Decreased Superoxide Dismutase Activity Research Articles

Overexpression of C9orf72 exacerbates Aβ25‑35‑induced oxidative stress and apoptosis in PC12 cells.

Alzheimer's disease (AD) is the most common neurodegenerative disease and is manifested by memory loss and spatial disorientation. There is currently no effective treatment for AD. Abnormalities of the chromosome 9 open reading frame 72 (C9ORF72) gene have been associated with various neurodegenerative diseases. However, its intrinsic roles in AD remain to be elucidated. Here we found that Aβ25‑35 increased the expression of C9orf72 in PC12 cells at both mRNA and protein levels. In Aβ25‑35‑treated PC12 cells, C9orf72 overexpression induced an abnormally condensed and fragmented nucleus and apoptosis, as well as significantly enhanced reactive oxygen species (ROS) levels. Mechanistically, an Aβ25‑35‑induced decrease of superoxide dismutase activity was augmented by C9orf72 overexpression, which in contrast increased malondialdehyde content. Consistently, further apoptotic analysis revealed significant downregulation of Bcl‑2 and Bcl‑xL expression and enhanced cleavage of caspase‑3 with Aβ25‑35 treatment, all of which were exacerbated by C9orf72 overexpression. In addition, tau phosphorylation, another hallmark of AD pathology, was induced by Aβ25‑35 and was remarkably enhanced by C9orf72 overexpression. Our data indicate that C9orf72 plays important roles in intracellular ROS signaling and Aβ25‑35‑induced neuronal apoptosis in AD. These findings provide insights into C9orf72 function in the pathogenesis of many related neurodegenerative diseases and provide a basis for potential therapeutic interventions.

THE LEVEL OF OXIDATIVE STRESS METABOLITES IN AN EXPERIMENTAL MODEL WITH PERIODONTITIS

In people worldwide, chronic periodontitis occurs in 10-15% of cases. Prolonged inflammation of periodontal tissues contributes to the formation of oxidative stress. The purpose of this study was to evaluate the level of malondialdehyde and superoxide dismutase (as indicators of oxidative stress) in periodontitis in rats. For this, in the main group of rats (n=10) a model of ligature periodontitis was created. The control group of rats (n=10) was intact. As a result, in periodontitis, the level of malondialdehyde doubled. We also found an inverse relationship between the level of lipid damage and superoxide dismutase activity. Conclusions. The level of metabolites of redox processes is significantly increased in periodontitis. This confirms a significant increase in the indicators of malondialdehyde. A decrease in superoxide dismutase activity leads to a low antioxidant status in rats.

Sex-specific changes in oxidative stress parameters and longevity produced by Bisphenol F and S compared to Bisphenol A in Drosophila melanogaster

Female and male Drosophila melanogaster were exposed separately for seven days to Bisphenol A (BPA), Bisphenol F (BPF), and Bisphenol S (BPS) at concentrations of 0.25, 0.5, and 1 mM. We observed that males exposed to 0.5 and 1 mM BPS showed lower catalase (CAT) activity and higher superoxide dismutase (SOD) and reactive species (RS); CAT activity decreased for BPF 0.5 and 1 mM. Nevertheless, BPA 0.5 and 1 mM decreased CAT activity, increased RS and lipid peroxidation (LPO), and reduced mitochondrial viability. None of the bisphenols altered the cell viability of male flies, although BPA 0.5 and 1 mM reduced longevity. In female flies, BPA and BPS 0.5 and 1 mM increased RS and LPO levels and decreased CAT activity and glutathione-S-transferase (GST), which may have contributed to lower mitochondrial and cell viability. Furthermore, BPS decreased SOD activity at the 1 mM concentration, and BPA reduced the SOD activity at concentrations of 0.5 and 1 mM. In the BPF 1 mM group, there was a reduction in GST activity and an increase in RS and LPO levels. The toxicological effects were different between sexes, and BPA was more harmful than BPF and BPS in male flies. Thus, our findings showed that females were more susceptible to oxidative cell damage when exposed to BPA and BPS than to BPF, and daily exposure to BPA and BPS at all concentrations reduced female longevity, as well as in BPF 1 mM.

