index. The results revealed that the increase of PE% and TWE% decreases TBARS (Thiobarbituric Acid Reactive Substances) and hydroperoxides formation. Viscosity increases with the rise of TWE% over (0.04%), whereas lower concentrations of PE% decreases it. Those results have been confirmed in the PCA analysis. TWE showed higher resistance to oxidation, although PE was more effective as antioxidant than TWE.

Intravenous Arginine Administration Downregulates NLRP3 Inflammasome Activity and Attenuates Acute Kidney Injury in Mice with Polymicrobial Sepsis.

Acute kidney injury (AKI) is a major complication of sepsis. Nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasomes are multiprotein complexes that mediate septic AKI. L-arginine (Arg) is a conditionally essential amino acid in catabolic conditions and a substrate for nitric oxide (NO) production; however, its use in sepsis is controversial. This study investigated the effect of intravenous Arg supplementation on modulating NLRP3 inflammasome activity in relation to septic AKI. Mice were divided into normal control (NC), sham, sepsis saline (SS), and sepsis Arg (SA) groups. In order to investigate the role of NO, L-N6-(1-iminoethyl)-lysine hydrochloride (L-NIL), an inducible NO synthase inhibitor, was administered to the sepsis groups. Sepsis was induced using cecal ligation and puncture (CLP). The SS and SA groups received saline or Arg via tail vein 1 h after CLP. Mice were sacrificed at 6, 12, and 24 h after sepsis. The results showed that compared to the NC group, septic mice had higher plasma kidney function parameters and lower Arg levels. Also, renal NLRP3 inflammasome protein expression and tubular injury score increased. After Arg treatment, plasma Arg and NO levels increased, kidney function improved, and expressions of renal NLRP3 inflammasome-related proteins were downregulated. Changes in plasma NO and renal NLRP3 inflammasome-related protein expression were abrogated when L-NIL was given to the Arg sepsis groups. Arg plus L-NIL administration also attenuated kidney injury after CLP. The findings suggest that intravenous Arg supplementation immediately after sepsis restores plasma Arg levels and is beneficial for attenuating septic AKI, partly via NO-mediated NLRP3 inflammasome inhibition.

Spirulina Enhances Bone Modeling in Growing Male Rats by Regulating Growth-Related Hormones.

In recent years, growth hormone deficiency in children has been treated with hormone therapy despite the possible significant side effects. Therefore, it was deemed beneficial to develop functional foods or dietary supplements for safely improving children's growth. Spirulina platensis is known for its high antioxidant, anti-aging, anti-cancer, and immunity-enhancing properties, as well as its high digestibility and high protein content, but little has been reported about its influence on bone development in children with a normal supply of protein. In this study, we evaluated the effects of spirulina on the bone metabolism and antioxidant profiles of three-week-old growing male rats. The animals were divided into four groups (n = 17 per group) and were fed AIN93G diets with 0% (control), 30% (SP30), 50% (SP50), and 70% (SP70) of casein protein replaced by spirulina, respectively, for seven weeks. We observed that spirulina enhanced bone growth and bone strength by stimulating parathyroid hormone and growth hormone activities, as well its increased antioxidant activity. These results indicate that spirulina provides a suitable dietary supplement and alternative protein source with antioxidant benefits for growth improvement in early developmental stages.

A Diterpenoid, 14-Deoxy-11, 12-Didehydroandrographolide, in Andrographis paniculata Reduces Steatohepatitis and Liver Injury in Mice Fed a High-Fat and High-Cholesterol Diet.

