Antioxidant Markers Research Articles

Evaluation of Testicular Function and Structural Changes of Wistar Rats Following Antiretroviral Exposure: Protective Role of Cyperus Esculentus.

Long-term antiretroviral drug toxicity may exacerbate the impact of HAART-Cyperus esculentus (C. esculentus) interactions on testicular function in HIV-infected individuals. This study examined the ability of C. esculentus plants to treat testicular dysfunction, which is thought to be a probable side effect of antiretroviral toxicity. Adult Wistar male rats weighing 90-110 g were divided into six groups and administered the prescribed treatments. In addition to testicular histology and stereological parameters, testosterone levels, follicle-stimulating hormone levels, antioxidant markers, malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione levels were also evaluated. The adverse consequences of highly active antiretroviral therapy (HAART) include considerable loss of germ cells, enlargement of the tubular lumen, widening of interstitial gaps, and severe hypocellularity. Compared to the other treatment groups, MDA levels dramatically increased, whereas GSH and antioxidant enzyme (SOD) levels significantly decreased. Testicular architecture was largely conserved after treatment with C. esculentus, with a notable increase in the cellular densities of germinal and interstitial cells and a notable decrease in the tubular lumen. Vacuolation, architectural malformations, and hypoplastic changes were reduced. Significant improvements were also observed in C. esculentus in terms of elevated antioxidant SOD and GSH levels and decreased MDA levels. C. esculentus reduced architectural distortions and testicular dysfunction caused by HAART, and improved testicular morphology. Further exploration of these pathways is required.

Evaluation of antidiabetic and antioxidant activity of methanolic extract of Limonia acidissima leaves in alloxan-induced diabetic wister albino rats: a randomized controlled experimental study

Objectives: The present study was carried out to find graded-doses antidiabetic and antioxidant activities of methanolic extract of Limonia acidissima (MELA) leaves in rats. Materials and Methods: Male Wistar rats were randomly divided into 6 groups (n=8): Normal control, Diabetic control (Alloxan-induced), and test groups where varying doses of MELA (100mg/kg, 200mg/kg, and 400mg/kg) or Metformin (100mg/kg) administered post-alloxan induction. Random blood sugar (RBS) levels were estimated at specific intervals over a 28-day period. Moreover, antioxidant markers (malondialdehyde, superoxide dismutase, and reduced glutathione) were assessed on day 28. Histopathological examination of pancreatic tissue was conducted. Results: Overall, mean RBS levels decreased at all intervals. There was a significant decrease in median malondialdehyde, an increase in median superoxide dismutase, and reduced glutathione levels (all p-values<0.0001). The change in RBS (p-values<0.0001) and antioxidants (p-value>0.05) levels was greater in Group VI than in Group V. On histopathology, Groups VI and V demonstrated regeneration of necrotic β-cells in the islets, and this was more pronounced than Group IV. Conclusion: Results of our study suggested that MELA possesses dose-dependent significant antidiabetic and antioxidant activity.

Synergistic antioxidant and anti-inflammatory effects of combined supplementation with oral zinc and dietary Moringa oleifera leaf in streptozotocin-induced diabetic rats

Individual interventions with zinc or M. oleifera leaf powder have shown some promise in managing diabetes-induced oxidative stress and inflammation. This study examined the synergistic effect of oral zinc and dietary M. oleifera leaf supplementation on the serum antioxidant and anti-inflammatory activities in streptozotocin-induced diabetic rats. Seven groups of 56 rats were used in the experiment: (1) normal rats + normal diet, (2) normal rats + 3% M. oleifera leaf-supplemented diet, (3) non-treated diabetic rats, (4) diabetic rats + 200 mg/kg metformin, (5) diabetic rats + 3% M. oleifera leaf-supplemented diet, (6) diabetic rats + 100 mg/kg oral zinc sulfate, and (7) diabetic rats + 3% M. oleifera leaf-supplemented diet + 100 mg/kg oral zinc sulfate. ELISA assay kits were used for antioxidant and anti-inflammatory markers respectively. The results suggest that when all treated diabetic groups were compared with non-treated diabetic control at p<0.05, only groups 4 and 7 showed a significant increase in superoxide dismutase activity. Only group 5 showed a significant increase in reduced glutathione. No significant changes were observed in catalase and the total antioxidant capacity. MDA decreased significantly in group 7 only. There was a significant reduction in interleukin-6 in groups 6 and 7. Only group 7 showed significantly reduced C-reactive protein. Tumor necrosis factor-α reduced significantly in group 6 only. Overall, the combined supplementation with zinc and M. oleifera outperformed the individual treatments with either zinc or M. oleifera in ameliorating diabetes-induced oxidative stress and inflammation, indicating a possible synergistic effect of their combination.

