Significant Decrease In Oxidative Stress Research Articles

Effect of moringa seed extract in chlorpyrifos-induced cerebral and ocular toxicity in mice.

Chlorpyrifos (CPF) is one of the most commonly used organophosphosphate-based (OP) insecticides. Its wide use has led to higher morbidity and mortality, especially in developing countries. Moringa seed extracts (MSE) have shown neuroprotective activity, antioxidant, anti-inflammatory, and antibacterial features. The literature lacks data investigating the role of MSE against CPF-induced cerebral and ocular toxicity in mice. Therefore, we aim to investigate this concern. A total of 40 mature male Wistar Albino mice were randomly distributed to five groups. Initially, they underwent a one-week adaptation period, followed by a one-week treatment regimen. The groups included a control group that received saline, MSE 100 mg/kg, CPF 12 mg/kg, CPF-MSE 50 mg/kg, and CPF-MSE 100 mg/kg. After the treatment phase, analyses were conducted on serum, ocular, and cerebral tissues. MSE100 and CPF-MSE100 normalized the pro-inflammatory markers (interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α)) and AChE serum levels. CPF-MSE50 significantly enhanced these serum levels compared to CPF; however, it showed higher levels compared to the control. Moreover, the tissue analysis showed a significant decrease in oxidative stress (malondialdehyde (MDA) and nitric oxide (NO)) and an increase in antioxidant markers (glutathione (GSH), glutathione peroxidase (GSH-PX)), superoxide dismutase (SOD), and catalase (CAT) in the treated groups compared to CPF. Importantly, the significance of these effects was found to be dose-dependent, particularly evident in the CPF-MSE100 group. We conclude that MSE has a promising therapeutic effect in the cerebral and ocular tissues of CPF-intoxicated mice, providing a potential solution for OP public health issues.

6-Hydroxy-2,2,4-trimethyl-1,2,3,4-tetrahydroquinoline Demonstrates Neuroprotective Properties in Experimental Parkinson's Disease by Enhancing the Antioxidant System, Normalising Chaperone Activity and Suppressing Apoptosis.

Parkinson's disease (PD) is a neurodegenerative disease, whereby disturbances within the antioxidant defence system, increased aggregation of proteins, and activation of neuronal apoptosis all have a crucial role in the pathogenesis. In this context, exploring the neuroprotective capabilities of compounds that sustain the effectiveness of cellular defence systems in neurodegenerative disorders is worthwhile. During this study, we assessed how 6-hydroxy-2,2,4-trimethyl-1,2,3,4-tetrahydroquinoline (HTHQ), which has antioxidant properties, affects the functioning of the antioxidant system, the activity of NADPH-generating enzymes and chaperones, and the level of apoptotic processes in rats with rotenone-induced PD. Six groups of animals were formed for our experiment, each with 12 animals. These were: a control group, animals with rotenone-induced PD, rats with PD given HTHQ at a dose of 50mg/kg, rats with PD given HTHQ at a dose of 25mg/kg, animals with pathology who were administered a comparison drug rasagiline, and control animals who were administered HTHQ at a dose of 50mg/kg. The study results indicate that administering HTHQ led to a significant decrease in oxidative stress in PD rats. The enhanced redox status in animal tissues was linked with the recovery of antioxidant enzyme activities and NADPH-generating enzyme function, as well as an upsurge in the mRNA expression levels of antioxidant genes and factors Nrf2 and Foxo1. Administering HTHQ to rats with PD normalized the chaperone-like activity and mRNA levels of heat shock protein 70. Rats treated with the compound displayed lower apoptosis intensity when compared to animals with pathology. Therefore, owing to its antioxidant properties, HTHQ demonstrated a beneficial impact on the antioxidant system, resulting in decreased requirements for chaperone activation and the inhibition of apoptosis processes triggered in PD. HTHQ at a dose of 50mg/kg had a greater impact on the majority of the examined variables compared to rasagiline.

