Levels Of Pro-oxidants Research Articles

Intermittent hypoxia differentially affects metabolic and oxidative stress responses in two species of cyprinid fish.

Oxygen fluctuations are common in freshwater habitats and aquaculture and can impact ecologically and economically important species of fish like cyprinids. To gain insight into the physiological responses to oxygen fluctuations in two common cyprinid species, we evaluated the impact of short-term intermittent hypoxia on oxidative stress and metabolic parameters (including levels of prooxidants and oxidative lesions, antioxidants, mitochondrial enzyme activities, mitochondrial swelling, markers of apoptosis, autophagy and cytotoxicity) in silver carp Hypophthalmichthys molitrix and gibel carp Carassius gibelio. During hypoxia, gibel carp showed higher baseline levels of antioxidants and less pronounced changes in oxidative and metabolic biomarkers in the tissues than silver carp. Reoxygenation led to a strong shift in metabolic and redox-related parameters and tissue damage, indicating high cost of post-hypoxic recovery in both species. Species-specific differences were more strongly associated with oxidative stress status, whereas metabolic indices and nitrosative stress parameters were more relevant to the response to hypoxia-reoxygenation. Overall, regulation of energy metabolism appears more critical than the regulation of antioxidants in the response to oxygen deprivation in the studied species. Further research is needed to establish whether prioritizing metabolic over redox regulation during hypoxia-reoxygenation stress is common in freshwater cyprinids.

Antioxidant peptides, the guardian of life from oxidative stress.

Reactive oxygen species (ROS) are produced during oxidative metabolism in aerobic organisms. Under normal conditions, ROS production and elimination are in a relatively balanced state. However, under internal or external environmental stress, such as high glucose levels or UV radiation, ROS production can increase significantly, leading to oxidative stress. Excess ROS production not only damages biomolecules but is also closely associated with the pathogenesis of many diseases, such as skin photoaging, diabetes, and cancer. Antioxidant peptides (AOPs) are naturally occurring or artificially designed peptides that can reduce the levels of ROS and other pro-oxidants, thus showing great potential in the treatment of oxidative stress-related diseases. In this review, we discussed ROS production and its role in inducing oxidative stress-related diseases in humans. Additionally, we discussed the sources, mechanism of action, and evaluation methods of AOPs and provided directions for future studies on AOPs.

Aflatoxin B1-induced dysfunction in male rats’ reproductive indices were abated by Sorghum bicolor (L.Moench) hydrophobic fraction

The burden of infertility distresses millions of families worldwide. The harmful effects of aflatoxin B1 (AFB1) on the reproductive system involve oxidative stress, culminating in inflammation and cellular apoptosis. The phytochemical in Sorghum bicolor is rich in antioxidants and anti-inflammatory activities. The effect of Sorghum bicolor (L.) Moench (SBE-HP) extract -hydrophobic fraction- enriched in Apigenin (API) was investigated in rats chronically dosed with AFB1 and the likely mechanism (s) of SBE-HP to protect against AFB1-induced reproductive toxicity. Adult Wistar male rats (twenty-four) were selected randomly and allocated into four groups. Cohort 1 was administered 0.05 % carboxymethyl cellulose (CMC); cohort 2 received AFB1 (50 µg/kg) alone; while cohorts 3 and 4 received 5 & 10 mg/kg of (SBE-HP) respectively, along with 50 µg/kg of AFB1. After 28 days, AFB1 induced remarkable reproductive toxicity as evidenced by increased sperm abnormalities, lowered sperm quality and motility, altered serum hormonal levels and testicular enzyme activities, decreased anti-oxidants, increased pro-oxidants, apoptotic and inflammatory biomarkers, as well as altered histoarchitectural structure of the testis, epididymis, and hypothalamus of rats. API-enriched extract of S. bicolor reduced AFB1-induced oxidative, inflammatory, apoptotic, and histological derangement by improving sperm function parameters, testicular enzymes, and reproductive hormones. Anti-oxidant levels and anti-inflammatory mediators were increased while decreases in the activities and levels of pro-oxidants, pro-inflammatory molecules and caspase-9 occurred in the rats' testes, epididymis, and hypothalamus. API-enriched S. bicolor protected the testes, epididymis, and hypothalamus of male rats exposed to AFB1 by modulating oxidative stress, inflammation, and apoptosis.