Immunohistochemical and morphological changes associated with hepatic damage in lead acetate-induced toxicity and mitigatory properties of naringin in cockerel chicks.

Lead (Pb) toxicity constitutes a major health hazard to both humans and animals especially in the developing countries. It is a ubiquitous environmental contaminant found in the air essentially because of unregulated mining and other industrial activities. Lead can be found naturally in the soil thus, contaminating crops for human and animal food, as well as run-off water and air pollution. Intensively and extensively reared domestic chickens are exposed to contamination via inhalation and ingestion of contaminated food materials. Naringin, a product from citrus plant has been described to possess excellent metal chelating ability. Naringin is rich in flavonoid with attendant antioxidant, anti-autophagy, anti-inflammatory, hepatoprotective and cardio-nephroprotective properties. This study was conducted to investigate the hepatoprotective and modulation of oxidative stress in commercial cockerel chickens by Naringin. Thirty-six commercial cockerel chickens were randomly assigned into six groups A-F of six birds each viz: Group A served as control group while groups B, C, and D received Lead acetate at 300 ppm via drinking water continuously till the end of the experiment. In addition, groups C and D were treated with Naringin at 80 mg/kg and 160mg/kg, respectively, via oral gavage for 8 weeks. Groups E and F were administered naringin only at 80mg/kg and 160mg/kg respectively for eight weeks. Pb toxicity induced degenerative changes in the histological sections as well as, higher expression of hepatic caspase 3 as shown by immunohistochemistry. There was increased oxidative stress markers (H2O2, MDA) and depletion of the antioxidant defense system markers SOD, GPx, GSH, and GST. It concluded that Co- treatment with Naringin ameliorated oxidative stress, enhanced antioxidant defense system, reduced the expression of hepatic caspase 3 thus, offering protection against lead acetate-induced derangements in the liver of commercial cockerel chickens.

Oxidative stress and antioxidants markers in individuals with thyroid hormones dysfunction

Introduction and aim. Thyroid hormone abnormalities have been associated with oxidative changes in human beings. The aim of the study was to evaluate the oxidative stress marker and antioxidants status in individuals with thyroid hormone dysfunction in Ekiti State. Material and methods. A total of eighty samples were recruited in this study comprising forty subjects with thyroid hormones dysfunction and forty apparently healthy controls. Malondialdehyde (MDA), reduced glutathione (GSH) and catalase were determined spectrophotometerically. Results. MDA was non-significantly higher (p>0.05) in subjects (4.33±0.84 nmol/mL) compared with control (4.12±0.63 nmol/mL), catalase was non-significantly higher (p>0.05) in subjects (199.36±20.21 µm/mL) compared with control (181.55±16.61 µm/mL), while GSH was significantly lower (p<0.05) in subjects (79.31±10.12 µmol/mL) compared with control (127.21±7.29 µmol/mL). Conclusion. It can be concluded that the increase in the reactive oxygen species accompanied with impairment of the antioxidant system occurs in patients with thyroid hormone dysfunction. Hypothyroidism and hyperthyroidism induces disequilibrium of the oxidative/anti-oxidative balance that can lead to subsequent development of inflammation and associated diseases.

Dietary Tartaric Acid Improves Growth Performance, Gut Microbiota, Digestive Enzyme Activities, Hemolymph Immunity, Antioxidant Markers, and Disease Resistance against Vibrio parahaemolyticus in Pacific White Shrimp

Tartaric acid (TA) is an organic acid whose properties in aquaculture have not yet been comprehensively studied. In the current research, the effect of dietary TA on growth indices, gut microbiota, the level of digestive enzymes, antioxidant and immunological markers, and survival rate following immersion challenge with Vibrio parahaemolyticus (14 days) in Litopenaeus vannamei were investigated. To achieve this, 600 shrimp (3.26 ± 0.05 g) were tested with pellets supplemented with five distinct concentrations of TA including 0 (TA0), 2.5 (TA2.5), 5 (TA5), 7.5 (TA7.5), and 10 g/kg (TA10) for 56 days. The results showed that the growth performance, feed utilization, gut lactic acid bacteria (LAB) count, and activity of digestive enzymes were markedly elevated in the groups receiving diets incorporated with 5 and 7.5 g/kg of TA. The highest total hemocyte count (THC), hyaline cell (HC), and semi-granular cell (SGC) counts were detected in shrimp fed with the TA7.5 diet. Hemolymph immune responses including LYZ (lysozyme), alkaline phosphatase (AKP), acid phosphatase (ACP), and phenol oxidase (PO) activities were significantly enhanced in all TA-treated groups. Dietary TA7.5 significantly boosted all antioxidant enzymes. In addition, malondialdehyde (MDA) content illustrated a significant decrease in shrimp fed with diets supplemented with 2.5–10 g/kg TA when compared with specimens fed with TA0. The survival rate following the immersion challenge with Vibrio parahaemolyticus markedly increased in all shrimp treated with 2.5–10 g/kg TA compared to TA0, irrespective of the dosage. However, the dietary inclusion of TA7.5 resulted in the highest survival rate. Based on the outcomes, dietary TA, especially at the concentration of 7.5 g/kg, is proposed to promote the growth performance and immunological indicators of L. vannamei.