The role of oxidative stress and inflammation biomarkers in pre- and postoperative monitoring of prostate cancer patients

Introduction Prostate Cancer (PC) is a global health concern affecting men worldwide. Oxidative stress is believed to contribute to the initiation of early-stage PC lesions. Additionally, inflammation has long been acknowledged as a factor in the development of PC. We aimed to examine the biomarkers of oxidative stress and inflammation in PC patients before and after surgery. Patients and methods A cross-sectional study was conducted at the Urology Outpatient Clinic of Bezmialem Vakif University Hospital. A total of 150 individuals were included in the study, divided into five groups: 50 Healthy controls, 25 patients with Benign Prostatic Hyperplasia (BPH), 25 patients with Low-Risk Prostate Cancer (LRPC), 25 patients with Medium-Risk Prostate Cancer (MRPC), and 25 patients with High-Risk Prostate Cancer (HRPC). Measurements of Total Oxidant Status (TOS), Total Antioxidant Status (TAS), Total Thiol (TT), and Native Thiol (NT) were performed using photometric methods. Oxidative Stress Index (OSI) and Disulfide (DIS) levels were calculated mathematically. Levels of Interleukin-10 (IL-10), Interleukin-1beta (IL-1β), Tumor Necrosis Factor-alpha (TNF-α), Interleukin-6 (IL-6), and Presepsin were determined using commercially available enzyme-linked immunosorbent assay (ELISA) kits. Results Compared to the healthy control group, the results indicated a statistically significant increase in both oxidative stress and inflammation levels. In the groups receiving both pharmaceutical therapy and surgical treatment (PC), a significant decrease in oxidative stress and inflammation levels was observed. Conclusion Consequently, it is suggested that the assessment of oxidative stress and inflammatory biomarkers should be incorporated in the pre- and postoperative monitoring of patients with PC.

Effects of two-month treatment with a mixture of natural activators of autophagy on oxidative stress and arterial stiffness in patients with essential hypertension: A pilot study

Background and aimsTrehalose, spermidine, nicotinamide, and polyphenols are natural substances that exert pro-autophagic and antioxidant properties. Their role in blood pressure (BP) regulation and preservation of vascular function in essential hypertension is unknown. The aim of this study was to evaluate the effect of a mixture of these agents on BP level, markers of oxidative stress, autophagy, endothelial function, and vascular stiffness in outpatients with grade 1 uncomplicated essential hypertension. Methods and resultsA single-centre, open-label, case–control, pilot study was conducted in adult outpatients (aged ≥18 years) receiving or not the mixture for two months along with the standard therapies. Both at baseline and at the end of the treatment the following clinical parameters were evaluated: brachial seated office BP level, central aortic pressure, pulse wave velocity, augmentation index (AI@75). Both at baseline and at the end of the treatment, a blood sample was drawn for the measurement of: H2O2, HBA%, levels of sNOX2-dp, Atg 5, P62, endothelin 1, and NO bioavailability. The mixture of nutraceuticals did not influence BP levels. Patients receiving the mixture showed a significant decrease of oxidative stress, stimulation of autophagy, increased NO bioavailability and no increase of the AI@75, in contrast to what observed in hypertensive patients not receiving the mixture. ConclusionsThe supplementation of the trehalose, spermidine, nicotinamide, and polyphenols mixture counteracted hypertension-related arterial stiffness through mechanisms likely dependent on oxidative stress downregulation and autophagy stimulation. These natural activators of autophagy may represent favourable adjuvants for prevention of the hypertensive cardiovascular damage.

Remediation of wastewater by biosynthesized manganese oxide nanoparticles and its effects on development of wheat seedlings.