14-Deoxy-11,12-didehydroandrographolide (deAND), a diterpenoid in Andrographis paniculata (Burm. f.) Nees, acts as a bioactive phytonutrient that can treat many diseases. To investigate the protective effects of deAND on reducing fatty liver disease, male mice were fed a high-fat and high-cholesterol (HFHC) diet without or with 0.05% and 0.1% deAND supplementation. Cholesterol accumulation, antioxidant, and anti-inflammatory activities in liver and liver injury were evaluated after deAND treatment. The results show that deAND treatment for seven weeks reduced plasma alanine aminotransferase activity and lowered hepatic cholesterol accumulation, tumor nuclear factor-α, and histological lesions. The 0.1% deAND treatment reduced HFHC diet-induced apoptosis by lowering the caspase 3/pro-caspase 3 ratio. After 11 weeks of deAND treatment, increased NOD-like receptor protein 3 (NLRP3), capase-1, and interleukin-1ß protein levels in liver were suppressed by deAND treatment. In addition, nuclear factor erythroid 2-related factor 2 (Nrf2) mRNA expression, heme oxygenase-1 protein expression, and the activities of glutathione peroxidase and glutathione reductase were increased in mice fed the HFHC diet. However, those activities of antioxidant enzymes or proteins were also upregulated by 0.1% deAND treatment. Furthermore, deAND treatment tended to lower hepatic lipid peroxides. Finally, deAND treatment reversed the depletion of hepatic glutamate level induced by the HFHC diet. These results indicate that deAND may ameliorate HFHC diet-induced steatohepatitis and liver injury by increasing antioxidant and anti-inflammatory activities.

The role of the aqueous extract Polypodium leucotomos in photoprotection.

Solar radiation in the ultraviolet (UV), visible (VIS), and infrared (IR) ranges produces different biological effects in humans. Most of these, particularly those derived from ultraviolet radiation (UVR) are harmful to the skin, and include cutaneous aging and increased risk of cutaneous diseases, particularly skin cancer. Pharmacological photoprotection is mostly topical, but it can also be systemic. Oral photoprotectives constitute a new generation of drugs to combat the deleterious effects of solar radiation. Among these, an extract of Polypodium leucotomos (PL/Fernblock®, IFC Group, Spain) contains a high content of phenolic compounds that endow it with antioxidant activity. PL can administered orally or topically and is completely safe. PL complements and enhances endogenous antioxidant systems by neutralizing superoxide anions, hydroxyl radicals, and lipoperoxides. In addition to its antioxidant activity, PL also improves DNA repair and modulates immune and inflammatory responses. These activities are likely due to its ability to inhibit the generation and release of reactive oxygen species (ROS) by UVR, VIS, and IR radiation. PL also prevents direct DNA damage by accelerating the removal of induced photoproducts and decreasing UV-induced mutations. Oral PL increases the expression of active p53, decreases cell proliferation, and inhibits UV-induced COX-2 enzyme levels. PL has been used to treat skin diseases such as photodermatoses and pigmentary disorders and recently as a complement of photodynamic phototherapy in actinic keratoses. The photoprotective capability of PL has been proven in a multitude of in vitro and in vivo studies, which include animal models and clinical trials with human subjects. Based on this evidence, PL is a new generation photoprotector with antioxidant and anti-inflammatory properties that also protects DNA integrity and enhances the immune response.

Effect of garden cress in reducing blood glucose, improving blood lipids, and reducing oxidative stress in a mouse model of diabetes induced by a high-fat diet and streptozotocin.

BACKGROUND: A mouse model in which diabetes mellitus was induced by low-dose streptozotocin (STZ) injection combined with a high-fat diet was used to study the effect of two water cress (Lepidium savitum) preparations. Diabetic mice were treated with dried cress powder or with water-soluble extracts (tested at two doses), together with proper control groups. The mice were evaluated after 4 weeks of continuous intervention for type 2 diabetic and associated markers. We determined blood glucose, body weight, total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL), high-density lipoprotein (HDL), serum insulin levels, and DNA integrity of hepatic cells. The concentrations of malondialdehyde (MDA) and lipid peroxide (LPO) and the activities of four enzymes that are part of the antioxidant defense system were determined in liver samples, as well as gene expression (by semi-quantitative reverse transcription polymerase chain reaction) and enzyme activity of IRS-1, IRS-2, PI3K, AKT-2, and GLUT4. RESULTS: After 4 weeks of intervention, the levels of TC, TG, and LDL cholesterol were significantly (P < 0.5) decreased and HDL cholesterol was significantly increased. Enzyme activities of liver superoxide dismutase, glutathione, glutathione peroxidase, and catalase were significantly increased, whereas MDA and LPO concentrations were significantly reduced. The transcription level of the five genes assessed was increased, with corresponding increases in protein expression. CONCLUSION: Oral uptake of garden cress can significantly reduce the blood glucose and improve the blood lipid metabolism of diabetic mice. Considerable improvements in the activity of antioxidant defense enzymes were observed in type 2 diabetic mice that improved the body's antioxidant emergency response. © 2019 Society of Chemical Industry.