Biochemical markers of oxidative stress in patients with inflammatory bowel diseases

Introduction: Inflammatory bowel disease (IBD) is a group of diseases of unexplained aetiology, characterized by periods of remissions and exacerbations. Reactive oxygen species (ROS) as far as disorders of balance between levels of prooxidants and antioxidants may also participate in the occurrence of IBD. The aim of the present study was an assessment of the antioxidative barrier of the organism in patients with inflammatory bowel disease. Material and methods: The study group consisted of 99 patients (80 with IBD as a study group and 19 healthy as a control group) from Jan Biziel University Hospital in Bydgoszcz, Poland. Venous blood was the material for biochemical analysis: HT, GSH, GPXp, GPXRBC, GST, GR, SOD-1, MDA, NO2-/NO3- and CP. Results: There were statistically significant differences in oxidative stress parameters observed between the study group and the control group, especially concerning HT, GSH, GPXRBC, GST, SOD-1, MDA and NO2-/NO3-. Discussion: The assumption that increased activity of antioxidative compounds may constitute a defence against the influence of oxidative stress may be true. Their decreased activity may participate in lowering an organism’s abilities to defend against oxidative stress and cause the development of free radical diseases. Further studies into targeted preventive strategies are needed. Conclusions: Prooxidative factors play an essential role in the pathogenesis of IBD. Due to the still unknown etiopathology of IBD, research on imbalances between pro-oxidants and antioxidants should be continued in larger groups of patients.

Empagliflozin-Metformin Combination Has Antioxidative and Anti-Inflammatory Properties that Correlate with Vascular Protection in Adults with Type 1 Diabetes

Methods 40 individuals with type 1 diabetes (average age of 44.7 ± 2.5 years) were randomized into four groups: (1) control (placebo), (2) empagliflozin 25 mg daily, (3) metformin 2000 mg daily, and (4) empagliflozin-metformin combination (25 mg and 2000 mg daily, respectively). At inclusion and after 12 weeks of treatment, the blood samples were collected, and the oxidative stress (total antioxidative status (TAS), superoxide dismutase (SOD), glutathione peroxidase (GPx), uric acid, advanced oxidation protein products (AOPP), advanced glycosylation end products ((AGE) and isoprostane), and inflammation (C-reactive protein (CRP) and interleukin-6 (IL-6)) parameters were determined. Results The empagliflozin-metformin combination increased levels of the antioxidants (TAS, SOD, and GPx up to 1.1-fold; P < 0.01), decreased the levels of prooxidants (AOPP and isoprostanes up to 1.2-fold, P < 0.01; AGE up to 1.5-fold, P < 0.01), and decreased inflammatory parameters (up to 1.5-fold, CRP P < 0.01; IL-6 P < 0.001). Antioxidative action was associated with the improvement in arterial function (obtained in the previous study) in the empagliflozin-metformin combination group. Conclusion Empagliflozin-metformin combination has strong antioxidative and anti-inflammatory capacity, in adults with type 1 diabetes that is greater than that for the individual drugs. Its antioxidative activity at least partially explains the improvement in arterial function. Therefore, it appears that the combination provides the most powerful vascular protection.

Inflammation and Oxidative Stress as Common Mechanisms of Pulmonary, Autonomic and Musculoskeletal Dysfunction after Spinal Cord Injury.