Research on the quality markers of antioxidant activity of Kai-Xin-San based on the spectrum-effect relationship.

Background: Kai-Xin-San (KXS) is one of the classic famous traditional Chinese medicine prescriptions for amnesia, which has been applied for thousands of years. Modern pharmacological research has found that KXS has significant therapeutic efficacy on nervous system diseases, which is related to its antioxidant activity. However, the antioxidant material basis and quality markers (Q-makers) of KXS have not been studied. Objective: The objective of this study is to explore the Q-makers of antioxidant activity of KXS based on spectrum-effect relationship. Methods: Specifically, the metabolites in KXS extracts were identified by UPLC-Q-Exactive Orbitrap MS/MS. The fingerprint profile of KXS extracts were established by high-performance liquid chromatography (HPLC) and seven common peaks were identified. Meanwhile, 2, 2-diphenyl-1-picrylhydrazyl (DPPH) test was used to evaluate the free radical scavenging ability of KXS. The spectrum-effect relationship between its HPLC fingerprint and DPPH free radical scavenging activity was preliminarily examined by the Pearson correlation analysis, grey relation analysis (GRA), and orthogonal partial least squares discrimination analysis (OPLS-DA). Further, the antioxidant effect of KXS and its Q-makers were validated through human neuroblastoma (SH-SY5Y) cells experiment. Results: The results showed that 103 metabolites were identified from KXS, and the similarity values between HPLC fingerprint of twelve batches of KXS were greater than 0.900. At the same time, the results of Pearson correlation analysis showed that the peaks 8, 1, 14, 17, 18, 24, 16, 21, 15, 13, 6, 5, and 3 from KXS were positively correlated with the scavenging activity values of DPPH. Combined with the results of GRA and OPLS-DA, peaks 1, 3, 5 (Sibiricose A6), 6, 13 (Ginsenoside Rg1), 15, and 24 in the fingerprints were screen out as the potential Q-makers of KXS for antioxidant effect. Besides, the results of CCK-8 assay showed that KXS and its Q-makers remarkably reduced the oxidative damage of SH-SY5Y cells caused by H2O2. However, the antioxidant activity of KXS was decreased significantly after Q-makers were knocked out. Conclusion: In conclusion, the metabolites in KXS were successfully identified by UPLC-Q-Exactive Orbitrap MS/MS, and the Q-makers of KXS for antioxidant effect was analyzed based on the spectrum-effect relationship. These results are beneficial to clarify the antioxidant material basis of KXS and provide the quality control standards for new KXS products development.

Novel quinazolinone Derivatives: Design, synthesis and in vivo evaluation as potential agents targeting Alzheimer disease

Since Alzheimer disease is one of the most prevalent types of dementia with a high mortality and disability rate, so development of multi-target drugs becomes the major strategy for battling AD. This study shows the development of a series of quinazolinone based derivatives as novel, multifunctional anti-AD drugs that exhibit both cholinesterase inhibitoryand anti-inflammatory properties. The preliminary results of the in vitro AChE inhibition activity showed that compounds 4b, 5a, 6f, 6h and 7b were better represented for further evaluation. Furthermore, in-vivo AChE inhibition activity and behavior Morris water maze test against donepezil as reference drug were evaluated. Additionally, hippocampal inflammatory markers; TNF-α, NFĸB, IL-1β and IL-6 and antioxidant markers; SOD and MDA were assessed to evaluate the efficacy of quinazolinone derivatives against AD hallmarks. The results showed that 6f, 6h and 7b have promising anti-acetylcholinesterase, anti-inflammatory and antioxidant activities thus, have a significant effect in treatment of AD. Moreover, Histopathological examination revealed that 6f, 6h and 7b derivatives have neuroprotective effect against neuronal damage caused by induced scopolamine model in mice. Finally, the binding ability of the synthesized derivatives to the target, AChE was investigated through molecular docking which reflected significant interactions to the target based on their docking binding scores. Hence, the newly designed quinazolinone derivatives possess promising anti-acetylcholinesterase activity and challenging for the management of AD in the future.