Boosting the Ferroptotic Antitumor Efficacy via Site-Specific Amplification of Tailored Lipid Peroxidation.

Ferroptosis is an iron-dependent cell death pathway that can eradicate certain apoptosis-insensitive cancer cells. The ferroptosis-inducing molecules are tailored lipid peroxides whose efficacy is compromised in hypoxic solid tumor and lack of tumor selectivity. It has been demonstrated that ascorbate (Asc) in pharmacological concentrations can selectively kill cancer cells via accumulating hydrogen peroxide (H2O2) only in tumor extracellular fluids. It was hypothesized that Asc-induced, selective enrichment of H2O2 in tumor coupled with Fe3+ codelivery could simultaneously address the above two problems via boosting the levels of hydroxyl radicals and oxygen in the tumor site to ease peroxidation initiation and propagation, respectively. The aim of this work was to synergize the action of Asc with lipid-coated calcium phosphate (CaP) hybrid nanocarrier that can concurrently load polar Fe3+ and nonpolar RSL3, a ferroptosis inducer with the mechanism of inhibiting lipid peroxide repair enzyme (GPX4). The hybrid nanocarriers showed accelerated cargo release at acidic conditions (pH 5.0). The combinational approach (Asc plus nanocarrier) produced significantly elevated levels of hydroxyl radicals, lipid peroxides, and depleted glutathione under hypoxia, which was accompanied with the strong cytotoxicity (IC50 = 1.2 ± 0.2 µM) in the model 4 T1 cells. In the 4 T1 tumor-bearing xenograft mouse model, the intravenous nanocarrier delivery plus intraperitoneal Asc administration resulted in a superior antitumor performance in terms of tumor suppression, which did not produce supplementary adverse effects to the healthy organs. This work provides a novel approach to enhance the potency of ferroptotic nanomedicine against solid tumors without inducing additional side effects.

Lipidomic methodologies for biomarkers of chronic inflammation in nutritional research: ω-3 and ω-6 lipid mediators.

The evolutionary history of hominins has been characterized by significant dietary changes, which include the introduction of meat eating, cooking, and the changes associated with plant and animal domestication. The Western pattern diet has been linked with the onset of chronic inflammation, and serious health problems including obesity, metabolic syndrome, and cardiovascular diseases. Diets enriched with ω-3 marine PUFAs have revealed additional improvements in health status associated to a reduction of proinflammatory ω-3 and ω-6 lipid mediators. Lipid mediators are produced from enzymatic and non-enzymatic oxidation of PUFAs. Interest in better understanding the occurrence of these metabolites has increased exponentially as a result of the growing evidence of their role on inflammatory processes, control of the immune system, cell signaling, onset of metabolic diseases, or even cancer. The scope of this review has been to highlight the recent findings on: a) the formation of lipid mediators and their role in different inflammatory and metabolic conditions, b) the direct use of lipid mediators as antiinflammatory drugs or the potential of new drugs as a new therapeutic option for the synthesis of antiinflammatory or resolving lipid mediators and c) the impact of nutritional interventions to modulate lipid mediators synthesis towards antiinflammatory conditions. In a second part, we have summarized methodological approaches (Lipidomics) for the accurate analysis of lipid mediators. Although several techniques have been used, most authors preferred the combination of SPE with LC-MS. Advantages and disadvantages of each method are herein addressed, as well as the main LC-MS difficulties and challenges for the establishment of new biomarkers and standardization of experimental designs, and finally to deepen the study of mechanisms involved on the inflammatory response.