THE EFFECT OF METHANOLIC EXTRACT OF Vernonia amygdalina ON LIPID PEROXIDATION AND SOME ANTIOXIDANT ENZYME ACTIVITIES IN THE EARLY STAGE OF CYCASIN INDUCED TESTICULAR CARCINOGENESIS IN RATS

This study evaluated the effect of Vernonia amygdalina (V. amygdalina) on testicular lipid peroxidation, Superoxide Dismutase (SOD) and catalase (CAT) activities in the early stages of cycasin-induced testicular carcinogenesis in rats. Fifty male Wistar rats with an average weight of 175g were divided into five groups of 10 animals each. Group 1 was fed with a Normal Diet (ND) and acted as experimental control. Group 2 was fed with a Normal Diet compounded with cycasin for 6 weeks. Group 3 to Group 5 were fed with Normal Diet compounded with cycasin V. amygdalina in varied amount and duration for 6 weeks. The results showed a significant (p< 0.05) increase in the level of lipid peroxidation and a significant (p< 0.05) decrease in the antioxidant activities of SOD and CAT in groups exposed to cycasin compared to the control group in both testes tissues. Feeding rats with the V. amygdalina significantly (p< 0.05) and gradually decreased the level of testicular lipid peroxidation compared with the Group 2. A significant (p< 0.05) and a gradual rise in the activity of SOD and CAT were also observed in the rats fed with V. amygdalina. The study shows cycasin fed to rats induces oxidative stress, and administration of V. amygdalina reverses the adversely effect in ways which suggest that V. amygdalina may protect rats from testicular carcinogenesis

Exposure to leucine induces oxidative stress in the brain of zebrafish.

Maple Syrup Urine Disease (MSUD) is an autosomal recessive inherited disorder caused by a deficiency in the activity of the branched-chain alpha-ketoacid dehydrogenase complex leading to the accumulation of branched-chain amino acids (BCAA) leucine, isoleucine, and valine and their respective branched-chain α-ketoacids and corresponding hydroxy acids. Considering that Danio rerio, known as zebrafish, has been widely used as an experimental model in several research areas because it has favorable characteristics that complement other experimental models, this study aimed to evaluate oxidative stress parameters in zebrafish exposed to high levels of leucine (2mM and 5mM), in a model similar of MSUD. Twenty-four hours after exposure, the animals were euthanized, and the brain content dissected for analysis of oxidative stress parameters: thiobarbituric acid reactive substances (TBARS), 2',7'-dichlorofluorescein oxidation assay (DCF); content of sulfhydryl, and superoxide dismutase (SOD) and catalase (CAT) activities. Animals exposed to 2mM and 5mM leucine showed an increase in the measurement of TBARS and decreased sulfhydryl content. There were no significant changes in DCF oxidation. In addition, animals exposed to 2mM and 5mM leucine were found to have decreased SOD activity and increased CAT activity. Based on these results, exposure of zebrafish to high doses of leucine can act as a promising animal model for MSUD, providing a better understanding of the toxicity profile of leucine exposure and its use in future investigations and strategies related to the pathophysiology of MSUD.

CircFN1 upregulation initiated oxidative stress-induced apoptosis and inhibition of proliferation and migration in trophoblasts via circFN1-miR-19a/b-3p-ATF2 ceRNA network