Nanoparticles play a vital role in environmental remediation on aglobal scale. In recent years, there has been an increasing demand to utilizenanoparticles in wastewater treatment due to their remarkable physiochemical properties. In the current study, manganese oxide nanoparticles (MnO-NPs) were synthesized from the Bacillus flexus strain and characterized by UV/Vis spectroscopy, X-ray diffraction, scanning electron microscopy, and Fourier transform infrared spectroscopy. The objective of this study was to evaluate the potential of biosynthesized MnO-NPs to treat wastewater. Results showed the photocatalytic degradation and adsorption potential of MnO-NPs for chemical oxygen demand, sulfate, and phosphate were 79%, 64%, and 64.5%, respectively, depicting the potential of MnO-NPs to effectively reduce pollutants in wastewater. The treated wastewater was further utilized for the cultivation of wheat seedlings through a pot experiment. It was observed that the application of treated wastewater showed a significant increase in growth, physiological, and antioxidant attributes. However, the application of treated wastewater led to a significant decrease in oxidative stress by 40%. It can be concluded that the application of MnO-NPs is a promising choice to treat wastewater as it has the potential to enhance the growth, physiological, and antioxidant activities of wheat seedlings.

Heartwood Extract of Pterocarpus marsupium Roxb. Offers Defense against Oxyradicals and Improves Glucose Uptake in HepG2 Cells.

Diabetes mellitus leads to cellular damage and causes apoptosis by oxidative stress. Heartwood extract of Pterocarpus marsupium has been used in Ayurveda to treat various diseases such as leprosy, diabetes, asthma, and bronchitis. In this study, we worked out the mechanism of the antidiabetic potential of methanolic heartwood extract of Pterocarpus marsupium (MPME). First, metabolic profiling of MPME was done using gas chromatography-mass spectrometry (GCMS), ultra-performance liquid chromatography-mass spectroscopy (UPLC-MS), and high-performance thin-layer chromatography (HPTLC) to identify phenols, flavonoids, and terpenoids in MPME. Biological studies were carried out in vitro using the HepG2 cell line. Many antidiabetic compounds were identified including Quercetin. Methanolic extract of MPME (23.43 µg/mL–93.75 µg/mL) was found to be safe and effective in reducing oxyradicals in HepG2 cells. A concentration of 93.75 µg/mL improved glucose uptake efficiently. A significant decrease in oxidative stress, cell damage, and apoptosis was found in MPME-treated HepG2 cells. The study suggests that the heartwood of Pterocarpus marsupium offers good defense in HepG2 cells against oxidative stress and improves glucose uptake. The results show the significant antidiabetic potential of MPME using a HepG2 cell model. The effect seems to occur by reducing oxidative stress and sensitizing the cells towards glucose uptake, hence lowering systemic glucose levels, as well as rescuing ROS generation.

Cannabinoid 2 receptor agonist and L-arginine combination attenuates diabetic cardiomyopathy in rats via NF-ĸβ inhibition.

Beta-caryophyllene (BCP), a cannabinoid 2 (CB2) receptor agonist has recently been found to have cardioprotective activity as an anti-inflammatory and antioxidant molecule. L-arginine (LA), a nitric oxide (NO) donor, is a potential regulator of cardiovascular function. Considering the role of CB2 receptor activation and NO regulation in cardiovascular diseases, the combination of BCP with LA may be a possible treatment of diabetic cardiomyopathy (DCM). Hence, we investigated the efficacy of the novel combination of BCP with LA on cardiovascular inflammation and oxidative stress in diabetic rats. DCM was induced by streptozotocin (55 mg/kg) in Sprague-Dawley rats intraperitoneally. BCP, LA, and BCP with LA were administered to diabetic rats for 4 weeks. After completion of the study, hemodynamic parameters, biochemical parameters, and inflammatory cytokine levels were analyzed. Also, oxidative stress parameters, nuclear factor kappa beta (NF-ĸβ) expression, and histopathology in cardiac tissues were estimated. The combination of BCP (200 mg/kg) with LA (200 mg/kg) significantly normalized the hemodynamic parameters and decreased the glucose, cardiac markers, interleukin-6, and tumor necrosis factor-alpha levels. Treatment of BCP and LA showed a significant decrease in oxidative stress and downregulated the cardiac expression of NF-ĸβ. Thus, the combination of BCP with LA improves cardiac functions by attenuating inflammation through NF-ĸβ inhibition in DCM.

Pycnogenol® supplementation prevents inflammation and symptoms in recurrent, non-severe urinary infections.