ETF-QO Mutants Uncoupled Fatty Acid ß-Oxidation and Mitochondrial Bioenergetics Leading to Lipid Pathology.

The electron-transfer flavoprotein dehydrogenase gene (ETFDH) that encodes the ETF-ubiquinone oxidoreductase (ETF-QO) has been reported to be the major cause of multiple acyl-CoA dehydrogenase deficiency (MADD). ETF-QO is an electron carrier that mainly functions in mitochondrial fatty acid ß-oxidation and the delivery of electrons to the ubiquinone pool in the mitochondrial respiratory chain. A high frequency of c.250G>A has been found in Taiwanese patients with late-onset MADD. We postulated that the ETFDH c.250G>A mutation may concomitantly impair fatty acid ß-oxidation and mitochondrial function. Using MADD patient-derived lymphoblastoid cells and specifically overexpressed ETFDH c.92C>T, c.250G>A, or coexisted c.92C>T and c.250G>A (c.92C>T + c.250G>A) mutated lymphoblastoid cells, we addressed the genotype-phenotype relationship of ETFDH variation in the pathogenesis of MADD. The decreased adenosine triphosphate synthesis, dissipated mitochondrial membrane potentials, reduced mitochondrial bioenergetics, and increased neutral lipid droplets and lipid peroxides were found in the MADD patient-derived lymphoblastoid cells. Riboflavin and/or coenzyme Q10 supplementation rescued cells from lipid droplet accumulation. All three mutant types, c.92C>T, c.250G>A, or c.92C>T + c.250G>A, had increased lipid droplet accumulation after treatment with palmitic acid. These results help to clarify the molecular pathogenesis of MADD as a result of the high frequency of the ETFDH c.250G>A and c.92C>T mutations.

Effect of methanol extract of Schisandrae Fructus on high fat diet induced hyperlipidemic mice.

OBJECTIVE: To investigate the effects and molecular targets of Schisandrae Fructus (SF) methanol extract (SFme) in mice with hyperlipidemia induced by high fat diet. METHODS: We observed changes in body weight, blood serum content of total cholesterol, high-density lipoprotein (HDL)-cholesterol, and triglyceride. The extent of accumulation of lipid peroxide due to lipid metabolism disorder also evaluated by measuring malondialdehyde (MDA) level. In addition, after getting gene expression in hepatic tissues, target protein of SFme was identified using a protein interaction database. RESULTS: SFme significantly decreased total cholesterol and triglyceride levels without alteration of body weight in mice, and the liver content of MDA was statistically decreased by SFme. And expression changes of cyclin- dependent kinase 1 (Cdk1) and leucine-rich repeat kinase 2 (Lrrk2) were restored by SFme. CONCLUSION: The effect of SFme on the high- fat-diet induced hyperlipidemia via decreasing total cholesterol and triglyceride levels may involve the expression of Cdk1 and Lrrk2 proteins.

Allyl methyl sulfide, an organosulfur compound alleviates hyperglycemia mediated hepatic oxidative stress and inflammation in streptozotocin - induced experimental rats.

Therapeutic approaches based on dietary compounds obtained from food products to handle diabetes involving oxidative stress and inflammation. Garlic is a common spice and has a long history as a folk remedy. Allyl methyl sulfide (AMS) is a potential garlic-derived organosulfur compound displaying a substantial range of optimistic actions in various diseases. Herein, we investigated the potential role of AMS in ameliorating the effects of oxidative stress and inflammation in the liver of streptozotocin (STZ)-induced experimental rats. Diabetes was induced by single intraperitoneal (i.p.) injection of STZ (40 mg/kg/b.w). STZ-induced hyperglycemic rats received daily intragastric doses of 50, 100 and 200 mg/kg/b.w of the AMS for 30 days. Dietary intervention of AMS (100 mg/kg b.w) resulted in significant attenuation in blood glucose and expression of pro-inflammatory markers TNF-α, IL-6, NF-κB p65 unit and significant elevation in the plasma insulin level. Moreover, AMS instigated a marked enhance in the levels of hepatic tissue non enzymatic antioxidants and the activities enzymatic antioxidants of diabetic rats with significant decline in lipid peroxides and hydroperoxides formation, serum biomarkers of liver damage, thus representing the protecting efficacy of AMS in hyperglycemic state. The pathological abnormalities in hepatic tissues of diabetic rats were significantly ameliorated by AMS supplementation and offered great support to the biochemical findings. These conclusions explicate the prospective use of AMS as a promising compound against glucotoxicity mediated hepatic oxidative dysfunction in rats. Clinical trials in validating this benefit for optimizing the AMS nutrition are however warranted.