Simple SummaryWhen a spinal cord injury occurs, the neurons that regulate our voluntary movements, those involved in environment and somatic perception and those that regulate vegetative functions are affected. Once neuronal damage is established, the cells of other tissues are also affected in their functions, altering the interaction between organs and altering the proper functioning of the organism. Multiple studies in animal models, as well as in humans, have recognized as factors involved in organ damage the imbalance between the formation of highly reactive molecules called pro-oxidants and defensive mechanisms called antioxidants. Closely associated with this phenomenon, the inflammatory response is also pathologically activated. In this narrative review, we have analyzed the information involving these pathological processes at the level of the lung, the autonomic nervous system and the skeletal musculature after spinal cord injury. Knowing the abnormal functioning mechanisms that occur after a spinal cord injury not only offers a better understanding of the organic events but also offers future possibilities for therapeutic interventions that may benefit the thousands of patients suffering this pathology.One of the etiopathogenic factors frequently associated with generalized organ damage after spinal cord injury corresponds to the imbalance of the redox state and inflammation, particularly of the respiratory, autonomic and musculoskeletal systems. Our goal in this review was to gain a better understanding of this phenomenon by reviewing both animal and human studies. At the respiratory level, the presence of tissue damage is notable in situations that require increased ventilation due to lower thoracic distensibility and alveolar inflammation caused by higher levels of leptin as a result of increased fatty tissue. Increased airway reactivity, due to loss of sympathetic innervation, and levels of nitric oxide in exhaled air that are similar to those seen in asthmatic patients have also been reported. In addition, the loss of autonomic control efficiency leads to an uncontrolled release of catecholamines and glucocorticoids that induce immunosuppression, as well as a predisposition to autoimmune reactions. Simultaneously, blood pressure regulation is altered with vascular damage and atherogenesis associated with oxidative damage. At the muscular level, chronically elevated levels of prooxidants and lipoperoxidation associated with myofibrillar atrophy are described, with no reduction or reversibility of this process through antioxidant supplementation.

Selenium Nanoparticles with Prodigiosin Rescue Hippocampal Damage Associated with Epileptic Seizures Induced by Pentylenetetrazole in Rats

Simple SummaryEpilepsy is a chronic neurological disease characterized by neuronal hyper electrical activity and the development of unprovoked seizures. Although several antiepileptic drugs are currently available, their application is associated with undesirable adverse effects. In an attempt to find a novel antiepileptic medication with minimum side effects, we have investigated the potential neuroprotective activity of prodigiosin, a red pigment produced by bacterial species that have important pharmaceutical and biological activities biosynthesized with selenium formulation (SeNPs-PDG) against a murine epileptic model mediated by pentylenetetrazole. The main recorded findings revealed that SeNPs-PDG delayed the onset of epileptic seizures and decreased their duration significantly. Additionally, SeNPs-PDG prevented hippocampal cell loss, oxidative stress, neuroinflammation, restored the balance between excitatory and inhibitory neurotransmitters, and notably normalized the monoaminergic and cholinergic transmission. These promising findings indicate that SeNPs-PDG might serve as a naturally derived anticonvulsant agent due to their active antioxidant, anti-inflammatory, anti-apoptotic, and neuromodulatory properties.Background: Prodigiosin (PDG) is a red pigment synthesized by bacterial species with important pharmaceutical and biological activities. Here, we investigated the neuroprotective and anticonvulsant activities of green biosynthesized selenium formulations with PDG (SeNPs-PDG) versus pentylenetetrazole (PTZ)-induced epileptic seizures. Methods: Rats were assigned into six experimental groups: control; PTZ (60 mg/kg, epileptic model); sodium valproate (200 mg/kg) + PTZ; PDG (300 mg/kg) + PTZ; sodium selenite (0.5 mg/kg) + PTZ; and SeNPs-PDG (0.5 mg/kg) + PTZ. The treatment duration is extended to 28 days. Results: SeNPs-PDG pre-treatment delayed seizures onset and reduced duration upon PTZ injection. Additionally, SeNPs-PDG enhanced the antioxidant capacity of hippocampal tissue by activating the expression of nuclear factor erythroid 2–related factor 2 and innate antioxidants (glutathione and glutathione derivatives, in addition to superoxide dismutase and catalase) and decreasing the levels of pro-oxidants (lipoperoxidation products and nitric oxide). SeNPs-PDG administration inhibited inflammatory reactions associated with epileptic seizure development by suppressing the production and activity of glial fibrillary acidic protein and pro-inflammatory mediators, including interleukin-1 beta, tumor necrosis factor-alpha, cyclooxygenase-2, inducible nitric oxide synthase, and nuclear factor kappa B. Moreover, SeNPs-PDG protected against hippocampal cell loss following PTZ injection by decreasing the levels of cytosolic cytochrome c, Bax, and caspase-3 and enhancing the expression of anti-apoptotic Bcl-2. Interestingly, SeNPs-PDG restored the PTZ-induced imbalance between excitatory and inhibitory amino acids and improved monoaminergic and cholinergic transmission. Conclusions: These promising antioxidative, anti-inflammatory, anti-apoptotic, and neuromodulatory activities indicate that SeNPs-PDG might serve as a naturally derived anticonvulsant agent.