Therapeutic effects of the combination of moderate-intensity endurance training and MitoQ supplementation in rats with isoproterenol-induced myocardial injury: The role of mitochondrial fusion, fission, and mitophagy

IntroductionMitochondrial dysfunction causes myocardial disease. This study investigated the effects of MitoQ alone and in combination with moderate-intensity endurance training (EX) on cardiac function and content and mRNA expression of several proteins involved in mitochondrial quality control in isoproterenol (ISO)-induced heart injuries MethodsSeven groups of CTL, ISO, ISO-EX, ISO-MitoQ-125, ISO-MitoQ-250, ISO-EX+MitoQ-125, and ISO-EX+MitoQ-250 were assigned. Rats were trained on a treadmill, and the MitoQ groups received MitoQ in drinking water for 8 weeks, starting one week after the induction of heart injury. Arterial pressure and cardiac function indices, mRNA expression, protein content, oxidant and antioxidant markers, fibrosis, and histopathological changes were assessed by physiograph, Real-Time PCR, immunofluorescence, calorimetry, Masson’s trichrome, and H&E staining, respectively. ResultsThe impacts of MitoQ-125, EX+MitoQ-125, and EX+MitoQ-250 on arterial pressure and left ventricular systolic pressure were higher than MitoQ-250 or EX alone. ± dp/dt max were higher in ISO-EX+MitoQ-125 and ISO-EX+MitoQ-250 than ISO-MitoQ-125 and ISO-MitoQ-250 groups, respectively. Histopathological scores and fibrosis decreased in ISO-EX, ISO-MitoQ-125, ISO-EX+MitoQ-125, and ISO-EX+MitoQ-250 groups. The restoration of MFN2, PINK-1, and FIS-1 changes was higher in ISO-EX+MitoQ-125 and ISO-EX+MitoQ-250 than ISO-EX, ISO-MitoQ-125 and ISO-MitoQ-250 groups. The expression of MFN2 and PINK-1 was lower in ISO-MitoQ-125 and ISO-EX+MitoQ-125 than ISO and CTL groups. The expression of FIS-1 in ISO-EX and ISO-EX+MitoQ-250 increased compared to CTL and ISO groups. MDA decreased in ISO-MitoQ-125 and ISO-EX+MitoQ-125 groups. ConclusionExercise and MitoQ combination have additive effects on cardiac function by modulating cardiac mitochondria quality. This study provided a possible therapy to treat heart injuries.

Relationship between Aspartame-Induced Cerebral Cortex Injury and Oxidative Stress, Inflammation, Mitochondrial Dysfunction, and Apoptosis in Sprague Dawley Rats.

There are emerging concerns about the potential cerebral cortex injury from aspartame due to the accumulation of the various neurotoxic metabolic components in the central nervous system after long-term dietary exposure. The aim of this study was to evaluate the effect of oral aspartame consumption on cerebral cortex injury in the rat brain, and further evaluate the various underlying molecular mechanisms, with a special focus on oxidative stress, inflammation, mitochondrial dysfunction, and apoptosis pathways. Sprague Dawley rats (nineteen, female) were randomly sub-divided into three groups: (i) normal diet with vehicle: control group (five rats), (ii) low dose of aspartame group (LA): seven rats received 30 mg/kg body weight (bw) daily doses of aspartame, (iii) high dose of aspartame group (HA): seven rats received 60 mg/kg bw daily doses of aspartame. After 8 weeks, the LA and HA groups showed lower expression levels of brain-derived neurotrophic factor (BDNF), antioxidant enzyme activity (SOD2, CAT), antioxidant marker (Nrf2), inflammatory response (IκB), mitochondrial biogenesis (Sirt1, PGC1α, Nrf1, TFAM), mitochondrial DNA (mtDNA) copy number, and apoptosis-related proteins (Bax, Caspase-3) expressions. Aspartame administration also elevated oxidative stress levels (Malondialdehyde, MDA), 8-hydroxy-2-deoxy guanosine (8-OHdG), PGE2 and COX-2 expressions, pro-inflammatory cytokines (TNFα, IL6, IL1β), antioxidant marker expression (Keap1), inflammatory responses (iNOS, NFκB), and glial fibrillary acidic protein (GFAP) levels in the cerebral cortex of the rats, thereby contributing to the reduced survival of pyramidal cells and astrocyte glial cells of the cerebral cortex. Therefore, these findings imply that aspartame-induced neurotoxicity in rats' cerebral cortex could be regulated through four mechanisms: inflammation, enhanced oxidant stress, decreased mitochondrial biogenesis, and apoptosis pathways.

