Increase In Lipid Peroxidation Products Research Articles

Lipid Peroxidation, Reduced Glutathione, and Glutathione Peroxidase Levels in Intervertebral Discs of Patients with Lumbar Degenerative Disc Disease.

BACKGROUND Either a reduction in antioxidant levels or an accumulation of reactive oxygen species can heighten susceptibility to oxidative damage in disc cells. To date, no research has investigated the levels of lipid peroxidation products (thiobarbituric acid reactive substances [TBARs]), reduced glutathione (GSH), and glutathione peroxidase (GPx) in excised human lumbar disc tissues affected by degenerative disease. Therefore, this study aimed to evaluate lipid peroxidation products in excised disc tissues from patients with degenerative disc disease. MATERIAL AND METHODS Forty-two patients were enrolled. Patients were divided into lumbar disc degeneration (LDD) and nonlumbar disc degeneration (nonLDD) groups according to Pfirrmann classification. Intervertebral discs were obtained from all patients during the operation and were homogenized for analysis. TBARs levels were measured using fluorometry. GSH levels and GPx activity were quantified spectrophotometrically using a kinetic method. RESULTS TBARs levels in excised discs from LDD patients (5.18±4.14) were significantly higher than those from nonLDD patients (2.56±1.23, P=0.008). The levels of TBARs tended to increase with the severity of degeneration according to the Pfirrmann classification. However, these 2 groups showed no significant differences in reduced glutathione levels or glutathione peroxidase activity (P>0.05). Patients with LDD exhibited a worse health-related quality of life, reflected in lower utility and EQ-VAS scores and higher Oswestry disability index scores. CONCLUSIONS There was a notable increase in lipid peroxidation products in the excised intervertebral discs of patients with LDD. This finding suggests that oxidative stress may contribute to the development of disc degeneration.

Changes in Endogenous Intoxication and Antioxidant Defense System Markers in Patients with Tumor-Induced Acute Colonic Obstruction

A comprehensive evaluation of clinical and biochemical markers defining the status of endotoxemia in patients diagnosed with acute colonic obstruction (ACO) was conducted. The findings revealed that advancing stages of ACO corresponded to an increase in serum levels of endogenous intoxication markers and a simultaneous decrease in antioxidant defense system (ADS) markers.
 The aim of the study was to analyze changes in endogenous intoxication and ADS markers in patients with tumor-induced ACO throughout the disease progression and evaluate the outcomes.
 Materials and Methods. The study is based on examining serum levels of endogenous intoxication markers, including middle weight molecules (MWM), products of lipid peroxidation (LPO) - conjugated dienes (CD), malonaldehyde (MA), protein oxidative modification (POM), and key ADS markers, specifically superoxide dismutase (SOD), catalase (CAT), and ceruloplasmin (CP), in 155 patients with ACO throughout the disease progression and 20 apparently healthy individuals.
 Results. Upon patient admission to the hospital, the duration of ACO was found to correlate with an increase in endogenous intoxication markers and a decrease in antioxidant defense markers. Depending on ACO stage, MWM levels were 0.42 (0.38; 0.43) IU, 0.56 (0.51; 0.58) IU, and 0.72 (0.69; 0.73) IU, respectively (р1<0.01, р2<0.01, р3<0.01), with a normal range of 0.23 (0.18; 0.25) IU. In the compensated stage of ACO, MA levels significantly increased compared to the control group, reaching 6.39 (6.25; 6.42) nmol/mL (р1<0.001, р2<0.01, р3<0.05). Additionally, with the progression of the disease, a gradual increase in MA levels up to 6.39 (6.25; 6.42) nmol/mL, 7.88 (7.62; 7.92) nmol/mL, and 8.11 (8.05; 8.15) nmol/mL, respectively, was noted (р1<0.001, р2<0.01, р3<0.05), with a normal range of 3.14 (2.58; 3.17) nmol/mL. Similar trend was observed in serum CD levels - 3.11 (3.02; 3.18) IU, 3.69 (3.52; 3.72) IU, and 4.69 (4.53; 4.82) IU, respectively, with a normal range of 1.41 (1.32; 1.46) IU (р1<0.01, р2<0.01, р3<0.01). The study of LPO intensity via the optical density of aldehyde and ketone derivatives of neutral and basic dinitrophenylhydrazones (POM 356, POM 370, POM 430, POM 530) revealed an increase in POM product levels with the disease progression compared to the control group (р1<0.001, р2<0.01, р3<0.01). The analysis of the ADS showed an opposite trend, characterized by a significant decrease in marker levels. In patients with different ACO stages, serum CAT levels were 8.08 (7.95; 8.12) Н2О2/mL, 6.32 (6.25;6.41) Н2О2/mL, and 5.67 (5.59; 5.75) Н2О2/mL, respectively, with a normal range of 12.36 (12.21; 12.55) Н2О2/ml (р1<0.001, р2<0.01, р3<0.01), while SOD concentration decreased with the disease progression as well - 42.43 (31.75; 51.84) IU, 35.65 (24.72; 45.53) IU, and 32.18 (18.72; 41.15) IU, respectively, with a normal range of 63.60 (54.41; 74.56) IU (р1<0.001, р2<0.01, р3<0.01). In the compensated stage of ACO, CP level exceeded the normal value - 39.21 (38.92; 39.41) IU, with a normal range of 28.9 (28.4; 29.1) IU, indicating a compensatory defensive response of the body to a dramatic increase in LPO products. CP reserves, however, were depleted with the disease progression and a consistent decrease in this marker was subsequently observed: 19.10 (18.91; 19.23) IU in the subcompensated stage and 16.12 (16.01; 16.15) IU in the decompensated stage (р1<0.001, р2<0.01, р3<0.01).
 Conclusions. As a systemic process that induces various metabolic homeostasis disorders, endogenous intoxication serves as the pathogenetic foundation for the development of multiple organ failure in ACO patients. With ACO progression, endogenous intoxication caused an increase in LPO and POM activity, resulting in elevation of highly toxic middle-molecular weight substances, concurrently accompanied by a decline in the AOS activity.