The aim of this pilot, registry study was to evaluate the prophylactic effects of oral supplementation with Pycnogenol® (150 mg/day) in subjects with previous history of recurrent (urinary tract infections (UTI) in a 2-month open follow-up. subjects with recurrent-UTIs, defined by: 1) at least three symptomatic UTIs over the past year; 2) two episodes of UTI's in the past six months; 3) symptoms of UTIs with urinalysis without bacterial presence, were included in the study. Pycnogenol® was supplemented at the dose of 150 mg/day for 2 months. The two groups of subjects (supplement and controls, each including 25 subjects) were demographically and clinically comparable at baseline. No side effects or tolerability problems were observed. The registry evaluated the number of recurrent UTIs in two months; there was a limited decrease in the rate of recurrent UTIs, in comparison with the period before inclusion of 9.93% in the standard management group in comparison with a more important decrease in the Pycnogenol® group (-50.1%; P<0.05). The number of episodes decreased from 3.22±0.4 to 2.9±0.3 in the control group in 2 months versus a decrease from 3.1±0.5 to 1.6±0.6 in the Pycnogenol® group. The number of infection-free subjects at the end of the two-month registry study was significantly higher with the supplement (P<0.05) than in controls. Oxidative stress measured as plasma free radicals at inclusion was 388±22 Carr units in the control group and resulted unchanged (not significant) at the end of the study (379±21 Carr units). In the supplement group, there was a significant decrease in oxidative stress from 389±24 to 227±14 Carr units at the end of the study (P<0.05). This pilot registry indicates that prophylaxis with Pycnogenol® decreases the occurrence of UTIs both in men and women without side effects and with a good tolerability. The effects of Pycnogenol® in these patients - including the control of oxidative stress - may be very important, particularly when a predominantly inflammatory component (UTI without infection or with a minimal bacterial component due to bacterial fragments) is present and maintains the inflammatory process.

Effects of Post-Resuscitation Normoxic Therapy on Oxygen-Sensitive Oxidative Stress in a Rat Model of Cardiac Arrest.

BackgroundCardiac arrest (CA) can induce oxidative stress after resuscitation, which causes cellular and organ damage. We hypothesized that post‐resuscitation normoxic therapy would protect organs against oxidative stress and improve oxygen metabolism and survival. We tested the oxygen‐sensitive reactive oxygen species from mitochondria to determine the association with hyperoxia‐induced oxidative stress.Methods and ResultsSprague–Dawley rats were subjected to 10‐minute asphyxia‐induced CA with a fraction of inspired O2 of 0.3 or 1.0 (normoxia versus hyperoxia, respectively) after resuscitation. The survival rate at 48 hours was higher in the normoxia group than in the hyperoxia group (77% versus 28%, P<0.01), and normoxia gave a lower neurological deficit score (359±140 versus 452±85, P<0.05) and wet to dry weight ratio (4.6±0.4 versus 5.6±0.5, P<0.01). Oxidative stress was correlated with increased oxygen levels: normoxia resulted in a significant decrease in oxidative stress across multiple organs and lower oxygen consumption resulting in normalized respiratory quotient (0.81±0.05 versus 0.58±0.03, P<0.01). After CA, mitochondrial reactive oxygen species increased by ≈2‐fold under hyperoxia. Heme oxygenase expression was also oxygen‐sensitive, but it was paradoxically low in the lung after CA. In contrast, the HMGB‐1 (high mobility group box‐1) protein was not oxygen‐sensitive and was induced by CA.ConclusionsPost‐resuscitation normoxic therapy attenuated the oxidative stress in multiple organs and improved post‐CA organ injury, oxygen metabolism, and survival. Additionally, post‐CA hyperoxia increased the mitochondrial reactive oxygen species and activated the antioxidation system.