Enhancement of cardiac angiogenesis in a myocardial infarction rat model using selenium alone and in combination with PTXF: the role of Akt/HIF-1α signaling pathway

Ischemic heart diseases such as myocardial infarction (MI) are a global health problem and a leading cause of mortality worldwide. Angiogenesis is an important approach for myocardial healing following ischemia. Thus, this study aimed to explore the potential cardiac angiogenic effects of selenium (Se), alone and in combination with the tumor necrosis factor-alpha inhibitor, pentoxifylline (PTXF), via Akt/HIF-1α signaling. MI was induced in rats using two subcutaneous doses of isoprenaline (ISP) at a 24-h interval (150 mg/kg). One week later, rats were orally given Se (150 µg/kg/day), PTXF (50 mg/kg/day), or Se/PTXF combination. ISP-induced myocardial damage was evident by increased HW/TL ratios, ST segment elevation, and increased serum levels of CK-MB, LDH, and troponin-I. ISP increased the cardiac levels of the lipid peroxidation marker MDA; the pro-inflammatory cytokines IL-6, IL-1β, and TNF-α; and the pro-apoptotic protein Bax and caspase-3. In contrast, the cardiac levels of the antioxidant markers GSH and SOD and the anti-apoptotic marker Bcl-2 were reduced. Furthermore, ISP markedly increased the cardiac levels of p-Akt and HIF-1α proteins and the cardiac gene expression of ANGPT-1, VEGF, and FGF-2. Treatment with Se both alone and in combination with PTXF ameliorated the ISP-induced myocardial damage and further increased cardiac angiogenesis via Akt/HIF-1α signaling. Se/PTXF combined therapy was more beneficial than individual treatments. Our study revealed for the first time the cardiac angiogenic effects of Se both alone and in combination with PTXF in myocardial infarction, suggesting that both may be promising candidates for clinical studies.Graphical

Hepatoprotective Effect of Nicotinamide Versus Lead-Motivated Hepatotoxicity in Rats via Correcting Effect on Nuclear Factor-kβ Pathway and Glutathione Metabolism.

Lead (Pb) poisoning is one of the pivotal environmental issues and prompts liver dysfunction by elevating oxidative stress and inflammation. Nicotinamide (NA) deficiency enhances sensitivity to Pb toxicity. So, we investigated the effect of nicotinamide (NA) on the rat's liver histopathological and biochemical profiles in a rat model of Pb toxicity. Thirty-six rats were divided into four groups (nine rats at each): normal (N), lead toxicity (Pbt), and NA-treated N and Pbt groups. Treated groups took NA (180 mg/L in drinking water for one month). Pb intoxication was motivated in rats by acquiring 50 mg/L lead acetate in drinking water. Oxidative stress markers (advanced oxidation protein products and malondialdehyde), antioxidant markers (total glutathione, reduced glutathione to oxidized glutathione ratio, ferric ion reducing power, catalase, and paraoxonase-1), and inflammatory markers (hepatic nuclear factor-kβ expression, interleukin 1β level, and myeloperoxidase activity) in sera and liver homogenates were determined. In addition, the biochemical parameters of the liver function were measured. Finally, the liver of rats was evaluated by histopathological observation. NA corrected lead-persuaded biochemical and histopathological changes in the rat's liver. In addition, treatment decreased Pb, oxidative stress, and inflammatory markers in the sera and liver homogenates of N and Pbt groups. In addition, it elevated antioxidant markers (p < 0.001). NA prevented Pb-induced liver histopathological alternations and reduced liver dysfunction by reducing Pb, oxidative stress, and inflammation. Moreover, raising GSH/GSSG and diminishing the hepatic NF-kβ pathway are cardinal mechanisms of the treatment against Pb-motivated hepatotoxicity in rats.

Roasting Extract of Handroanthus impetiginosus Enhances Its Anticancer Activity in A549 Lung Cancer Cells and Improves Its Antioxidant and Anti-Inflammatory Effects in Normal Cells

The family Bignoniaceae includes Handroanthus impetiginosus trees, which are sparsely distributed in the northeast of Brazil. Natural products play a vital role in the discovery of drugs for various diseases. Many plants have been used as sources of medicines because of their chemical diversity and potent bioactivity. Handroanthus impetiginosus has been used traditionally to cure a wide range of illnesses, such as cancer, oxidative stress, and inflammation. This work highlights the cytotoxicity, cell death, and routes of apoptosis in lung cancer cells (A549) and the anti-inflammatory and antioxidant effects of roasted Handroanthus impetiginosus (lapacho/taheebo) in normal cells. The cell viability assay indicated that puffing roasted taheebo is nontoxic to a normal cell line up to 500 µg/mL but significantly toxic to A549 cells. The roasted lapacho/taheebo also increases reactive oxygen species (ROS) generation in A549 lung cancer cells, and cellular apoptosis via a mitochondrial intrinsic pathway was confirmed. The roasted lapacho/taheebo significantly inhibited both colony formation and cell migration ability, highlighting its potential as an anticancer agent. Additionally, this study demonstrates that roasted taheebo enhanced the expression of genes for BAX accumulation and decreased Bcl-2 gene expression through the p53 signaling pathway. Furthermore, research on the anti-inflammatory properties of roasted taheebo revealed a strong NO inhibition as well as the inhibition of inflammatory mediators (TNF-α, iNOS, COX-2, IL-6, and IL-8) through the NF-κB signaling pathway. However, in H2O2-induced HaCaT cells, roasted taheebo extract significantly reduced oxidative stress by upregulating the level of expression of antioxidative markers (SOD, CAT, GPx, and GST) at 50 μg/mL. As a result, roasted taheebo justifies investigation in animal and clinical trials as a possible source of antioxidants, anti-inflammatory substances, and anti-cancer compounds.