Heme Oxygenase-1 Regulates Zearalenone-Induced Oxidative Stress and Apoptosis in Sheep Follicular Granulosa Cells.

Zearalenone (ZEA) is a common non-steroidal estrogenic mycotoxin found in a range of animal feeds and poses a serious threat to the reproductive health of farm animals and humans. However, the mechanism underlying ZEA-induced reproductive toxicity in sheep remains unknown. Granulosa cells are crucial for egg maturation and the fertility of female sheep. In this study, we aimed to examine the impact of different ZEA concentrations on sheep follicular granulosa cells and to elucidate the potential molecular mechanism underlying ZEA-induced toxicity using transcriptome sequencing and molecular biological approaches. Treating primary sheep follicular granulosa cells with different concentrations of ZEA promoted the overproduction of reactive oxygen species (ROS), increased lipid peroxidation products, led to cellular oxidative stress, decreased antioxidant enzyme activities, and induced cell apoptosis. Using transcriptome approaches, 1395 differentially expressed genes were obtained from sheep follicular granulosa cells cultured in vitro after ZEA treatment. Among them, heme oxygenase-1 (HMOX1) was involved in 11 biological processes. The protein interaction network indicated interactions between HMOX1 and oxidative and apoptotic proteins. In addition, N-acetylcysteine pretreatment effectively reduced the ZEA-induced increase in the expression of HMOX1 and Caspase3 by eliminating ROS. Hence, we suggest that HMOX1 is a key differential gene involved in the regulation of ZEA-induced oxidative stress and apoptosis in follicular granulosa cells. These findings provide novel insights into the prevention and control of mycotoxins in livestock.

Bisphenol A induces placental ferroptosis and fetal growth restriction via the YAP/TAZ-ferritinophagy axis

Exposure to bisphenol A (BPA) during gestation leads to fetal growth restriction (FGR), whereby the underlying mechanisms remain unknown. Here, we found that FGR patients showed higher levels of BPA in the urine, serum, and placenta; meanwhile, trophoblast ferroptosis was observed in FGR placentas, as indicated by accumulated intracellular iron, impaired antioxidant molecules, and increased lipid peroxidation products. To investigate the role of ferroptosis in placental and fetal growth, BPA stimulation was performed both in vivo and in vitro. BPA exposure during gestation was associated with FGR in mice; also, it induces ferroptosis in mouse placentas and human placental trophoblast. Pretreatment with ferroptosis inhibitor ferritin-1 (Fer-1) alleviated BPA-induced oxidative damage and cell death. Notably, BPA reduced the trophoblastic expression of Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ), which regulated tissue growth and organ size. YAP or TAZ siRNA enhanced BPA-induced ferroptosis, suggesting that trophoblast ferroptosis is dependent on YAP/TAZ downregulation after BPA stimulation. Consistently, the protein levels of YAP/TAZ were also reduced in FGR placentas. Further results revealed that silencing YAP/TAZ promoted BPA-induced ferroptosis through autophagy. Pretreatment with autophagy inhibitor chloroquine (CQ) attenuated BPA-induced trophoblast ferroptosis. Ferritinophagy, an autophagic degradation of ferritin (FTH1), was observed in FGR placentas. Similarly, BPA reduced the protein level of FTH1 in placental trophoblast. Pretreatment with iron chelator desferrioxamine (DFO) and NCOA4 (an autophagy cargo receptor) siRNA weakened the ferroptosis of trophoblast after exposure to BPA, indicating that autophagy mediates ferroptosis in BPA-stimulated trophoblast by degrading ferritin. In summary, ferroptosis was featured in BPA-associated FGR and trophoblast injury; the regulation of ferroptosis involved the YAP/TAZ-autophagy-ferritin axis.