Chronic exposure to multi-metals on testicular toxicity in rats

Despite the availability of sufficient data on the effects of individual metal exposure on living organisms, a critical knowledge gap still exists in predicting effects of multi-metals particularly on the pituitary-testicular axis. Thus, the aim of the present study was to check the effects of individual or combined (binary and ternary) exposure to aluminum, copper, and zinc on (i) sperm and testosterone levels (ii) oxidative stress and (iii) structural changes in testis of male Wistar rats. Animals were exposed to aluminum, copper, and zinc either individually (20 mg/kg, orally, once, daily), binary (10 mg/kg each, orally, once daily) or in ternary combination (5 mg/kg, each, orally, once daily) for 24 weeks. The exposure to aluminum, copper individually and in combination led to a significant decrease in sperm counts and an increased oxidative stress compared to the control group. Exposure to zinc caused significant decrease in oxidative stress and an increase in different sperm variables. The exposure to zinc with aluminum or copper had no toxic effects on testis while concomitant exposure to aluminum, copper, and zinc produced more pronounced testicular injury. In summary, while co-exposure to zinc with aluminum or copper produced reproductive toxicity the co-exposure to all the three metals may lead to a significant testicular toxicity and these changes were related to increase in oxidative stress in rats.

Suppression of inflammation and fibrosis using soluble epoxide hydrolase inhibitors enhances cardiac stem cell-based therapy.

Stem cell replacement offers a great potential for cardiac regenerative therapy. However, one of the critical barriers to stem cell therapy is a significant loss of transplanted stem cells from ischemia and inflammation in the host environment. Here, we tested the hypothesis that inhibition of the soluble epoxide hydrolase (sEH) enzyme using sEH inhibitors (sEHIs) to decrease inflammation and fibrosis in the host myocardium may increase the survival of the transplanted human induced pluripotent stem cell derived‐cardiomyocytes (hiPSC‐CMs) in a murine postmyocardial infarction model. A specific sEHI (1‐trifluoromethoxyphenyl‐3‐(1‐propionylpiperidine‐4‐yl)urea [TPPU]) and CRISPR/Cas9 gene editing were used to test the hypothesis. TPPU results in a significant increase in the retention of transplanted cells compared with cell treatment alone. The increase in the retention of hiPSC‐CMs translates into an improvement in the fractional shortening and a decrease in adverse remodeling. Mechanistically, we demonstrate a significant decrease in oxidative stress and apoptosis not only in transplanted hiPSC‐CMs but also in the host environment. CRISPR/Cas9‐mediated gene silencing of the sEH enzyme reduces cleaved caspase‐3 in hiPSC‐CMs challenged with angiotensin II, suggesting that knockdown of the sEH enzyme protects the hiPSC‐CMs from undergoing apoptosis. Our findings demonstrate that suppression of inflammation and fibrosis using an sEHI represents a promising adjuvant to cardiac stem cell‐based therapy. Very little is known regarding the role of this class of compounds in stem cell‐based therapy. There is consequently an enormous opportunity to uncover a potentially powerful class of compounds, which may be used effectively in the clinical setting.

Rhoifolin regulates oxidative stress and proinflammatory cytokine levels in Freund's adjuvant-induced rheumatoid arthritis via inhibition of NF-κB.

Rheumatoid arthritis (RA) is an autoimmune disease of knee joints involving pain and inflammation. Rhoifolin is a plant flavonoid known to have antioxidant and anti-inflammatory properties. This study was taken to identify the effect of rhoifolin on complete Freund’s adjuvant (CFA)-induced arthritis in the rat model. Treatment with rhoifolin (10 and 20 mg/kg) showed a significant improvement in the overall health parameters such as paw edema and weight loss. This improvement in morphological parameters corroborated the findings with gross morphological changes observed in the histopathological analysis. Rhoifolin treatment also caused a significant decrease in oxidative stress, evident from changes in intracellular levels of glutathione, glutathione peroxidase, malondialdehyde, and superoxide dismutase in the articular cartilage tissue. Moreover, proinflammatory cytokines, tumor necrosis factor (TNF)-α, interleukin(IL)-1β, and IL-6 showed a significant downregulation of gene expression and intracellular protein concentration levels. The NF-κB pathway showed a significant attenuation as evident in the significant reduction in the levels of NF-κB p65 and p-IκB-α. These results indicated that rhoifolin can be a natural therapeutic alternative to the extant regimens, which include non-steroidal anti-inflammatory drugs and immunosuppressants. Additionally, the antioxidant and anti-inflammatory action of rhoifolin was probably mediated by the NF-κB pathway. However, the exact target molecules of this pathway need to be determined in further studies.