Recently, the etiopathogenesis of preeclampsia (PE) has been developed from the perspective of circular RNA, microRNA and their crosstalk in placental oxidative stress. Real-time quantitative PCR and western blotting detected expression of circular RNA-fibronectin 1 (circFN1; ID hsa_circ_0058152), microRNA (miR)-19a/b-3p and activating transcription factor 2 (ATF2). Receiver operating characteristic (ROC) curve analyzed the predictive value of circFN1. Oxidative stress, apoptosis, proliferation, and migration were measured using superoxide dismutase (SOD) and malonaldehyde (MDA) assay kits, Annexin V/Prodium iodide and western blotting methods, MTS and EdU assays, and scratch wound assay, respectively. Target relationships were retrieved by miRNA target prediction software and confirmed by dual-luciferase reporter assay, RNA immunoprecipitation and RNA pull-down. Expression of circFN1 was upregulated in the serum of PE pregnancies, and the area under the ROC curve of serum circFN1 was 0.7826 (95% confidence interval: 0.6495-0.9157; sensitivity 86.96%; specificity 56%). Functionally, its upregulation decreased SOD activity, cell viability, EdU incorporation, migration rate, and Bcl-2 expression in human trophoblast HTR-8/SV-neo cells, but meanwhile increased MDA level, apoptosis rate, and Bax and cleaved-caspase3 expression. Moreover, its downregulation played the opposite effects in HTR-8/SV-neo cells. Mechanistically, circFN1 functioned as "miRNA sponge" for miR-19a/b-3p and modulated the latter's target gene ATF2. There were feedback effects of miR-19a/b-3p restorations and ATF2 depletion on circFN1 actions in HTR-8/SV-neo cells. Oxidative injury-mediated placental trophoblast dysfunction in PE was through competing endogenous RNA (ceRNA) mechanism of CircFN1-miR-19a/b-3p-ATF2 axes.

α-Tocopherol Prevents Sperm Apoptosis and Necrosis in Rats Exposed to 2,3,7,8-Tetrachlorodibenzo-p-dioxin.

2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is a persistent organic pollutant that induces overproduction of reactive oxygen species (ROS). Studies on avoiding the adverse effects of dioxin pollution exposure are needed in all aspects, including reproductive health. This study aimed to determine the effect of α-tocopherol on superoxide dismutase (SOD) and malondialdehyde (MDA) levels, live spermatozoa, apoptosis, and necrosis in male rats exposed to dioxin as a model. Thirty healthy 12-week-old male rats were randomly divided into five groups. Rats in the control group were given corn oil twice daily at 4-hour intervals. The remaining rats were given TCDD 700 mg/kg BW daily, followed by administration of corn oil and α-tocopherol at doses of 77, 140, and 259 mg/kg BW/d for T0, T1, T2, and T3 groups, respectively. The treatments were conducted for 45 days; all rats were euthanized to collect blood and testicular samples on day 46. The results showed that exposure of TCDD resulted in a decrease in SOD activity and live spermatozoa and increased MDA level and death, apoptosis, and necrosis of spermatozoa (T0) compared to the control (C) group (p < 0.05). The administration of α-tocopherol, starting from the doses of 77 (T1), 149 (T2), and 259 mg (T3) per kg BW, was sequentially followed by returning MDA levels, recovering SOD activities, and restoration in the percentage of living, dead, apoptotic, and necrotic spermatozoa, similar (p > 0.05) to those of the control group. It could be concluded that the administration of α-tocopherol resolves the harmful effects of TCDD on the viability of spermatozoa in rats as a model.

Effect of a synbiotic supplement as an antibiotic alternative on broiler skeletal, physiological, and oxidative parameters under heat stress