Otaria Exercise for the Influence of 8-hydroxydeoxyguanosine (8-ohdg) in Postpartum Women

Objectives: If a woman is in a physiological post partum condition, there will be an increase in the production of free radicals in her body. This situation will be worse if the woman is undergoing pathological postpartum, the production of free radicals in her body will be even greater. This condition is known as "oxidative stress". Theoretical Framework: Doing Otaria exercise will affect the muscle's need for oxygen, which will increase, meaning it requires strong blood flow like the uterine muscles. By doing postpartum exercises, it will stimulate uterine contractions, so that uterine contractions will be better, the release of lochia will be smooth, which will affect the uterine involution process. Method: The design used in this research was Post Test Only Control Group Design or post test with experimental and control groups. The sample in this study was 20 respondents in the experimental group and 20 respondents in the control group. Results and conclusion: In postpartum mothers, there is an increase in lipid peroxidation products, especially 8-OhdG. The 8-OHdG is one of the product compounds of the lipid peroxide reaction which is also used as a marker of oxidative stress Implications of the research: Research implications: midwifery services, maternal and child health and the reduction of maternal and infant mortality rates are affected by this study. The potential for quality midwifery care in the postpartum period can benefit the health of mothers and their babies. This study allows for further research and collaboration in the future to further reduce maternal mortality in the post partum period.

Primary photosynthetic processes of Thalassiosira weissflogii under the effect of ciprofloxacin

Fluoroquinolone antibiotics such as ciprofloxacin have been actively used in medical practice, including the COVID-19 pandemic, to suppress adverse bacterial infections. Widespread application and improper disposal have resulted in the ubiquity of antibiotics in the environment, which can affect aquatic life, including phytoplankton. The effect of fluoroquinolone antibiotics on the photosynthetic processes of marine diatoms, which are the main producers in marine ecosystems, has been little studied. In this work the effect of the antibiotic ciprofloxacin on the primary photosynthetic processes in the marine diatom Thalassiosira weissflogii was studied. It has been shown that ciprofloxacin affects the functioning of PSII, preventing the transfer of absorbed energy from the excited antenna chlorophyll molecules to the PSII RC (φDo). Under the influence of ciprofloxacin, a decrease in the efficiency of electron donation to P680+ (FV / FO), inhibition of the quantum yield of PSII (FV / FM), a decrease in the proportion of active RCs (ABS / RC), and an increase in the dissipation of absorbed energy in RCs (DIo / RC) were revealed. It has been shown that the mechanism of action of ciprofloxacin is associated with damage of PSII RC. Ciprofloxacin enhances the photosensitivity of microalgae and causes an increase in lipid peroxidation products. It is proposed to apply the parameters of chlorophyll fluorescence analyzing the effect of antibiotics on microalgae.

Identification of ferroptotic genes and phenotypes in idiopathic nonobstructive azoospermia

Effective treatments for nonobstructive azoospermia (NOA), which affects 1% of all men globally, are limited by undefined pathogenic mechanisms, especially in idiopathic NOA (iNOA). Here, we tried to identify the functional ferroptosis-related genes and phenotypes involved in iNOA. Differentially expressed ferroptotic genes were identified from iNOA mRNA microarray datasets by bioinformatic analyses, and these ferroptotic genes were subsequently filtered by various algorithms. Then, receiver operating characteristic (ROC) curves were generated to evaluate the diagnostic ability of the abovementioned genes for iNOA. Generally, 11 differentially expressed ferroptotic genes were downregulated, and five genes were upregulated in iNOA samples. Four genes, including DUSP1, GPX4, HSD17B11, and SLC2A8, were technically selected and determined to be potential biomarkers for iNOA. Subsequently, similar expression levels were validated at both the RNA and protein levels in the iNOA specimens. Finally, morphologic and biochemical assays were applied to define the ferroptotic phenotypes in testes. The ferroptotic features, like shrunken mitochondria with electron-dense membranes and a reduction in cristae were observed across various cell types within iNOA patients, accompanied by the overload of ferrous ions and increased lipid peroxidation production. Our findings demonstrated that these ferroptosis genes could be involved in the underlying pathogenesis mechanisms of iNOA by regulating ferroptosis and serve as potential diagnostic biomarkers. Also, the ferroptotic phenotypes were identified in iNOA patients.