Protective antioxidative and anti-inflammatory actions of β-caryophyllene against sulfasalazine-induced nephrotoxicity in rat.

The pathogenesis of sulfasalazine (SFZ)-induced nephrotoxicity is unclear. Moreover, there are no reports on the protective effects of β-caryophyllene (BCP) against SFZ-induced renal injury. Hence, in this study, we measured several oxidative stress and inflammatory regulatory molecules alongside the effects of BCP in SFZ-intoxicated rats. Male rats (n = 48) were distributed to six equal groups as follows: negative control (NC), normal rats treated with low (N-LD; 200 mg/kg/day) and high (N-HD; 400 mg/kg/day) BCP doses, and animals treated with SFZ individually (PC; 600 mg/kg/day) or combined with BCP low (P-LD) and high (P-HD) doses. All drugs were administrated for 14 consecutive days. The NC, N-LD, and N-HD groups showed comparable renal histology and biochemistry. In contrast, abnormal histology, and increased creatinine and urea alongside oliguria and proteinuria were detected in the PC group. Renal specimens from the PC group revealed increased levels of nuclear factor-kappa B (NF-κB), transforming growth factor (TGF)-β with kidney injury molecule (KIM)-1, while the levels of nuclear factor erythroid 2-related factor 2 (Nrf2), AMP-activated protein kinase (AMPK), and protein kinase B (AKT) declined, relative to controls. The PC renal tissue also had markedly higher levels of inflammatory cytokines (tumor necrosis factor [TNF]-α/interleukin [IL]-1β/IL-6) and pro-oxidants (malondialdehyde [MDA]/H2O2/protein carbonyls), whereas those of antioxidants (glutathione [GSH]/glutathione peroxidase [GPx]/superoxide dismutase-1 [SOD1]/catalase [CAT]) and IL-10 decreased and were associated with marked apoptosis. Both BCP regimens ameliorated renal functions and histology, and reduced NF-κB, TGF-β, and KIM-1 levels in addition to those of oxidative stress and inflammation markers. Both protocols also augmented Nrf2, AMPK, AKT, antioxidants, and IL-10. However, P-HD showed better alleviating effects than the N-HD group. In conclusion, this study is the first to link NF-κB, TGF-β, Nrf2, AMPK, and AKT with SFZ-induced nephrotoxicity. In addition, this is the first report to reveal antioxidative and anti-inflammatory effects for BCP against SFZ-associated nephropathy.

ERDOSTEINE SALVAGES CARDIAC NECROSIS: NOVEL EFFECT THROUGH MODULATION OF MAPK AND NRF-2/HO-1 PATHWAY

Objective: To assess the pharmacological and molecular effects of erdosteine in ISO induced myocardial necrosis in rats Design and method: To optimize the effect of erdosteine against experimental model of myocardial necrosis, male albino Wistar rats were divided into eight groups (n = 6) i.e. normal, ISO-control (ISO-C), erdosteine treatment with ISO. Rats in treatment groups were administered erdosteine orally for 28 days, whereas in normal and ISO-C group, 1% CMC was administered orally at 2 ml/kg/day for 28 days. Two consecutive doses of ISO 85 mg/kg, s.c. were given to ISO-C and erdosteine treatment groups on 27th and 28th day at 24 h interval. On 29th day, hemodynamic parameters were recorded and animals were sacrificed to excise their heart for measurement of various parameters. Results: In ISO-C rats, significantly increased levels of inflammatory markers, pro-oxidants and structural damage was observed as compared to normal group. Furthermore, immunohistochemistry revealed an increased expression of apoptotic proteins and decreased expression of anti-apoptotic protein which was further confirmed through TUNEL assay. Pretreatment with erdosteine at 80 mg/kg and 160 mg/kg reversed the deleterious effects of isoproterenol and normalized myocardial architecture. Erdosteine showed anti-inflammatory and anti-apoptotic activities through inhibition of MAPK pathway. Furthermore, erdosteine partially activated transcription factor Nrf-2 and HO-1 expressions showing the anti-oxidant potential of erdosteine. Conclusions: Thus, this study revealed the new use of an old drug and concluded the protective effect of erdosteine in ISO-induced myocardial necrosis through combined effect of MAPK and Nrf-2/HO-1 pathway.