Hypoglycemic and antioxidant effect of Tai chi exercise training in older adults with metabolic syndrome.

INTRODUCTION: The antioxidant and anti-inflammatory effects of Tai chi (TC) exercise training in healthy older adults has been demonstrated. However, there are no studies on this effect in older adults with metabolic syndrome (MetS). PURPOSE: The aim of this study was to determine the effect of TC exercise on oxidative stress and inflammatory markers in older adults with MetS. METHODS: A quasi-experimental study was carried out with a sample of 110 older sedentary volunteers with clinical diagnoses of MetS: (i) a control group, n = 50, of individuals who do not participate in physical exercise, of which 37 fulfilled the entire study protocol, and (ii) an experimental group, n = 60, of subjects enrolled in a TC exercise training program (eight-form easy), 5 days a week for 6 months, in sessions of 50 min, under the supervision of a qualified instructor, of which 48 fulfilled the entire study protocol. We measured in both groups (pre- and post-intervention) the following cardiovascular parameters: resting heart rate (RHR), diastolic and systolic blood pressure (DBP and SBP), mean arterial pressure (MAP), RHR-SBP product, RHR-MAP product; glycosylated hemoglobin (HbA1c); oxidative stress markers (superoxide dismutase, total antioxidant status, thiobarbituric acid reacting substances, and oxidative stress score); and inflammation markers (TNF-α, IL-6, IL-8, and IL-10). RESULTS: A statistically significant decrease in HbA1c concentration was observed in the TC group compared with the control group (p < 0.05). This group also showed a statistically significant increase in TAS and a decrease in the oxidative stress score (p < 0.05). We did not observe changes in the cardiovascular parameters (RHR, DBP, SBP, MAP, RHR-SBP product, and RHR-MAP product) in the TC experimental group compared to the control group. CONCLUSION: Our findings suggest that the practice of TC exercise has an antioxidative and hypoglycemic effect in the elderly with MetS.

Peroxidation and unsaturation indices as potential biomarkers of multifarious zinc and copper micro-supplementation in Helix pomatia L.

The work is a continuation of two previous studies in which biomarker fatty acids (12 of 56 FA pools) were analysed in Helix pomatia L. after heterogeneous micro-supplementation of Zn and Cu (administered in five micro-doses in the form of salts and EDTA and lysine chelates). This time, peroxidation (PI) and unsaturation coefficients (UI) as biomarker were analysed. These indices were calculated based on the FA profile in the foot and hepatopancreas of snails. The correlation of frequently used oxidation status indicators of organisms (catalase - CAT, glutathione peroxidase - GPx, selenium-dependent peroxidase - se-GPx, superoxide dismutase - SOD, glutathione transferase - GST, glutathione reductase - GR, glutathione - GSH, carbonyl protein - CP, thiobarbituric acid reactive substances - TBARS) with the rarely used UI and PI ratios was analysed. It was found that the 12-week micro-exposure to Zn and Cu did not inhibit but rather stimulated antioxidative defence at a sufficient level to increase the values of peroxidation/unsaturation indices in comparison to the control groups. Induction of an opposite process to oxidation of fatty acids was demonstrated. Maximum activities and amounts of antioxidants as well as minima of protein and lipid decomposition were recorded in groups supplemented with 0.75mg/l Zn and 1.0mg/l Cu. The possibility of a direct use of fatty acids as well as peroxidation/unsaturation indices as sensitive and reproducible biomarkers of exposure and oxidative physiological status in snails was confirmed.