Endoplasmic reticulum stress-triggered ferroptosis via the XBP1-Hrd1-Nrf2 pathway induces EMT progression in diabetic nephropathy.

Diabetic nephropathy (DN) is characterized by tubulointerstitial fibrosis caused by epithelial-mesenchymal transition (EMT) of renal tubular epithelial cells. Although ferroptosis promotes DN development, the specific pathological process that is affected by ferroptosis in DN remains unclear. Herein, EMT-related changes, including increased α-smooth muscle actin (α-SMA) and Vimentin expression and decreased E-cadherin expression, were observed in the renal tissues of streptozotocin-induced DN mice and high glucose-cultured human renal proximal tubular (HK-2) cells. Treatment with ferrostatin-1 (Fer-1) ameliorated these changes and rescued renal pathological injury in diabetic mice. Interestingly, endoplasmic reticulum stress (ERS) was activated during EMT progression in DN. Inhibiting ERS improved the expression of EMT-associated indicators and further rescued the characteristic changes in ferroptosis caused by high glucose, including reactive oxygen species (ROS) accumulation, iron overload, increased lipid peroxidation product generation, and reduced mitochondrial cristae. Moreover, overexpression of XBP1 increased Hrd1 expression and inhibited NFE2-related factor 2 (Nrf2) expression, which could enhance cell susceptibility to ferroptosis. Co-immunoprecipitation (Co-IP) and ubiquitylation assays indicated that Hrd1 interacted with and ubiquitinated Nrf2 under high-glucose conditions. Collectively, our results demonstrated that ERS triggers ferroptosis-related EMT progression through the XBP1-Hrd1-Nrf2 pathway, which provides new insights into potential mechanisms for delaying EMT progression in DN.

THE PECULIARITIES OF BIOCHEMICAL AND MORPHOLOGICAL CHANGES IN THE HEART OF THE CASTRATED RATS IN THE DEVELOPMENT OF ADRENALIN DAMAGE OF HEART

The aim of the study was to evaluate the state of oxidation processes and morphological changes in the heart of castrated rats during the development of epinephrine heart damage (EHD). Materials and methods. The study was performed on 120 white male Wistar rats. The animals were divided into four series: 1 - control, 2 - castration. For EHD, rats were injected once intraperitoneally with a 0.18% solution of adrenaline hydrotartrate at the rate of 0.5 mg/kg of weight. Castration was performed under anesthesia. The concentration of diene and triene conjugates (DC, TC), Schiff's bases (SB), TBA-active products (TBA-ap), oxidatively modi"ed proteins (OMP), activity of superoxide dismutase (SOD) and catalase (CAT) were determined in the heart. A morphological study of preparations stained with Azantrichrome was carried out. All studies were performed in control, 1, 3, 7, 14 and 28 days after adrenaline injection. Results: In the I series DC and TC increased after 1 day of EHD, fell to control values after 3 days, and then had wave-like character (highest - after 14 days). SB decreased (minimal after 7 days), TBA-ap increase (maximal after 14 days). OMP370 increased after 1 and 3 days, after 7 days they did not differ from the control, after 14 days they were higher than in control, and after 28 days they decreased to the control values. OMP430 and OMP530were greater than the control indicators in all terms, except the last; the maximum was noted after 14 days. The activity of antioxidant enzymes was lower than the control indicators at all times of the study. Castration caused an increase of lipid peroxidation. After 7 days, DC and TC, were lower and SB - higher, than in the I series. Castration caused a decrease in OMP. In EHD all values of OMP, compared to the castrated control rats, were higher at all studed times Castration leads to increase of SOD, and decrase of CAT. All indicators of SOD and CAT exceeded the indicators of animals of the I series at all times of the study. Biochemical changes are consistent with morphological changes. After injection of epinephrine, severe vascular disorders, adventitia edema, perivasal edema, endothelial cell damage, dilatation of hemicapillaries, full blood vessels, stasis, hemorrhages in the surrounding tissues, and sclerosing of the walls of arteries and venules were observed. Cardiomyocytes were swollen, shortening, necrosis was observed, myocytolysis was noted. Edema of the stroma was noted. In the stroma, around the vessels, located cells of connective tissue elements were observed. Indicate more damage to the myocardium in the process of development of EHD in animals of the I series. Conclusions: Castration of rats causes an increase of lipid peroxidation products and CAT activity in the heart, but a decrease in the content of OMP. Adrenaline injection causes activation of lipid peroxidation and an increase in the content of OMP. During the development of EHD, the activity of antioxidants is significantly higher in II group. Biochemical changes are consistent with morphological, and indicate more damage to the myocardium in the development of EHD in animals of the I series.