The Effects of Direct Red Bull Administration to Isolated Hearts of Trained and Untrained Rats Who Regularly Consumed or Did Not Consume Energy Drink: Focus on Cardiodynamics and Oxidative Stress

Abstract Energy drinks (EDs) contain caffeine and other active ingredients which affect cardiovascular system. The aims of this study were to examine direct effects of Red Bull (RB) on cardiodynamics and oxidative stress in isolated hearts of rats. The rats were divided into four groups: untrained rats who never consumed ED (dEDUT); untrained rats who consumed ED 5 days a week during 4 weeks (ch+dED-UT); rats trained 5 times a week for 4 weeks, but did not consume ED (dED-T); rats trained and consumed ED 5 times a week for 4 weeks (ch+dED-T). After sacrificing, hearts were isolated and perfused according to Langendorff technique. Through the isolated heart of all rats in each group, RB was administered. The parameters of cardiac function were recorded, and the levels of prooxidants were measured in the coronary effluent during coronary autoregulation. Rats in ch+dED-UT group had significantly lower rates of myocardial contraction and relaxation compared to rats in dED-UT group. The same effect was recorded in the dED-T group compared to dED-UT group. The levels of hydrogen peroxide were significantly higher in trained rats. Rats in ch+dED-T group also had significantly higher levels of superoxide anion radical and index of lipid peroxidation, as well as lower levels of nitrites when compared to ch+dED-UT group, while opposite effect was recorded in rats in dED-T group compared to dEDUT group. The RB could have a potentially negative inotropic effect in chronic consumers. Prooxidative effect of RB was most pronounced in trained chronic consumers.

Ameliorative Impact of Aloe vera on Cartap Mediated Toxicity in the Brain of Wistar Rats.

Exposure to pesticides can pose a greater threat to multiple organs of nontarget animals. Cartap is a thiocarbamate pesticide, broadly used in agricultural fields. The assessment of neurotoxicity of cartap has not been properly studied in the mammalian systems. The present investigation unveils the toxic effects of cartap in the brain of Wistar rats its amelioration by using aqueous extract of Aloe vera leaves. We have used 4 groups of animals comprising six in each: Group 1- control, Group 2- control with Aloe vera, Group 3- cartap, Group 4- cartap with Aloe vera treated. After 15days of treatment, biochemical investigations were conducted. Wistar rats orally exposed to sublethal doses of cartap, showed significant variations in the levels of prooxidants i.e. MDA and GSH (an oxidative stress marker) and enzymatic antioxidants i.e. SOD, CAT, GST, GPx. The decreased levels of CAT, SOD, GST and increased levels of GPx were detected in the experimental rats treated with cartap. The significant alterations were recorded with the declined activities of LDH and AChE, considered as the biomarker of energy metabolism and altered cholinergic function, respectively. However, the pre-administration of aqueous extract of Aloe vera leaves was found to markedly ameliorate the toxic effects of cartap by shielding the levels of aforesaid oxidative markers near to the control. The ameliorative impact of Aloe vera, might be due to the presence of several antioxidant molecules in it which were able to counter the oxidative stress generated by cartap stress. These results suggested that Aloe vera could be utilized as a possible supplement with the relevant therapeutics in the suitable management of cartap toxicity in association.

The effects of acute and chronic Red Bull® consumption on cardiodynamics and oxidative stress in coronary effluent of trained rats

Background/Aim. Energy drinks (EDs) are widely used by athletes as ergogenic agents and Red Bull? is one of the most consumed EDs among them. The aim of this study was to determine the acute and chronic effects of Red Bull? on cardiodynamics and parameters of oxidative stress in physically trained rats. Methods. Rats were subjected to a swimming practice (1h a day, 5 days a week, for 4 weeks). They were divided into 4 groups: rats that did not consume ED either before swimming or prior to sacrificing; rats that did not consume ED before swimming but did consume ED 30 min prior to sacrificing; rats that consumed ED 30 min before every swimming training but did not consume ED prior to sacrificing; rats that consumed ED 30 min before every swimming training and 30 min before sacrificing. After sacrificing, the hearts of the rats were isolated and perfused according to the Langendorff technique. The parameters of cardiac function were recorded, and also the levels of prooxidants were measured in the coronary effluent during coronary autoregulation. Results. Acute administration of the ED had a positive inotropic effect (manifested as a significantly higher level of the maximum and minimum rate of pressure development in the left ventricle), while chronic administration affected the isolated increase in systolic left ventricular pressure. The prooxidative effect of the ED was observed, which was more pronounced in chronic consumption. Conclusion. The main conclusion of our study is that chronic consumption of ED changes the cardiovascular response and redox status in acute consumption ED.