The biochemical effects of nano tamoxifen and some bioactive components in experimental breast cancer.

The effect of nano tamoxifen and some bioactive components such as yeast, isoflavone, and silymarin on the level of resistance and prevention of breast cancer progression in experimental animals is the target of this study. Thirty female Sprague-Dawley rats received a single medication dosage of 7,12-dimethylbenz[a]anthracene (DMBA) intragastrically. After fourteen days of DMBA admission, the procedure protocol started out. Finally, all the experimental results evaluated, tabulated and statistically analyzed. The results demonstrated a highly significant elevation in the 8-OHdG level in group 1 (nano yeast) and 3 (nano silymarin) while the results demonstrated a highly significant reduction in group 2 (nano tamoxifen). The apoptosis results demonstrated a significant elevation in group 3 (nano silymarin) where appeared significant reduction in group 4 (nano isoflavone). ErbB-2 results demonstrated a significant elevation in group 2 (nano tamoxifen) and a significant reduction in each of group 3 (nano silymarin) and 4 (nano isoflavone). The lipid peroxide level demonstrated an extremely significant reduction in group 4 (nano isoflavone). And a significant reduction of total antioxidant was observed in group 3 (nano silymarin) in comparison to injected animals control. This may be considered a new vision and strategy to resist breast cancer disease or prevent progression.

Involvement of the endocannabinoid system in the physiological response to transient common carotid artery occlusion and reperfusion.

BACKGROUND: The transient global cerebral hypoperfusion/reperfusion achieved by induction of Bilateral Common Carotid Artery Occlusion followed by Reperfusion (BCCAO/R) may trigger a physiological response in an attempt to preserve tissue and function integrity. There are several candidate molecules among which the endocannabinoid system (ECS) and/or peroxisome-proliferator activated receptor-alpha (PPAR-alpha) may play a role in modulating oxidative stress and inflammation. The aims of the present study are to evaluate whether the ECS, the enzyme cyclooxygenase-2 (COX-2) and PPAR-alpha are involved during BCCAO/R in rat brain, and to identify possible markers of the ongoing BCCAO/R-induced challenge in plasma. METHODS: Adult Wistar rats underwent BCCAO/R with 30 min hypoperfusion followed by 60 min reperfusion. The frontal and temporal-occipital cortices and plasma were analyzed by high performance liquid chromatography-mass spectrometry (HPLC-MS) to determine concentrations of endocannabinoids (eCBs) and related molecules behaving as ligands of PPAR-alpha, and of oxidative-stress markers such as lipoperoxides, while Western Blot and immunohistochemistry were used to study protein expression of cannabinoid receptors, COX-2 and PPAR-alpha. Unpaired Student's t-test was used to evaluate statistical differences between groups. RESULTS: The acute BCCAO/R procedure is followed by increased brain tissue levels of the eCBs 2-arachidonoylglycerol and anandamide, palmitoylethanolamide, an avid ligand of PPAR-alpha, lipoperoxides, type 1 (CB1) and type 2 (CB2) cannabinoid receptors, and COX-2, and decreased brain tissue concentrations of docosahexaenoic acid (DHA), one of the major targets of lipid peroxidation. In plasma, increased levels of anandamide and lipoperoxides were observed. CONCLUSIONS: The BCCAO/R stimulated early molecular changes that can be easily traced in brain tissue and plasma, and that are indicative of the tissue physiological response to the reperfusion-induced oxidative stress and inflammation. The observed variations suggest that the positive modulation of the ECS and the increase of proinflammatory substances are directly correlated events. Increase of plasmatic levels of anandamide and lipoperoxides further suggests that dysregulation of these molecules may be taken as an indicator of an ongoing hypoperfusion/reperfusion challenge.