Difenoconazole disrupts the blood-brain barrier and results in neurotoxicity in carp by inhibiting the Nrf2 pathway mediated ROS accumulation.

Excessive use of hard-to-degrade pesticides threatens the ecological health of aquatic systems. This study aimed to investigate difenoconazole (DFZ) residues in the environment induced neurotoxicity in carp and the underlying mechanisms. A total of thirty-six carps were divided into three groups and exposed to 0, 0.5, and 2.0mg/L DFZ for 96h, respectively. The alterations in behavior and blood-brain barrier (BBB) were examined, and potential mechanisms were explored using immunological assays and biochemical methods. The results showed that DFZ exposure caused behavioral freezing, reduced feeding, and neuronal necrosis in carp. Mechanistically, DFZ triggered ROS accumulation and destroyed the balance between oxidation and antioxidation with increased lipid peroxidation product MDA contents and reduced antioxidant enzymes SOD and CAT activities in the carp brain by inhibiting the NF-E2-related factor 2 (Nrf2) pathway. The activation of oxidative stress further reduced tight junction proteins and MMP levels, thereby destroying BBB and leading to DFZ leakage into the brain. Increased BBB permeability additionally led to DFZ activation of nuclear factor kappa-B signaling-mediated inflammatory cytokine storm, exacerbating neuroinflammation. Meanwhile, DFZ exposure activated mitochondria-associated apoptosis in the carp's brain by up-regulating Bcl-2 associated X protein, cleaved-caspase3, and cytochrome C and decreasing B-cell lymphoma-2 levels. Interestingly, the carp's brain initiated a protective autophagic response via the PI3K/AKT/TOR pathway intending to counteract the neurotoxicity of DFZ. Overall, we concluded that accumulation of DFZ at high concentrations in the aquatic systems disrupted the BBB and resulted in neurotoxicity in carp through inhibition of Nrf2 pathway-mediated ROS accumulation. This study provides a reference for monitoring DFZ residues in the environment and a new target for the treatment of DFZ-induced neurotoxicity in carp.

Effects of Glyphosate-Based Herbicide on Primary Production and Physiological Fitness of the Macroalgae Ulva lactuca

The use of glyphosate-based herbicides (GBHs) worldwide has increased exponentially over the last two decades increasing the environmental risk to marine and coastal habitats. The present study investigated the effects of GBHs at environmentally relevant concentrations (0, 10, 50, 100, 250, and 500 μg·L−1) on the physiology and biochemistry (photosynthesis, pigment, and lipid composition, antioxidative systems and energy balance) of Ulva lactuca, a cosmopolitan marine macroalgae species. Although GBHs cause deleterious effects such as the inhibition of photosynthetic activity, particularly at 250 μg·L−1, due to the impairment of the electron transport in the chloroplasts, these changes are almost completely reverted at the highest concentration (500 μg·L−1). This could be related to the induction of tolerance mechanisms at a certain threshold or tipping point. While no changes occurred in the energy balance, an increase in the pigment antheraxanthin is observed jointly with an increase in ascorbate peroxidase activity. These mechanisms might have contributed to protecting thylakoids against excess radiation and the increase in reactive oxygen species, associated with stress conditions, as no increase in lipid peroxidation products was observed. Furthermore, changes in the fatty acids profile, usually attributed to the induction of plant stress response mechanisms, demonstrated the high resilience of this macroalgae. Notably, the application of bio-optical tools in ecotoxicology, such as pulse amplitude modulated (PAM) fluorometry and laser-induced fluorescence (LIF), allowed separation of the control samples and those treated by GBHs in different concentrations with a high degree of accuracy, with PAM more accurate in identifying the different treatments.

L-Glutamic Acid Mitigates Carbon Tetrachloride-Induced Acute Tissue Injury by Reducing Oxidative Stress in a Rat Model

Background: Tetrachloromethane (CCl4) is a highly toxic environmental pollutant that causes specific and serious damage to various organs of animals and humans. The study of its effect on physiological and biochemical processes in the mammalian organism is very important, despite the severe restrictions on the use of tetrachloromantane in recent years. The fact is that they can be used as a model for many toxicological studies. Objective: The experimental studies aimed at exploring the ameliorative effects of L-glutamic acid (LGlu) on CCl4 toxicity in the myocardium, lung tissues and blood of male rats. Methods: Rats were exposed to CCl4, and later rats were treated with L-Glu. The GSH level and the activities of antioxidant enzymes were studied. In addition to this, the content of lipid peroxidation products was monitored. Results: The obtained results suggest that CCl4 causes oxidative stress in rat tissues, accompanied by an increase in lipid peroxidation products and a decrease in glutathione peroxidase (GPx), glutathione reductase (GR), glutathione transferase (GST), glucose-6-phosphate dehydrogenase (G6PDH), superoxide dismutase (SOD), catalase (CAT) activities and reduced glutathione (GSH) content. The enzymatic activity in tissues of rats treated with L-Glu was restored. Moreover, the changes, which were observed in the studied parameters, showed to be less significant compared to CCl4 treated group. Conclusion: These results suggest that L-Glu inhibits free radical processes. In summary, this study demonstrates the feasibility of the administration of L-Glu supplementation, which could be used to protect and mitigate the CCl4-induced oxidative stress.

