Glutathione Peroxidase Levels Research Articles

Effects of circuit weight training by intensity on stress hormones and antioxidant capacity in high-school wrestlers

We aimed to investigate the effects of 8-week circuit weight training by intensity on blood stress hormones and antioxidant capacity in highschool wrestlers. This study involved 27 male wrestlers with > 2 years of wrestling experience who were randomly assigned to either a low intensity (n= 13) or a high-intensity circuit weight training group (n= 14). The participants performed circuit weight training for 60 min per session, 3 times per week for 8 weeks. The low- and high-intensity circuit weight training exercises were performed at 50%–60% and 70%–80% of one-repetition maximum for 10 stations, respectively, and 8–15 repeated sessions per station were performed in order. No changes were observed in adrenocorticotropic hormone (ACTH), cortisol, epinephrine, and norepinephrine levels between the two training groups. When compared to levels before the training, ACTH and epinephrine levels decreased, whereas cortisol levels increased. However, no difference was observed in norepinephrine levels. Further, no differences were observed in malondialdehyde (MDA) and glutathione peroxidase (GPX) levels between the two groups. However, MDA and GPX levels were increased from those before training. Changes in superoxide dismutase levels were observed between the two groups, but the change was significant only in the high-intensity circuit weight training group. Long-term training did not increase lipid peroxidation, but increased the activity of antioxidant enzymes that defend against oxidative stress. The antioxidant defense system in tissues can be regulated by exercise intensity as well as physical training status.

3,5-Dihydroxy-4-methoxybenzyl alcohol, a novel antioxidant isolated from oyster meat, inhibits the hypothalamus–pituitary–adrenal axis to regulate the stress response

BackgroundAntioxidants that can scavenge reactive oxygen in the brain and inhibit hyperactivity of the HPA axis are desirable. AimsWe investigated the cerebral translocation of the antioxidant 3,5-dihydroxy-4-methoxybenzyl alcohol (DHMBA) and the effects of DHMBA administration on the hypothalamus–pituitary–adrenal (HPA) axis in stress-loaded rats. MethodsExperiment 1: Plasma and brain DHMBA concentrations were measured over time after oral DHMBA administration to female B6 mice. Experiment 2: Female Wistar Imamichi rats were used. The normal group was not subjected to stress. The stress, DHMBA, and vitamin E groups were subjected to individual and overcrowding stress. Brain and hippocampal 8-hydroxy-2′-deoxyguanosine levels, hippocampal glucocorticoid receptor-α levels, plasma corticosterone levels and RNA levels of glutathione peroxidase 4, catalase, and glutathione reductase in the hippocampus were measured. ResultsIn Experiment 1, DHMBA was not detected in the plasma or brain before DHMBA administration but was detected in both after administration. In Experiment 2, brain and hippocampal 8-hydroxy-2′-deoxyguanosine levels and plasma corticosterone levels were significantly lower in the DHMBA than in the stress group. Glucocorticoid receptor-α levels were higher in the DHMBA than in the stress group. DHMBA increased RNA levels of antioxidant enzymes in the hippocampus. Conclusion: DHMBA was translocated to the brain after administration. DHMBA administration decreased 8-hydroxy-2′-deoxyguanosine levels in the brain and hippocampus, increased hippocampal glucocorticoid receptor-α levels, and decreased the plasma corticosterone concentration, suggesting that DHMBA inhibits hyperactivity of the HPA axis. Nrf2 pathway activity induced by DHMBA resulted in increased antioxidant enzyme levels in the hippocampus

Maternal exposure to nanopolystyrene induces neurotoxicity in offspring through P53-mediated ferritinophagy and ferroptosis in the rat hippocampus