Insulin- and quercetin-loaded liquid crystalline nanoparticles: implications on oral bioavailability, antidiabetic and antioxidant efficacy.

The present study reports insulin (INS)- and quercetin (QT)-lyotropic liquid crystalline nanoparticles (LCNPs) with improved bioavailability, antidiabetic and antioxidant efficacy following oral administration. The developed INS-QT-LCNPs were evaluated for simulated gastric fluid stability. In vitro Caco-2 uptake studies were also performed. Furthermore, in vivo pharmacokinetics and pharmacodynamics of INS-QT-LCNPs were evaluated. INS entrapped within LCNPs demonstrated excellent stability in simulated gastric fluid. Higher uptake of fluorescein isothiocyanate-INS-LCNPs were observed in Caco-2 cells. INS-LCNPs demonstrated approximately 20% relative bioavailability compared with subcutaneously administered INS. Significant decrease in oxidative stress was confirmed by reduction in malondialdehyde level. Overall, combination strategy not only overcomes poor oral bioavailability of INS and QT, but also prevents the generation of reactive oxygen species, responsible for diabetes-mediated complications.

Anti-inflammatory effects of Ginkgo biloba extract against trimethyltin-induced hippocampal neuronal injury.

Despite the immense neuromodulatory potentials of Ginkgo biloba extract as a memory enhancer, its underlying mechanism seems inadequate particularly with regard to its anti-inflammatory properties. The objective of the present study is to investigate the protective potentials of Ginkgo biloba extract (GBE) against hippocampal neuronal injury induced by trimethyltin (TMT), a potent neurotoxicant. Male SD rats were administered trimethyltin (8.5mgkg-1 b.wt) single intraperitoneal (i.p.) injection, followed by Ginkgo biloba extract (100mgkg-1 b.wt i.p) for 21days. The co-administration of GBE with TMT showed marked improvement in cognitive functions. Concomitantly, there was a significant decrease in oxidative stress as evident by reduction in MDA and total ROS levels. In addition, there was a marked suppression of astrocyte activation (GFAP), transcription factor NFκB and proinflammatory cytokines (TNF-α, IL-1α, 1L-6), which were found to be elevated by TMT administration. Histopathological observations showed remarkable improvement in hippocampal neuronal injury in the conjunctive group. Therefore, it is suggested that Ginkgo biloba extract is an effective agent against trimethyltin-induced hippocampal neuronal loss owing to its antioxidative as well as anti-inflammatory properties.

Catechin ameliorates doxorubicin-induced neuronal cytotoxicity in in vitro and episodic memory deficit in in vivo in Wistar rats.

Cognitive dysfunction by chemotherapy compromises the quality of life in cancer patients. Tea polyphenols are known chemopreventive agents. The present study was designed to evaluate the neuroprotective potential of (+) catechin hydrate (catechin), a tea polyphenol, in IMR-32 neuroblastoma cells in vitro and alleviation of episodic memory deficit in Wistar rats in vivo against a widely used chemotherapeutic agent, Doxorubicin (DOX). In vitro, neuroprotective studies were assessed in undifferentiated IMR-32 cells using percentage viability and in differentiated cells by neurite length. These studies showed catechin increased percentage viability of undifferentiated IMR-32 cells. Catechin pretreatment also showed an increase in neurite length of differentiated cells. In vivo neuroprotection of catechin was evaluated using novel object recognition task in time-induced memory deficit model at 50, 100 and 200mg/kg dose and DOX-induced memory deficit models at 100mg/kg dose. The latter model was developed by injection of DOX (2.5mg/kg, i.p.) in 10 cycles over 50days in Wistar rats. Catechin showed a significant reversal of time-induced memory deficit in a dose-dependent manner and prevention of DOX-induced memory deficit at 100mg/kg. In addition, catechin treatment showed a significant decrease in oxidative stress, acetylcholine esterase and neuroinflammation in the hippocampus and cerebral cortex in DOX-induced toxicity model. Hence, catechin may be a potential adjuvant therapy for the amelioration of DOX-induced cognitive impairment which may improve the quality of life of cancer survivors. This improvement might be due to the elevation of antioxidant defense, prevention of neuroinflammation and inhibition of acetylcholine esterase enzyme.