TIGAR drives colorectal cancer ferroptosis resistance through ROS/AMPK/SCD1 pathway

Colorectal cancer (CRC) is the third most commonly diagnosed malignancy and major cause of cancer death in the world. Ferroptosis is a recently identified type of regulated cell death. Increasing evidence has shown that ferroptosis plays an important regulatory role in the occurrence and development of cancer. This study identified TIGAR as a potential regulator of ferroptosis resistance in the development of CRC. We showed that TIGAR expression in CRC tissues is significantly higher than that in adjacent normal tissues. Knockdown of TIGAR significantly caused an increase in erastin-induced ferroptosis in SW620 and HCT116 cells. Notably, knockdown of TIGAR significantly decreased GSH/GSSG ratio, increased lipid peroxidation production, and facilitated the accumulation of lipid peroxidation product malondialdehyde (MDA), and rendered CRC cells more sensitive to erastin induced ferroptosis. Furthermore, TIGAR inhibition repressed SCD1 expression in a redox and AMPK-dependent manner. Thus, these results suggest that TIGAR induces ferroptosis resistance in CRC cells via the ROS/AMPK/SCD1 signaling pathway.

Biomarker assessment in urgent surgical pathology of the small bowel: case-control analysis of a retrospective database

Background: Small bowel obstruction, mesenteric thrombosis, and strangulated ventral hernia area a challenge in emergency abdominal surgery. This study aimed to evaluate biomarkers of damage to the digestive tract in patients with urgent pathology. Materials and methods: The study involved 71 patients aged 18 to 80 years who were hospitalized in the intensive care unit in the immediate postoperative period. Results: All 71 underwent emergency surgery, 27 with small bowel necrosis. Lactate level area under curve (AUC = 0.964), C-reactive protein (AUC = 0.805) and systolic blood pressure (area under curve, AUC = 0.803) on the context of Sequential Organ Failure Assessment (SOFA) score (AUC = 0.880) showed stratification of patients with complications before surgery. Small bowel necrosis patients revealed an increase in primary thiobarbituric acid (TBA) reactive products (AUC = 0.813) lipid peroxidation products, and a decrease in superoxide dismutase activity (AUC = 0.818) and catalase (AUC = 0.804). Wide variability of intestinal fatty-acid binding protein (I-FABP) from 199.8 to 2189.6 pg/mL were observed in all patients studied, with an AUC = 0.814 in small intestinal necrosis. Conclusion: Surgical pathology of the small intestine due to obstruction of various origina, mesenteric thrombosis, and strangulated ventral hernia pronounced revealed disorders of the antioxidant-prooxidant balance. This was expressed by an increase in lipid peroxidation products, and the level of TBA-reactive products, and the activities of superoxide dismutase (SOD), and catalase. Viewed against the background of an increase in I-FABP above 577 pg/mL, these variables were the most significant indicators of small intestinal necrosis.

Integrated molecular response of exposure to traffic-related pollutants in the US trucking industry.

Exposure to traffic-related pollutants, including diesel exhaust, is associated with increased risk of cardiopulmonary disease and mortality; however, the precise biochemical pathways underlying these effects are not known. To investigate biological response mechanisms underlying exposure to traffic related pollutants, we used an integrated molecular response approach that included high-resolution metabolomic profiling and peripheral blood gene expression to identify biological responses to diesel exhaust exposure. Plasma samples were collected from 73 non-smoking males employed in the US trucking industry between February 2009 and October 2010, and analyzed using untargeted high-resolution metabolomics to characterize metabolite associations with shift- and week-averaged levels of elemental carbon (EC), organic carbon (OC) and particulate matter with diameter≤2.5μm (PM2.5). Metabolic associations with EC, OC and PM2.5 were evaluated for biochemical processes known to be associated with disease risk. Annotated metabolites associated with exposure were then tested for relationships with the peripheral blood transcriptome using multivariate selection and network correlation. Week-averaged EC and OC levels, which were averaged across multiple shifts during the workweek, resulted in the greatest exposure-associated metabolic alterations compared to shift-averaged exposure levels. Metabolic changes associated with EC exposure suggest increased lipid peroxidation products, biomarkers of oxidative stress, thrombotic signaling lipids, and metabolites associated with endothelial dysfunction from altered nitric oxide metabolism, while OC exposures were associated with antioxidants, oxidative stress biomarkers and critical intermediates in nitric oxide production. Correlation with whole blood RNA gene expression provided additional evidence of changes in processes related to endothelial function, immune response, inflammation, and oxidative stress. We did not detect metabolic associations with PM2.5. This study provides an integrated molecular assessment of human exposure to traffic-related air pollutants that includes diesel exhaust. Metabolite and transcriptomic changes associated with exposure to EC and OC are consistent with increased risk of cardiovascular diseases and the adverse health effects of traffic-related air pollution.