The aim of this study was to examine if synbiotics can function as alternatives to antibiotics in broiler production under heat stress (HS). Day-old broiler chicks (528 birds) were randomly placed in floor pens within 2 identical temperature-controlled rooms (11 birds/pen and 24 pens/room). The pens of each room were evenly divided among 3 treatments (n = 8): basal diet (CON), the basal diet mixed with 50 ppm of bacitracin methylene disalicylate (BMD) or a synbiotic (50 ppm of PoultryStar meUS, SYN). From d 15, room 2 was under thermoneutral (TN) conditions (TN-CON, TN-BMD, and TN-SYN), while HS was applied to room 1 at 32oC for 9 hrs/d (0800 to 1700) (HS-CON, HS-BMD, and HS-SYN). Treatment effects on footpad dermatitis and gait score were measured on 5 birds/pen, and latency to lie (LTL) test was measured on 2 birds/pen at d 27 and d 41; and 1 broiler/pen was sampled on d 28 and d 42, respectively. Body, liver, and spleen weight were determined. Plasma levels of interleukins (IL), heat shock protein 70, immunoglobulin (Ig)Y, liver superoxide dismutase (SOD) and glutathione peroxidase (GPx) enzyme activities were examined. Heat stress suppressed BW and IgY concentrations on both d 28 and d 42, while suppressed plasma IL-6 concentrations, SOD activities, and LTL duration on d 28 only (P < 0.05). Among all treatments, SYN birds had the best foot and skeletal health scores on both d 27 and d 41 (P < 0.05). On d 42, SYN increased BW, and TN-SYN birds had higher relative spleen weight than both TN-BMD and TN-CON birds (P < 0.05). Antibiotic BMD increased BW (P < 0.05) but decreased SOD activities (P < 0.05) on d 42. These results indicate that the SYN supplementation decreases HS negative effect on broilers by improving BW, foot, and skeletal health, while BMD improves BW but also increases oxidative stress in broilers. The data suggest that synbiotic supplement may function as an alternative to antibiotics in broiler production during summer seasons, especially in the tropical and subtropical regions.

α-Tocopherol restores semen quality in rats exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Background and Aim:2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persistent organic pollutant toxic to the human reproductive system. This study aimed to evaluate the effect of α-Tocopherol administration on the male fertility parameters of a rat model exposed to TCDD.Materials and Methods:Fifty healthy 12-week-old male rats were randomly divided into five groups. Rats in the control group were given corn oil twice daily in 4 h intervals. In the treatment groups, all rats were given TCDD at a dose of 700 ng/kg of body weight (BW)/day for 45 days. Four hours after receiving the TCDD, T0 rats were given corn oil, and T1, T2, and T3 rats were given α-Tocopherol at doses of 77, 140, and 259 mg/kg BW/day, respectively, for 45 days. On day 46, experimental animals were sacrificed to collect blood and testicular samples.Results:TCDD exposure decreased superoxide dismutase activity, plasma membrane integrity, Leydig cell count, sperm cell count, sperm viability and motility, and increased malondialdehyde levels, serum testosterone levels, and sperm morphological abnormalities. The administration of α-Tocopherol mitigated the effects of TCDD exposure, and the 140 and 259 mg/kg BW/day treatments returned those male fertility parameters to normal levels.Conclusion:The administration of 140 mg/kg BW/day α-Tocopherol restored male semen quality in rats exposed to TCDD. We found dynamics serum testosterone levels in rats exposed to TCDD that need to be further studied.

Sulfiredoxin-1 Inhibits PDGF-BB-Induced Vascular Smooth Muscle Cell Proliferation and Migration by Enhancing the Activation of Nrf2/ARE Signaling.

Sulfiredoxin1 (Srxn1), an endogenous antioxidant protein, is involved in cardiovascular diseases. In this study, we aimed to investigate the role of Srxn1 in VSMCs and its molecular mechanism. The murine vascular smooth muscle cells MOVAS were treated with different doses of platelet-derived growth factor-BB (PDGF-BB); then, Srxn1 expression was detected using reverse transcription-quantitative polymerase chain reaction and western blot analysis. MTT and wound healing assay were used to examine the effect of Srxn1 on MOVAS cell proliferation and migration. Reactive oxygen species (ROS) production, malondialdehyde (MDA) level, and superoxide dismutase (SOD) activity in MOVAS cells were detected using corresponding commercial kits. Moreover, the expression of proliferating cell nuclear antigen (PCNA), matrix metalloproteinase 2 (MMP-2), and nuclear factor erythroid-2-related factor 2 (Nrf2) /antioxidant response element (ARE) signaling-related proteins was detected using western blot analysis. In our study, PDGF-BB dose-dependently increased Srxn1 expression in MOVAS cells, and Srxn1 expression was increased with time dependence in PDGF-BB-treated MOVAS cells. The knockdown of Srxn1 increased PDGF-BB-induced the proliferation, migration, ROS production, MDA level, and the protein expression of PCNA and MMP-2, as well as decreased SOD activity and the expression of Nrf2/ARE signaling-related proteins in PDGF-BB-stimulated MOVAS cells. However, the overexpression of Srxn1 showed the opposite results to those of knockdown of Srxn1. Moreover, the inhibitory effects of Srxn1 overexpression on PDGF-BB induced proliferation, migration, ROS production, and MDA level and the promotion of Srxn1 overexpression on PDGF-BB induced SOD activity were partially reversed by the knockdown of Nrf2. Srxn1 inhibited PDGF-BB-induced proliferation, migration, and oxidative stress through activating Nrf2/ARE signaling.