Maternal low-protein diet in female rat heart: possible protective effect of estradiol.

Several studies have shown that maternal low-protein (LP) diet induces detrimental effects in cardiovascular system and oxidative stress in male animals. Additional studies suggested that female has lower incidence of cardiovascular disease. However until present data, the possible effects of estradiol on the undernutrition during gestational and lactation periods are not discussed. The present study was conducted to evaluate the effects of a maternal LP diet during gestational and lactation period on oxidative balance in the female rat hearts ventricles at two ages. Dams were fed with normal protein (NP) or a LP diet during the gestational and lactation period, and their female offspring were divided into age groups (22 or 122 days, corresponding to a low or high estrogen level) composing four experimental groups. Evaluating the nutritional effect showed an increase in oxidative stress biomarkers and decrease in enzymatic defense in LP-22D compared with NP-22D. In contrast, no changes were observed in malondialdehyde and carbonyls, but an increase in glutathione-S-transferase (GST) activity in the LP-122D compared with NP-122D. The global oxy-score in the LP-22D group indicated a predominance of oxidative damage when compared with NP-22D, while in LP-122D group the global oxy-score was restored to NP-122D levels. Evaluating the estradiol effect, our data show a significant decrease in oxidative stress with increase in CAT and GST activity, associated with increase in intracellular thiols. Our data suggest that in situation with low levels of estradiol, hypoproteic diet during gestation and lactation period has detrimental effects on heart, however when estradiol levels raise, the detrimental effects induced are mitigated.

IL-6 controls resistance to radiation by suppressing oxidative stress via the Nrf2-antioxidant pathway in oral squamous cell carcinoma.

Background:In promoting tumour malignancy IL-6 signalling is considered to have an important role. However, the biological roles of IL-6 on radiosensitivity in oral squamous cell carcinoma (OSCC) remain largely unclear. The objective of this study is to determine the effects and molecular mechanisms of IL-6 on radiosensitivity in OSCC.Methods:Two OSCC cell lines, and OSCC tissue samples with radioresistant cells were used. We examined the effects of IL-6, or tocilizumab, a humanised anti-human IL-6 receptor antibody, or both on radiosensitivity and DNA damage after X-ray irradiation in vitro. In addition, we investigated the involvement of the Nrf2-antioxidant pathway in IL-6-mediated radioresistant mechanisms using OSCC cell lines and tissues.Results:Increased levels of IL-6 suppressed radiation-induced cell death, and the blockade of IL-6 signalling by tocilizumab sensitised tumour cells to radiation. The radioresistant effect of IL-6 was associated with decreased DNA damage after radiation. We also found that IL-6 promotes the activation of not only the downstream molecule STAT3 but also the Nrf2-antioxidant pathway, leading to a significant decrease in oxidative stress by upregulating Mn-SOD.Conclusions:These results indicate that the blockade of IL-6 signalling combined with conventional radiotherapy could augment the treatment response and survival rate in patients with radioresistant OSCC.