Lipid peroxidation functional state changes in patients with obstructive jaundice depending on the level of bilirubin in the blood.

Obstructive jaundice (OJ) is the most common syndrome among diseases of the hepatopancreatoduodenal region and is found in 12-45% of cases. OJ may be benign and malignant etiology. Despite the evidence of the participation of bilirubin in reducing the bactericidal properties of neutrophils, there are no data currently on changes in the functioning of the antioxidant defense system depending on the level of bilirubin in the blood of patients with OJ of various origins. Research in this direction reveals the possibility for the development of pathogenetic recommendations for influencing these links of the pathogenesis of the disease. The study included men with OJ of non-malignant (OJNMG) (n = 47; mean age - 52.02 ± 5.18 years) and OJ of malignant genesis (OJMG) (I-II stages of the malignant process) (n = 45; mean age - 53.02 ± 4.8 years), divided into three subgroups, depending on the level of bilirubin in the blood. The indicators of practically healthy men as a control (n = 50, average age - 48.7 ± 3.9 years) were used. Spectrophotometric and statistical research methods were used. A statistically significant decrease of superoxide dismutase, glutathione-S-transferase, glutathione-peroxidase, ceruloplasmin, an increase in the values of diene conjugates, malondialdehyde in the group of patients with OJNMG relative to the control was revealed, regardless of the level of bilirubin in the blood. The presence of malignant genesis of the disease with more intense changes in the studied parameters relative to control is accompanied. Comparison of indicators between groups of patients with OJ of different genesis showed a decrease in the values of glutathione-S-transferase and an increase in the level of diene conjugates in patients with OJMG and the level of bilirubin less than 60 μmol / L, as well as an increase in the content of diene conjugates in patients with OJNMG and a level of bilirubin 60- 200 μmol / L in comparison with the corresponding groups of patients with OJNMG. Thus, both in the groups with OJNMG and in the groups with OJMG, there is a significant decrease in the activity of the main antioxidant enzymes and an increase in lipid peroxidation products, regardless of the level of bilirubin in the blood. The presence of malignant genesis is characterized by more intense differences. The revealed changes can serve as additional criteria for optimizing the diagnosis and treatment of this cohort of patients.

The protective effect of the aqueous extract of parsley (Petroselinum sativum ) seeds on experimentally – induced oxidative stress in rats

In this study, the potential protective effect of aqueous extract of parsley (Petroselinum sativum) seeds against hydrogen peroxide (H2O2) – induced oxidative stress in male rats was assessed. Three groups of male albino rats were randomly divided (n=7) and were handled for twenty-eight days as follows: rats in group I served as control; animals in group || were provided with drinking water containing 0.5% H2O2 and those in group III received orally 8 mg/100 gm B.W. of aqueous extract of parsley seeds plus 0.5% H2O2 in drinking water. After four weeks experimental period, a significant increase in lipid peroxidation products (MDA), and decrease in glutathione (GSH) concentrations were observed in plasma, kidney, liver and heart tissues of H2O2 treated animals as compared with the control group. These biomarkers (GSH and MDA) are interrelated and indicate the occurrence of oxidative stress. Plasma total cholesterol (TC) concentration was significantly increased in H2O2 treated rats. By administration of aqueous extract of parsley along with H2O2, plasma and tissue GSH levels were significantly increased while the elevation in MDA level was diminished in plasma and different tissues examined. A decrease in plasma cholesterol concentration was recorded in H2O2 and parsley treated group as compared with the control one and H2O2 treated groups. These results indicate that aqueous extract of parsley have hypocholesterolemic and antioxidant effect.