Neutrophil extracellular traps (NETs) modulate inflammatory profile in obese humans and mice: adipose tissue role on NETs levels.

Neutrophilextracellular traps (NETs) are a recently discovered neutrophil defense mechanism whichmodulates several inflammatory conditions contributing to metabolic profile alterations. Therefore, the present study aimed to evaluate the production of NETs in obese patients and mice, verifying the possible mechanisms associated with the release of NETs by the adipose tissue. The present study investigated NETs production in human adipose tissue and also showing the neutrophils using intravital microscopy in mouse epididymal adipose tissue. Blood and white adipose tissues were obtained from eutrophic and obese individuals and from mice. Lipid, glycemic and leukocyte profiles were evaluated, as well as the levels of NETs and its markers. Bioinformatics and proteomics analyses were performed and the identified key proteins were measured. The main findings showed that the inflammatory markers interleukin-8 (IL-8), heat shock protein 90 (HSP90) and the E1 heat shock protein family (HSPE1) can be modulated by the NETs levels in obesity. Obesity has also been associated with increased cholesterol, glucose intolerance, ionic calcium and NETs. We also observed an increase in catalase and a decreased superoxide dismutase activity. Bioinformatics and proteomics analyses revealed that IL-8, HSP90 and HSPE1 were associated with obesity, inflammation and NETs release. In conclusion, the present study shows an increase in NETs production during obesity associated with important inflammatory markers in adipose.

Dietary interventions in mice affect oxidative stress and gene expression of the Prlr and Esr1 in the adipose tissue and hypothalamus of dams and their offspring.

Maternal diet is key to the progeny's health since it may impact on the offspring's adult life. In this study, mice dams received standard (CONT), restrictive (RD), or hypercaloric (HD) diets during mating, pregnancy, and lactation. Male offspring of each group of dams also received these diets: CONT, RD, HD. Aiming to evaluate the oxidative stress in the adipose tissue, reactive oxygen species (ROS) production, catalase (CAT), and superoxide dismutase (SOD) activities were analyzed in dams and offspring. In the adipose tissue and hypothalamus, gene expression of prolactin (Prlr) and estrogen alpha (Esr1) receptors was performed in dams and offspring. Protein expression of Stat5 was evaluated in the adipose tissue of the offspring from RD-fed dams. HD-fed dams increased triglycerides and leptin serum concentrations, and decreased SOD activity in the adipose tissue. In the offspring's adipose tissue, we observed a maternal diet effect caused by HD, with increased ROS production and SOD and CAT activities. Gene expression of Prlr and Esr1 in the offspring's adipose tissue was decreased due to maternal RD. Mice from HD-fed dams showed higher Stat5 expression compared to the offspring from CONT and RD dams in the adipose tissue. In the hypothalamus, we found decreased expression of Prlr in RD and HD dams, compared to CONT; and a maternal diet effect on Prlr and Esr1 gene expression in the offspring. In conclusion, we can affirm that maternal nutrition impacts the redox state and influences the gene expression of Prlr and Esr1, which are involved in energy metabolism, both peripherally and centrally in the adult life of the female offspring.