Quercetin nanoparticle ameliorates 5-fluorouracil-induced testicular damage in mice: A biochemical and histological study

Background5-Fluorouracil (5-FU) is one of the most broadly chemotherapeutic compounds employed in treating solid tumors. Quercetin (QU) as a flavonoid has diverse positive clinical applications including antioxidative, antiproliferative, and anti-inflammatory. The current study aims to assess the histopathological changes and anti-oxidative effects of QU loaded with chitosan nanoparticles (QU-NPs) on the testicular injury triggered by 5-FU in mice. MethodsTwenty male albino mice were randomly divided into 4 groups as follows: the control, 5-FU, 5-FU + QU (5 mg/kg), and 5-FU + QU-NPs (5 mg/kg) for 14 days. Oxidative marker [malondialdehyde (MDA)] and antioxidant markers [superoxide dismutase (SOD) and catalase (CAT)] were examined in serum. Testicular damage stemmed from a single dose injection of 5-FU intraperitoneally (i.p.). The control group received normal saline and the treatment groups received QU with i.p. injection for 14 days. ResultsSerum MDA level was lower in the QU and QU-NPs treated groups than in the 5-FU group. Moreover, serum CAT levels were remarkably increased in both the QU- and QU-NPs treated groups compared to the 5-FU group. In the case of SOD, the most considerable difference was found between the 5-FU group and the QU-NPs, but not the QU group. Further, both QU and QU-NPs, particularly the QU-NPs, ameliorated 5-FU-induced testicular tissue damage, as evidenced by a decrease in hyperemia, edema, and vacuolation, and an improvement in the area of seminiferous tubules, and spermatocyte and seminiferous tubule counts. ConclusionNanotechnology and fabrication of QU-NPs can ameliorate the testicular damage caused by 5-FU.

Systematic review and meta-analysis of oxidative stress and antioxidant markers in recurrent aphthous stomatitis

BackgroundWe performed this systematic review and meta-analysis to synthesize all studies that reported the level of oxidative and antioxidative markers in recurrent aphthous stomatitis (RAS) patients compared to controls.MethodsWe registered our study in PROSPERO (CRD42023431310). PubMed, ProQuest, Scopus, EMBASE, Google Scholar, and Web of Science were searched to find relevant publications up to June 5, 2023. The standardized mean differences (SMDs) with 95% confidence intervals (CIs) were calculated. We included 30 articles after multiple stags of screening.ResultsWe found that erythrocyte superoxide dismutase and Glutathione peroxidase activity were significantly lower in patients with RAS compared to healthy controls (SMD = − 1.00, 95%CI = -1.79 to -0.21, p = 0.013, and SMD = − 1.90, 95%CI = -3.43 to -0.38, p = 0.01, Respectively). However, there was not any difference between patients with RAS and healthy controls in erythrocyte Catalase (SMD = − 0.71, 95%CI = -1.56–0.14, p = 0.10). The total antioxidant status (TAS) level, in serum was significantly lower in patients than healthy controls (SMD = − 0.98, 95%CI = -1.57 to -0.39, p = 0.001). In addition, RAS patients had higher levels of serum Malondialdehyde (MDA), Serum total oxidant status, and serum oxidative stress index than healthy controls (SMD = 2.11, 95%CI = 1.43–2.79, p < 0.001, SMD = 1.53, 95%CI = 0.34–2.72, p = 0.01, and SMD = 1.25, 95%CI = 0.25–2.25, p = 0.014, Respectively); However, salivary MDA and TAS, and serum uric acid, vitamin E and C, and reduced glutathione levels of patients with RAS were not different from that of healthy controls.ConclusionsThe relationship between oxidative stress and RAS is well established in this meta-analysis. Although the molecular processes underlying the etiology of this pathology remain unknown, evidence indicating oxidative stress has a significant role in the pathogenesis of RAS has been revealed.