Comparison of Oxidative Stresses Mediated by Different Crystalline Forms and Surface Modification of Titanium Dioxide Nanoparticles

Titanium dioxide nanoparticles (TiO2NPs) are manufactured worldwide for use in a wide range of applications. There are two common crystalline forms of TiO2anatase and rutile with different physical and chemical characteristics. We previously demonstrated that an increased DNA damage response is mediated by anatase crystalline form compared to rutile. In the present study, we conjugated TiO2NPs with polyethylene glycol (PEG) in order to reduce the genotoxicity and we evaluated some oxidative stress parameters to obtain information on the cellular mechanisms of DNA damage that operate in response to TiO2NPs different crystalline forms exposure in hepatocarcinoma cell lines (HepG2). Our results indicated a significant increase in oxidative stress mediated by the anatase form of TiO2NPs compared to rutile form. On the other hand, PEG modified TiO2NPs showed a significant decrease in oxidative stress as compared to TiO2NPs. These data suggested that the genotoxic potential of TiO2NPs varies with crystalline form and surface modification.

Decrease of Atherosclerosis Markers and Oxidative Stress After 1 Year Administration of Omega-3 Fatty Acids Supplements in Patients with Metabolic Syndrome

Abstract Background and Aims: To assess the impact of 1 year administration of omega-3 fatty acids supplements on oxidative stress parameters and atherosclerosis progression. Material and Methods: A total of 284 patients with metabolic syndrome, aged 61±6.7 years, without clinical evidence of atherosclerosis were allocated to 2 groups, matched by sex and age: group A (140 patients) - diet according to ESC/EASD recommendations; group B (144 patients) - the same diet + capsules of fish oil (1g eicosapentanoic acid, 1g docosahexanoic acid, 0,1g a-tocopherol acetate). Body fat (BF) was measured by bioimpedance analysis. For oxidative stress evaluation we used the FormOx systems monitor on a blood drop and for progression of atherosclerosis the intima-media thickness (IMT) at common carotid artery. Patients were evaluated at baseline, after 6 months and 1 year. Results: IMT significantly decreased in group B vs group A at 1 year (p&lt;0.0001) and was correlated with %BF (p&lt;0.001), waist-to-hip ratio (WHR) (p=0.002), leptin (p&lt; 0.001), adiponectin (p&lt;0.05), leptin/adiponectin ratio (p&lt; 0.001) and oxidative stress (p&lt;0.001). Conclusions: One year administrations of omega-3 PUFA enriched diet reduces cardiovascular risk of metabolic syndrome patients, resulting in a significant decrease of oxidative stress and atherosclerosis progression.

Potential toxicological effects of amines used for carbon capture and storage and their degradation products

With the increasing use of amine solvents for carbon capture, there is a critical need to characterize the potential health effects of these materials and their degradation products formed within the capture system or downwind of release. This study evaluated the acute inhalation health risk of exposure to degraded mixtures of monoethanolamine (MEA), methyldiethanolamine (MDEA), and piperazine (PIP). Degradation was achieved in a heated (150C) and pressurized (approximately 15 psi) stainless steel vessel by adding NO2 and purified air over approximately 75 days. Laboratory mice were exposed to the degraded mixture (as well as the neat amines in separate experiments) 6hrs/day for 7 consecutive days in a whole-body inhalation chamber. Bronchoalveolar lavage (BAL) was carried out 18 to 24hours post-exposure and inflammatory cells were counted in lavage fluid. Cytokine expression and oxidative stress were measured in lung tissue. We found that exposure to degraded MEA resulted in significant increases in total cells, neutrophils, and lymphocytes, and the strongest cytokine response compared to control mice and compared to MEA-exposed mice. Neither MDEA nor PIP, or their degradant mixtures, caused increased inflammatory cells in BAL fluid. The degraded MEA atmosphere also caused a statistically significant decrease in oxidative stress in mouse lung. The degraded MDEA atmosphere caused the strongest cytokine response of the amines tested, producing statistically significant increases in cytokine growth-related oncogene (GRO-KC), monocyte chemotactic protein -1 (MCP-1), and granulocyte-macrophage colony stimulating factor (GMCSF) expression compared to the control and to MDEA alone. The degraded PIP atmosphere showed a statistically significant increase in GMCSF expression. This investigation represents a hazard evaluation and not a dose-response assessment; however, the results suggest that our approach can be used successfully to screen potential solvents for carbon capture for acute human health impacts.