Subacute toxicity of chlorpyrifos on histopathological damages, antioxidant activity, and pro‐inflammatory cytokines in the rat model

Chlorpyrifos (CPF) is an extensively used organophosphorus pesticide for agricultural, industrial, and domestic purposes. Previous studies have reported the adverse effects of CPF, such as intoxication incidents, endocrine disruption, cardiovascular diseases, as well as histopathological and oxidative damage. The aims of the present study were to elucidate short time subacute toxicity of CPF in male rats. Sprague-Dawley male rats (n= 32) were divided into four groups (n= 8) and received CPF as 3.25 mg/kg body weight (b.w) (Group A), 6.75 mg/kg b.w (Group B), 13.5mg/kg b.w (Group C), and corn oil (control or Group D) daily via gavage for 15 days. The rats were sacrificed and oxidative damages, pro-inflammatory cytokines (TNF-α, IL-1β), and histopathological changes were determined in the lung, liver, kidney, heart, and testis tissues as well as plasma. According to our result, administration of CPF caused a significant increase in malondialdehid level and catalase activity while a significant decrease in superoxide dismutase activity in all tissues. In addition, a significant decrease in TNF-α observed in all tissues and plasma duo to the CPF. Histopathological evaluation of CPF-treated samples revealed a dose-dependent tissue toxicity in the liver, heart, lung, and kidney with less sensitivity of testicular and kidney tissues. These results suggest the potential of CPF in inducing oxidative stress at low doses and short duration time with similar trends in different tissues. As well as, due to the effects of CPF on some pro-inflammatory mediators, more comprehensive studies are recommended.

Ultrastructural and biochemical studies on the potential effects of Moringa oleifera seed oil against nephrotoxicity induced by sofosbuvir in albino rats

The hepatitis C virus (HCV) causes both acute and chronic hepatitis which spread worldwide and accompanied with severe complications in long period of injury. Sofosbuvir (sofo) is a new drug for HCV treatment. Although it has an effective potential in reducing HCV load, its use was accompanied by some side effects. Moringa oleifera (MO) seed oil is natural food-supplemented oil has many pharmaceutical properties which give the plant the ability to reduce or improve the side effects of many insults. This work aimed to determine the possible protective effects of MO seed oil against sofo-nephrotoxicity. Four experimental groups were used; the control group, MO oil group was orally given MO seed oil (2ml/kg/day), sofo group was orally given sofo (36mg/kg/day) and sofo and MO oil group was orally administered sofo, then after 2 hours they were given MO oil. The rats received all doses daily for eight weeks. Twenty four hours following the last injection, rats were anesthetized, sacrificed, the two kidneys were quickly removed and the blood samples were withdrawn for complete blood count (CBC) and determination of the activity of superoxide dismutase (SOD) and the level of glutathione (GSH). Sofosbuvir induced marked ultrastructural changes and significant decrease in SOD activity and GSH level. In addition, CBC of the same groups showed significant decrease in the mean corpuscular value and the mean corpuscular hemoglobin and significant increase in red blood cells count. On the other hand, co-treatment with MO seed oil efficiency improved sofo-induced nephrotoxicity which was evident from the disappearance of most of the ultrastructural changes and improving SOD activity and GSH level. Conclusions: Moringa oleifera seed oil may improve the ultrastructural and biochemical changes associated with nephrotoxicity induced by sofo due to its antioxidant and anti-inflammatory constituents.

MicroRNA-18-5p inhibits the oxidative stress and apoptosis of myocardium induced by hypoxia by targeting RUNX1.