Oxidative Stress in ESRD Patients on Dialysis and the Risk of Cardiovascular Diseases.

Chronic kidney disease is highly prevalent worldwide. The decline of renal function is associated with inadequate removal of a variety of uremic toxins that exert detrimental effects on cells functioning, thus affecting the cardiovascular system. The occurrence of cardiovascular aberrations in CKD is related to the impact of traditional risk factors and non-traditional CKD-associated risk factors, including anemia; inflammation; oxidative stress; the presence of some uremic toxins; and factors related to the type, frequency of dialysis and the composition of dialysis fluid. Cardiovascular diseases are the most frequent cause for the deaths of patients with all stages of renal failure. The kidney is one of the vital sources of antioxidant enzymes, therefore, the impairment of this organ is associated with decreased levels of these enzymes as well as increased levels of pro-oxidants. Uremic toxins have been shown to play a vital role in the onset of oxidative stress. Hemodialysis itself also enhances oxidative stress. Elevated oxidative stress has been demonstrated to be strictly related to kidney and cardiac damage as it aggravates kidney dysfunction and induces cardiac hypertrophy. Antioxidant therapies may prove to be beneficial since they can decrease oxidative stress, reduce uremic cardiovascular toxicity and improve survival.

Erdosteine salvages cardiac necrosis: Novel effect through modulation of MAPK and Nrf-2/HO-1 pathway.

Isoproterenol (ISO) induced oxidative stress and inflammation is involved in the pathogenesis of myocardial necrosis. To optimize the effect of erdosteine against myocardial necrosis, male albino Wistar rats were divided into eight groups (n = 6), that is, normal, ISO-control, erdosteine pretreatment with ISO. Rats were administered erdosteine orally for 28 days. Two doses of ISO (85 mg/kg), s.c. were given to ISO-C and erdosteine treatment groups on the 27th and 28th day. On the 29th day, hemodynamic parameters were recorded and the heart was excised for further parameters. In ISO-C rats, significantly increased levels of inflammatory markers, pro-oxidants, and structural damage were observed as compared with normal group. Furthermore, immunohistochemistry and terminal deoxynucleotidyl transferase dUTP nick end labeling revealed an increased expression of apoptotic proteins. Erdosteine at 80 mg/kg reversed the deleterious effects of ISO and normalized myocardium. Erdosteine showed anti-inflammatory, antiapoptotic, and antioxidant activities through inhibition of MAPK and Nrf-2/HO-1 pathways. To conclude, erdosteine was found protective in ISO-induced myocardial necrosis through MAPK and Nrf-2/HO-1 pathway.

The influences of chokeberry extract supplementation on redox status and body composition in handball players during competition phase.

The aim of our study was to investigate the influence of 12 weeks of consumption of chokeberry extract on redox status, body composition, lipid profile, and biochemical parameters in active handball players. The study included 16 handball players aged 16-24 years (20.26 ± 2.86 years). Every morning before training, players received 30mL of liquid chokeberry extract for 12weeks during the regular competition season. The research consisted of morphofunctional and biochemical testing, which was performed at three points (at the beginning of the study and at 6 and 12weeks after extract consumption). After the chokeberry extract treatment, we observed significant changes in three main aspects. The 12 week supplementation with chokeberry extract decreased the levels of prooxidants (TBARS and nitrites) and increased catalase activity. Analyzing the dynamic of body composition showed a decrease in body fat (9.4 ± 0.5 vs. 7.3 ± 0.6kg) as well as its percent in a body (11.4 ± 0.4% vs. 8.8 ± 0.4%). On the other hand, the analysis showed an increase of high-density lipoprotein (1.3 ± 0.3 vs. 1.6 ± 0.2 mmol/L) and hemoglobin (144.4 ± 11.7 vs. 151.7 ± 9.9g/L) after 6 weeks of treatment. At the same time, a decrease in leukocytes (7.2 × 109 ± 2.8 vs. 6.5 ± 1.2 × 109/L) and an increase in red blood cells count (4.9 ± 0.4 × 109 vs. 5.5 ± 0.5 × 109/L) were observed. Overall, these results emphatically show that the use of chokeberry extract dietary supplement induced a wide range of beneficial effects in the examined group of athletes.