Effect of Varying Levels of Glutamine Addition on the Composition of the Intestinal Flora and the Productivity of Broilers Grown at Various Densities

The purpose of this study was to examine the effects of dietary glutamine on chicken performance, intestinal microbiota, and certain antioxidant markers at various stocking densities. (504) Ross 308 broiler chickens were used in this study; they were jointly grown from day one through week one and then divided into six groups at random. They were raised in floor breeding cages, the transactions were in the following order:1-(G1): the control group (12 birds/ m2), (G2): the high-density group (16 birds/m2) was fed with standard diet and normal water, (G3) and (G4) 12 birds / m2 with the addition of 2.5 or 5 gm Glutamine / liter of drinking water respectively. (G5) and (G6) 16 birds / m2 with the addition of 2.5 or 5 gm Glutamine / liter of drinking water respectively. Adding glutamine to broiler chickens raised at a density of 12 birds/m2 at a concentration of 5 g/l had a positive effect on the productive traits, and the birds raised at a density of 16 birds/m2 showed similar performance for a group of birds raised at a density of 12 birds/m2 after they were treated with glutamine G5 & G6. The results showed a significant decline in the productive traits of these chickens. Lactic Acid Bacteria recorded a significant superiority in the treatments of adding glutamine, even though there were no significant differences in the total number of enter bacteria and E-coli bacteria. It should be noted that this improvement in productive performance was accompanied by an improvement intestinal flora in glutamine addition. We draw the conclusion from this study that administering glutamine to broiler chickens kept in high density could enhance their productivity, and that this was linked to an improvement in the composition of the intestinal flora.

The hepato- and neuroprotective effect of gold Casuarina equisetifolia bark nano-extract against Chlorpyrifos-induced toxicity in rats

BackgroundThe bark of Casuarina equisetifolia contains several active phytoconstituents that are suitable for the biosynthesis of gold nanoparticles (Au-NPs). These nanoparticles were subsequently evaluated for their effectiveness in reducing the toxicity induced by Chlorpyrifos (CPF) in rats. ResultsVarious hematological and biochemical measurements were conducted in this study. In addition, markers of oxidative stress and inflammatory reactions quantified in liver and brain tissues were evaluated. Histopathological examinations were performed on both liver and brain tissues. Furthermore, the native electrophoretic protein and isoenzyme patterns were analyzed, and the relative expression levels of apoptotic genes in these tissues were determined. The hematological and biochemical parameters were found to be severely altered in the group injected with CPF. However, the administration of Au-C. equisetifolia nano-extract normalized these levels in all treated groups. The antioxidant system markers showed a significant decrease (P ≤ 0.05) in conjunction with elevated levels of inflammatory and fibrotic markers in both liver and brain tissues of the CPF-injected group. In comparison, the pre-treated group exhibited a reduction in these markers when treated with the nano-extract, as opposed to the CPF-injected group. Additionally, the nano-extract mitigated the severity of histopathological lesions induced by CPF in both liver and brain tissues, with a higher ameliorative effect observed in the pre-treated group. Electrophoretic assays conducted on liver and brain tissues revealed that the nano-extract prevented the qualitative changes induced by CPF in the pre-treated group. Furthermore, the molecular assay demonstrated a significant increase in the relative expression of apoptotic genes in the CPF-injected rats. Although the nano-extract ameliorated the relative expression of these genes compared to the CPF-injected group, it was unable to restore their values to normal levels. ConclusionOur results demonstrated that the nano-extract effectively reduced the toxicity induced by CPF in rats at hematological, biochemical, histopathological, physiological, and molecular levels, in the group pre-treated with the nano-extract.

P172: A preliminary study for potential protective role of anti-oxidative stress markers for cognitive impairment: glutathione and glutathione reductase.

Objective:We aimed to study the relationship between glutathione (GSH), a key molecule of the anti-oxidant defense system in the blood, and glutathione reductase (GR), which reduces oxidized GSSG to GSH and maintains redox balance, with the prevalence of Alzheimer’s dementia and cognitive decline.Methods:20 with normal cognition and 20 with Alzheimer's dementia who completed the 3rd f/u clinical evaluation over 6 years were selected by matching age and gender. Plasma glutathione (GSH) and glutathione reductase (GR) concentrations were independent variables. Clinical diagnosis and neurocognitive test scores were used as dependent variables indicating cognitive status.Results:The higher the GR, the greater the possibility of normal cognition rather than Alzheimer's dementia. Also, the higher the GR, the higher the neurocognitive score. However, this association was not significant in GSH in any way. After 6 years, the conversion rate from normal cognition to cognitive impairment was significantly higher in the lower 50th percentile of the GR group than in the upper 50th percentile.Conclusion:According to the result of this study, the higher the GR, the lower the prevalence of Alzheimer's dementia and incidence of cognitive impairment, and the higher the cognitive outcome. Therefore, GR can be regarded as a protective biomarker for Alzheimer’s dementia and cognitive decline.

Developing Topics.