Acute myocardial infarction (AMI) is the main cause of sudden death in the world. The aim of this paper was to explore the role of microRNA-18-5p (miR-18-5p) in myocardial infarction (MI) and its potential mechanism. The expression of miRNA and protein was detected using quantitative reverse-transcription polymerase chain reaction (RT-PCR) analysis and Western blot. The level of oxidative stress of cardiomyocytes was evaluated by detecting the contents of Superoxide dismutase (SOD), Reactive oxygen species (ROS) and Malondialdehyde (MDA). Caspase-3 activity assay, flow cytometry and TUNEL staining were employed to evaluate apoptosis of myocardium. Dual-Luciferase reporter gene assay was used to prove whether miR-18-5p targeted RUNX1. MiR-18-5p was down-regulated in hypoxia-treated H9c2 cells. Hypoxia treatment induced oxidative stress and apoptosis of H9c2 cells. The oxidative stress of H9c2 was manifested by the decrease of SOD activity, the increase of ROS and MDA levels, and the apoptosis of H9c2 was shown by the increase of caspase-3 activity and apoptosis rate. MiR-18-5p mimic was transfected into H9c2 cells and successfully up-regulated miR-18-5p. And overexpression of miR-18-5p markedly inhibited the oxidative stress and apoptosis caused by hypoxia in H9c2 cells. Through bioinformatics analysis and Dual-Luciferase reporter gene assay, RUNX1 was proved to have binding sites for miR-18-5p. Furthermore, knocking down RUNX1 using small interfering RNA-RUNX1 (siR-RUNX1) significantly protected H9c2 cells from oxidative stress and apoptosis. MiR-18-5p expression was decreased in hypoxia-treated H9c2 cells. Overexpression of miR-18-5p alleviated hypoxia-induced oxidative stress and apoptosis in H9c2 cells via targeting RUNX1.

Assessment of lipophilic fluorescence products in β-amyloid-induced cognitive decline: A parallel track in hippocampus, CSF, plasma and erythrocytes.

Oxidative stress implicates in Alzheimer's disease (AD) pathophysiology, and associates with the creation of end products of free radical reactions, are known as lipophilic fluorescent products (LFPs). This study aimed to evaluate the probable parallel alterations in the spectral properties of the LFPs in the hippocampus tissues, cerebrospinal fluid (CSF), plasma, and erythrocytes during AD model induction by intra-cerebroventricular (ICV) amyloid β-protein fragment 25-35 (Aβ) injection. Male rats received an intra-ICV injection of Aβ. Hippocampus, CSF, plasma, and erythrocytes were harvested at 5, 14, and 21days after Aβ injection. The fluorescent intensity of LFPs was assessed by spectrofluorimetry using synchronous fluorescence spectra 25 (SYN 25) and 50 (SYN 50) in the range of 250-500nm. Hippocampal tissue malondialdehyde (MDA) and superoxide dismutase (SOD) were also measured. Cognitive alterations were evaluated using Morris water maze (MWM) test. The parallel significant rise in the fluorescence intensity of LFPs was detected in the hippocampus, CSF, plasma, and erythrocytes, 14, and 21days after ICV-Aβ injection. These alterations were found in both types of synchronous spectra 25, and 50, and were coincided with hippocampal cognitive decline, the MDA rise, and decrease of SOD activity. There was a positive correlation between hippocampus homogenate, and plasma or CSF rise in fluorescence intensity. Data showed that the Aβ increased hippocampal MDA, and decreased SOD activity, led to a higher rate of oxidative products and subsequently resulted in an increase in LFPs fluorescence intensity during the development of cognitive decline. LFPs' alterations reflect a comprehensive view of tissue redox status. The fluorescence properties of LFPs indicate their composition, which may pave the way to trace the different pathological states.

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.

ORAL VACCINATION AGAINST YERSINIA RUCKERI: OXIDATIVE STRESS BIOMARKERS IN THE GILLS OF RAINBOW TROUT (ONCORHYNCHUS MYKISS WALBAUM)