Impact of Coenzyme Q10 Administration on Lead Acetate-Induced Testicular Damage in Rats

Exposure to lead (Pb) causes multiorgan dysfunction including reproductive impairments. Here, we examined the protective effects of coenzyme Q10 (CoQ10) administration on testicular injury induced by lead acetate (PbAc) exposure in rats. This study employed four experimental groups (n = 7) that underwent seven days of treatment as follows: control group intraperitoneally (i.p.) treated with 0.1 ml of 0.9% NaCl containing 1% Tween 80 (v : v), CoQ10 group that was i.p. injected with 10 mg/kg CoQ10, PbAc group that was i.p. treated with PbAc (20 mg/kg), and PbAc+CoQ10 group that was i.p. injected with CoQ10 2 h after PbAc. PbAc injection resulted in increasing residual Pb levels in the testis and reducing testosterone, luteinizing hormone, and follicle-stimulating hormone levels. Additionally, PbAc exposure resulted in significant oxidative damage to the tissues on the testes. PbAc raised the levels of prooxidants (malondialdehyde and nitric oxide) and reduced the amount of endogenous antioxidative proteins (glutathione and its derivative enzymes, catalase, and superoxide dismutase) available in the cell. Moreover, PbAc induced the inflammatory response as evidenced by the upregulation of inflammatory mediators (tumor necrosis factor-alpha and interleukin-1 beta). Further, PbAc treatment induced apoptosis in the testicular cells, as indicated by an increase in Bax and caspase 3 expression, and reduced Bcl2 expression. CoQ10 supplementation improved testicular function by inhibiting Pb accumulation, oxidative stress, inflammation, cell death, and histopathological changes following PbAc exposure. Our findings suggest that CoQ10 can act as a natural therapeutic agent to protect against the reproductive impairments associated with PbAc exposure.

Effects of hypoxia and reoxygenation on intermediary metabolite homeostasis of marine bivalves Mytilus edulis and Crassostrea gigas

Marine benthic invertebrates are frequently exposed to fluctuating oxygen levels resulting in hypoxia-reoxygenation (H/R) stress in the intertidal, estuarine and shallow coastal habitats. H/R stress can strongly affect the organisms' physiological performance due to the negative shifts in bioenergetics and redox balance. H/R stress commonly leads to the depletion of energy substrates and accumulation of anaerobic end products, but the effects of H/R stress on the homeostasis of the intermediate nitrogenous compounds are not well understood. We studied the effects of the short-term and long-term hypoxia (1 and 6 days, respectively) and subsequent reoxygenation on the metabolite profiles of free amino acids (FAAs), as well as the intermediates of the urea cycle and purine metabolism in two species of hypoxia-tolerant intertidal bivalves, the blue mussels Mytilus edulis and the Pacific oysters Crassostrea gigas. Accumulation of succinate was assessed to determine the role of anaerobiosis in the metabolic responses to H/R stress. Our study showed that the more hypoxia-tolerant of the two studied species (C. gigas) had lower rate of succinate accumulation during hypoxia (indicating stronger metabolic rate suppression) and was better able to maintain the homeostasis of nitrogenous intermediates during H/R stress compared with the less hypoxia-tolerant M. edulis. Furthermore, analysis of the metabolite profiles indicate that the oysters maintain high levels of cytoprotective compounds (such as taurine and GABA), accumulate lower levels of potential prooxidants (such as succinate and hypoxanthine) and experience less damage to oxidation-prone thiol-containing amino acids such as cysteine, homocysteine and methionine during hypoxia and reoxygenation compared with the blue mussels. This study indicates a potentially important role of intermediate metabolite homeostasis in the tolerance to prolonged hypoxia and H/R stress in marine organisms and opens avenue for further testing of this hypothesis in a broader comparative framework.