Alzheimer's disease is a brain ailment that causes cell degradation and is the leading cause of dementia, which is defined by a deterioration in thinking and independence in routine everyday activities. Insulin possesses neuroprotective and memory-enhancing effects indicating a permissive function for insulin in cognition. Defective insulin signaling promotes Aβ aggregation and accelerates Aβ formation in the brain. Based on this evidence, Alzheimer's is also defined as diabetes of the brain or Type 3 Diabetes. Diabetes was induced in mice by Alloxan (100mg/kg) and sucrose 35% solution. Glucose level was monitored, and test drugs were given accordingly. Behavioral models employed in the current study were elevated plus maze, morris water maze, actophotometer, and novel object recognition test. Biochemicals performed were all mitochondrial complexes, glutathione level, protein carbonyl level, lipid peroxidase, and acetylcholinesterase activity. Histopathological evaluation of the hippocampal region was carried out under a bright field microscope. Alloxan administration produced significant hyperglycemia characterized by a significant increase in serum glucose level as compared to the naïve. During the acquisition test (learning), alloxan-treated mice significantly delayed the escape latency period to reach the submerged platform as compared to the naïve group. However, quercetin and naringenin administration significantly improved memory performance. In novel object recognition, alloxan treated spent more time near the familiar object, and the treatment group spent more time near the novel object. Alloxan treatment also disrupted the mitochondrial levels and lowered the antioxidant enzyme levels, whereas the treatment group significantly reversed the changes. In the present study, alloxan administration caused significant impairment in cognitive behavior as evidenced by the Morris water maze (MWM) test, increased fasting blood glucose oxidative stress [through alteration of endogenous antioxidant markers i.e. superoxide dismutase (SOD), and catalase antioxidant enzyme activity and reduced glutathione (GSH) levels and oxidative stress markers i.e. reactive oxygen species (ROS) and protein carbonyls levels] and increased acetylcholinesterase activity in different areas of the brain (frontal cortex and hippocampus). Administration of quercetin and naringenin in different doses significantly reversed alloxan administration-induced behavioral, biochemical, and cellular alteration in both the frontal cortex as well as in hippocampus.

Effects of crude protein and non-essential amino acids on growth performance, blood profile, and intestinal health of weaned piglets

This study investigated the effect of crude protein (CP) and non-essential amino acid (NEAA) supplementation on the growth performance, blood profile, intestinal morphology, mRNA relative abundance of inflammatory and antioxidant markers, and tight junction proteins in piglets over the first 2 weeks after weaning. Ninety 21-day-old piglets (7.55 ± 0.72 kg) were assigned in a randomized block design to one of three dietary treatments: (1) high CP, a diet with 24% CP; (2) low CP, a diet with 18% CP; and (3) low CP + NEAA, a diet with 18% CP supplemented with 5 g/kg Arg (L-arginine; purity &amp;gt;99%) and 10 g/kg Glu + Gln (minimum 10% L-glutamine and minimum 10% L-glutamate). Piglets were fed with corn-soybean meal basal diets in a 14-day trial. There was an improvement (p &amp;lt; 0.05) in the feed conversion ratio of piglets fed the high-CP diet compared to treatments with low CP or low CP + NEAA. Serum urea nitrogen was higher (p &amp;lt; 0.05) in piglets fed high CP compared to other dietary treatments. In the duodenum, the villus height of animals fed the low-CP + NEAA diets was greater (p &amp;lt; 0.05) than those fed with the high- and low-CP diets. The goblet cell proportion of piglets fed low CP + NEAA or high CP was higher (p &amp;lt; 0.05) compared to low CP. In the jejunum, the crypt depth of the piglets with the high-CP dietary treatment was greater (p &amp;lt; 0.05) in comparison with low CP + NEAA. In the jejunum, IFN-γ mRNA expression was higher (p &amp;lt; 0.05) in animals fed the high-CP diets compared to other dietary treatments. However, superoxide dismutase and occludin mRNA expression were higher (p &amp;lt; 0.05) in animals fed low CP + NEAA than in piglets on the high-CP diets. In the ileum, the number of Peyer’s patches in piglets fed high CP was higher (p &amp;lt; 0.05) compared to other dietary treatments. In conclusion, the high-CP diet (24% CP) improves the feed conversion of piglets in the first 2 weeks after weaning compared to the low-CP diet (18% CP) supplemented or not with NEAA. However, the low-CP diet supplemented with NEAA (Arg, Gln, and Glu) improves intestinal health in piglets by promoting greater villus height and proportion of goblet cells in the duodenum, reducing jejunal crypt depth, and reducing Peyer’s number patches in the ileum. In addition, piglets that received the low-CP + NEAA diet showed an increase in superoxide dismutase and occludin and a lower expression of IFN-γ mRNA.