The aim of this study was to assess the effect of oral vaccination against Yersinia ruckeri based on oxidative stress biomarkers in the gills of rainbow trout (Oncorhynchus mykiss Walbaum). The vaccine consisted of three Y. ruckeri strains (O1 serotype) that originated from rainbow trout cultured on different farms, where fish exhibited clinical signs of enteric redmouth disease. The concentrated vaccine was incorporated into the fish food; treatment was delivered three times at one-day intervals. Two months after immunization, gills were sampled. The vaccination against Y. ruckeri resulted in non-significant changes in TBARS level as lipid peroxidation marker, aldehydic and ketonic derivatives of oxidatively modified proteins level in the gills of trout at the second month after immunization against Y. ruckeri. A significant decrease in superoxide dismutase activity (by 36%, p = 0.002) compared to untreated controls occurred. The alterations in markers of oxidative stress suggest that antioxidant defenses may contribute to the balance between oxidative modification of proteins and antioxidant defenses in the gills of trout vaccinated against Y. ruckeri. We did not find any alterations in the gills after 60 days of immunization. This is likely a result of long-term adaptation to immunization. Understanding the role of oxidative stress in the tissues of vaccinated trout has important implications for the understanding of the complex physiological changes that occur in immunization and also for improving aquaculture practices to maximize tissue growth and health of vaccinated trout. The oxidative stress biomarkers in the gills were sensitive to vaccination against Y. ruckeri and may potentially be used as biomarkers in evaluating vaccine toxicity in rainbow trout. From a practical point of view, the results may be useful in relation to studies of infections and the development, administration, and uptake of new vaccines applicable to large amounts of fish.

Neuroprotective potential of lignan-rich fraction of Piper cubeba L. by improving antioxidant capacity in the rat's brain.

Piper cubeba contains various types of lignans. These compounds have been found to have potential pharmacological activities, one being a neuroprotector through an antioxidant mechanism, especially in the brain. This study examined the antioxidant activity of the lignan-rich fraction of P. cubeba (LF) in rat brains. The rats were given LF (200 and 400 mg/kg), Vitamin C (200 mg/kg), and a carrier as the control group for one-week p.o. The following day, rat brains were collected for antioxidant tests, including examining lipid peroxide inhibition, superoxide dismutase and catalase activity, and determination of nitric oxide (NO) concentration. The phytochemical compounds were analyzed with thin-layer chromatography (TLC), ultra-high performance liquid chromatography-tandem mass spectrometry (UPLC-MS), and gas chromatography-mass spectrometry (GC-MS). Test results show that the LF of both doses of 200 and 400 mg/kg could significantly increase antioxidant activity in the brain by inhibiting lipid peroxidation. LF could also increase catalase, despite the decrease in superoxide dismutase activity. Reduction in NO only occurred in the LF-200 group, while LF-400 showed insignificant results compared to the control group. In conclusion, LF showed potential as an antioxidant in the brain and could be beneficial for treating neurological diseases.

Spondias mombin leaf extract ameliorates cerebral ischemia/reperfusion-induced cardiohepatorenal oxidative stress in rats

BackgroundStroke remains a leading cause of mortality and morbidity worldwide. Ischemic stroke is the most prevalent type of stroke and it is characterized by increased oxidative stress and other pathophysiological processes resulting from the reduction of blood flow to the brain. Medicinal plants have been reported to protect against oxidative stress and possess therapeutic potential for the management of stroke. In particular, Spondias mombin leaf extracts have been reported to possess antioxidant and neuroprotective properties. However, the ability of Spondias mombin leaf extract to protect distant organs against ischemicstroke mediated oxidative stress is not yet established. This study therefore evaluated the protective effects of Spondias mombin leaf extract (SML) on bilateral common carotid artery occlusion/reperfusion (BCCAO/R) ischemicstroke model-induced cardiac, hepatic, and renal oxidative stress in rats. MethodMale Wistar rats underwent 30 min of BCCAO and 24 h of reperfusion. Some groups of animals were post-treated with SML (25–100 mg/kg) or quercetin (20 mg/kg). Markers of oxidative stress were evaluated in the heart, liver, and kidney of the experimental animals. ResultsBCCAO/R significantly (p < 0.0001) induced oxidative stress in the heart, liver, and kidney of rats. This was reflected in decreased superoxide dismutase activity and reduced glutathione level. Also, there was increased lipid peroxidation, elevated nitric oxide level, and increased activity of myeloperoxidase. Post-treatment with SML significantly (p < 0.05) ameliorated BCCAO/R-induced oxidative stress in all the organs. ConclusionsCerebral ischemia/reperfusion significantly induced oxidative stress in the heart, liver, and kidney of rats and Spondias mombin leaf extract showed appreciable therapeutic potential against post-stroke cardiohepatorenal oxidative damage.