Scavenging reactive oxygen species selectively inhibits M2 macrophage polarization and their pro-tumorigenic function in part, via Stat3 suppression

Tumor associated macrophages (TAM) enhance the aggressiveness of breast cancer via promoting cancer cell growth, metastasis, and suppression of the patient's immune system. These TAMs are polarized in breast cancer with features more closely resembling the pro-tumorigenic and immunosuppressive M2 type rather than the anti-tumor and pro-inflammatory M1 type. The goal of our study was to examine primary human monocyte-derived M1 and M2 macrophages for key redox differences and determine sensitivities of these macrophages to the redox-active drug, MnTE-2-PyP5+. This compound reduced levels of M2 markers and inhibited their ability to promote cancer cell growth and suppress T cell activation. The surface levels of the T cell suppressing molecule, PD-L2, were reduced by MnTE-2-PyP5+ in a dose-dependent manner. This study also examined key differences in ROS generation and scavenging between M1 and M2 macrophages. Our results indicate that M2 macrophages have lower levels of reactive oxygen species (ROS) and lower production of extracellular hydrogen peroxide compared to the M1 macrophages. These differences are due in part to reduced expression levels of pro-oxidants, Nox2, Nox5, and the non-enzymatic members of the Nox complex, p22phox and p47phox, as well as higher levels of antioxidant enzymes, Cu/ZnSOD, Gpx1, and catalase. More importantly, we found that despite having lower ROS levels, M2 macrophages require ROS for proper polarization, as addition of hydrogen peroxide increased M2 markers. These TAM-like macrophages are also more sensitive to the ROS modulator and a pan-Nox inhibitor. Both MnTE-2-PyP5+ and DPI inhibited expression levels of M2 marker genes. We have further shown that this inhibition was partly mediated through a decrease in Stat3 activation during IL4-induced M2 polarization. Overall, this study reveals key redox differences between M1 and M2 primary human macrophages and that redox-active drugs can be used to inhibit the pro-tumor and immunosuppressive phenotype of TAM-like M2 macrophages. This study also provides rationale for combining MnTE-2-PyP5+ with immunotherapies.

Oxidative stress in biological systems and its relation with pathophysiological functions: the effect of physical activity on cellular redox homeostasis

The body of evidence from the past three decades demonstrates that oxidative stress can be involved in several diseases. This study aims to summarise the current state of knowledge on the association between oxidative stress and the pathogenesis of some characteristic to the biological systems diseases and aging process. This review also presents the effect of physical activity on redox homeostasis. There is strong evidence from studies for participation of reactive oxygen and nitrogen species in pathogenesis of acute and chronic diseases based on animal models and human studies. Elevated levels of pro-oxidants and various markers of the oxidative stress and cells and tissues damage linked with pathogenesis of cancer, atherosclerosis, neurodegenerative diseases hypertension, diabetes mellitus, cardiovascular disease, atherosclerosis, reproductive system diseases, and aging were reported. Evidence confirmed that inflammation contributes widely to multiple chronic diseases and is closely linked with oxidative stress. Regular moderate physical activity regulates oxidative stress enhancing cellular antioxidant defence mechanisms, whereas acute exercise not preceded by training can alter cellular redox homeostasis towards higher level of oxidative stress. Future studies are needed to clarify the multifaceted effects of reactive oxygen/nitrogen species on cells and tissues and to continue study on the biochemical roles of antioxidants and physical activity in prevention of oxidative stress-related tissue injury.

The Evaluation of Oxidative Stress and High-Density Lipoprotein Cholesterol Levels in Diffuse Large B-Cell Lymphoma

Diffuse large B-cell lymphoma (DLBCL) is the most common aggressive B-cell non-Hodgkin�s lymphoma. Oxidative stress, defined as an imbalance between the levels of pro-oxidants and the antioxidant defense, is involved in lymphomagenesis via chronic inflammation and is associated with a decrease in circulating levels of high-density lipoprotein (HDL) cholesterol. We evaluated oxidative stress levels in DLBCL patients by FORT (Free Oxygen Radicals Testing) and FORD assays (Free Oxygen Radical Defense), and investigated the relationship between oxidative stress markers and HDL-cholesterol levels. Our results suggest that oxidative stress and decreased levels of HDL-cholesterol might play a role in DLBCL pathogenesis via chronic inflammation.