Ecoengineering Solutions for the Impairment of Spreading and Growth of Invasive Spartina patens in Mediterranean Salt Marshes

The invasion of natural communities by non-indigenous species represents one of the most serious threats to biodiversity. Understanding the ecophysiology of invasive species can provide insights into potential physiological handicaps relative to native species. By doing so, we can leverage the development of ecoengineering solutions for the removal of non-indigenous species, preferably using non-chemical methods. Spartina patens is a known invasive species of cordgrass aggressively proliferating in Mediterranean salt marshes, producing impenetrable monospecific stands. As its occurrence is delimited by the upper high tide water level, we hypothesized that S. patens is intolerant to waterlogging. Therefore, we developed a field experiment where strands of S. patens were kept waterlogged over the entire tidal cycle for 30 days. At the end of the experimental period, plants in the trial plots exhibited severe stress symptoms at different physiological levels compared with control plots (no intervention). At the photobiological level, intervened plants exhibited lower efficiency in producing chemical energy from light, whilst at the biochemical level waterlogging impaired the antioxidant system and increased lipid peroxidation products. Furthermore, the application of chlorophyll a pulse amplitude modulated (PAM) fluorometry, a non-invasive technique, allowed us to evaluate the effectiveness of the implemented measures, being the tool that provided the best separation between the control and intervened population. Considering the physiological traits observed here, ecoengineering solutions based on increased waterlogging of S. patens stands, can be a low-cost and efficient measure to reduce the spreading and growth of this invasive species in the Mediterranean and other salt marshes worldwide with little disturbance.

The Enhanced Beneficial Effect of Extra Virgin Olive Oil Over Evening Primrose Oil on Oxidative Stress, and Liver Function in Male Arthritic Rats

Aims: Rheumatoid arthritis (RA) is characterized by the onset of oxidative stress. This study aimed to evaluate the enhancing of extra virgin olive (EVOO) and Evening primrose oil (EPO) on oxidative stress and liver enzymes in male Wistar rats and compare between them.
 Place and Duration: Faculty of Science biochemistry department, Between July 2018 and August 2018.
 Methodology: A Subcutaneous injection of 200 µl of Freund's complete adjuvant into a footpad of the right hind leg of Wistar male rats at two consecutive days induced RA. Rats received EVOO and EPO daily by oral gavage needle with gauge 18 at doses of 5 mg/kg b.wt./day. for 10 and 21 days. No loss was recorded in the experimental rats.
 Results: A significant depletion in serum Reduced glutathione content (GSH), glutathione peroxidase (GPX), and glutathione s transferase activities (GST) in arthritic rats compared to normal rats after 10 and 21 days of induction which improved significantly after 10 and 21 days of EPO and EVOO treatments. EPO and EVOO treatments for 21 days increased the GSH and GPX compared to 10 days treatments while no difference in GST activity. EVOO treatment improved GSH and GPX after 10 and 21 days than EPO treatment. The elevated uric acid levels in arthritic rats were markedly ameliorated as a result of EVOO and EPO treatment administration. Increased lipid peroxidation products (MDA), rheumatoid factor, and liver enzyme (Alanine transaminase ALT and Aspartate transaminase AST) were recorded in arthritic rats and they significantly progressed after EPO and EVOO treatments for 10 and 21 days but EVOO had the best effect at 21 days.
 Conclusion: EVOO and EPO showed significant antioxidant efficacies and improved affected liver enzymes due to rheumatoid arthritis onset. When comparing olive oil has more antioxidant properties than evening primrose oil, so we recommend more studies on olive oil combination with anti-arthritic medications to improve their efficacies with less toxicity.

Biochemical markers of oxidative stress in maize seedlings exposed to rose-grass aphids

We studied the influence of rose-grass aphid (Metopolophium dirhodum L.) infestation on the biochemical markers of oxidative stress in seedlings of two maize (Zea mays L.) varieties (relatively resistant Ambrozja and resistant Plomyk). We compared the generation of superoxide anion radicals O2-, level of hydrogen peroxide (H2O2), lipid peroxidation products (MDA) as well as markers of protein damage (protein-bound carbonyl groups). The studied parameters were measured at 24, 48, 72 and 96 h post-initial aphid infestation compared to the non-infested control seedlings. Our studies indicated that the rose-grass aphid feeding evoked oxidative stress in the maize seedlings. Investigated Z. mays cultivars exhibited excessive generation of superoxide anion radicals in response to insect treatments. Rose-grass aphid feeding increased the H2O2 level in maize tissues with similar levels observed at most periods post-infestation with M. dirhodum, also increased lipid peroxidation products with the maximal levels at 48 and 72 h for Ambrozja and 48, 72 and 96 h post-infestation for Plomyk varieties. Further at 48 and 72 h post-initial aphid infestation, there was an increase in protein bound carbonyl groups content in the maize seedlings after infestation with aphids.