There are increasing concerns regarding the rapid expansion of polystyrene nanoplastics (PS-NPs), which could impact human health. Previous studies have shown that nanoplastics can be transferred from mothers to offspring through the placenta and breast milk, resulting in cognitive deficits in offspring. However, the neurotoxic effects of maternal exposure on offspring and its mechanisms remain unclear. In this study, PS-NPs (50 nm) were gavaged to female rats throughout gestation and lactation to establish an offspring exposure model to study the neurotoxicity and behavioral changes caused by PS-NPs on offspring. Neonatal rat hippocampal neuronal cells were used to investigate the pathways through which NPs induce neurodevelopmental toxicity in offspring rats, using iron inhibitors, autophagy inhibitors, reactive oxygen species (ROS) scroungers, P53 inhibitors, and NCOA4 inhibitors. We found that low PS-NPs dosages can cause ferroptosis in the hippocampus of the offspring, resulting in a decline in the cognitive, learning, and memory abilities of the offspring. PS-NPs induced NOCA4-mediated ferritinophagy and promoted ferroptosis by inciting ROS production to activate P53-mediated ferritinophagy. Furthermore, the levels of the antioxidant factors glutathione peroxidase 4 (GPX4) and glutathione (GSH), responsible for ferroptosis, were reduced. In summary, this study revealed that consumption of PS-NPs during gestation and lactation can cause ferroptosis and damage the hippocampus of offspring. Our results can serve as a basis for further research into the neurodevelopmental effects of nanoplastics in offspring.Graphical

Regulation Mechanisms of the Glutamate Transporter in the Response of Pacific Oyster upon High-Temperature Stress

Glutamate transporters (GLTs) are integral to the glutamatergic system, modulating glutamate homeostasis to enhance resilience and resistance against environmental stress. There are six GLTs identified in the Pacific oyster (Crassostrea gigas), which were categorized into two subfamilies: excitatory amino acid transporters (CgEAATs) and vesicular glutamate transporters (CgVGLUTs). The CgEAATs harbor a GltP domain, while CgVGLUTs feature an MFS domain, both with conserved sequence and structural characteristics. The expression of CgGLTs is elevated during the planktonic larval stage compared to the fertilized egg stage and is constitutively expressed in various tissues of adult oysters, suggesting its critical role in both larval development and the physiological processes of adult oysters. Transcriptomic analysis revealed diverse expression patterns of GLTs in oyster gills after 7 days of high-temperature stress, with CgEAAT3 showing a significant upregulation. A KEGG pathway enrichment analysis identified glutathione metabolism and ferroptosis as prominently enriched pathways. At 48 h after high-temperature stress, the expression levels of Glutathione Peroxidase 4 (CgGPX4) and CgEAAT3, along with elevated Fe content in the gills, significantly increased. Moreover, the RNAi-mediated the inhibition of CgEAAT3 expression under high-temperature stress, resulting in a significant reduction in CgGPX4 expression and a further increase in Fe accumulation in oyster gills. These results indicate that CgEAAT3 contributes to the regulation of ferroptosis and redox homeostasis by modulating CgGPX4 expression. This study provides new insights into the adaptive mechanisms of bivalves to environmental stress.

Immunomodulatory microneedle patch for enhanced Ferroptosis and immunogenic cell death in postoperative tumor therapy

Microneedle technologies have emerged as a promising transdermal drug delivery platform for postoperative tumor therapy. Despite their potential, enhancing intracellular drug delivery to tumor cells and boosting the therapeutic efficiency of microneedles pose significant challenges. Herein, we develop a nanomedicine-loaded microneedle to enhance the induction of ferroptosis and immunogenic cell death for postoperative tumor therapy. This advancement is achieved by pre-formulating small molecule drugs with transition metal and protein templates into nanomedicine. Upon insertion into the tumors, the microneedle rapidly dissolves, facilitating the release and subsequent cellular uptake of the nanomedicine by tumor cells. Notably, the nanomedicine can release Mn ions and ferroptosis-inducer sulfasalazine (SAS) under acidic conditions. Furthermore, the released Mn ions can produce reactive oxygen species, which decrease the levels of glutathione (GSH) and glutathione peroxidase 4 (GPX4) with increased lipid peroxidation and enhanced induction of ferroptosis. Besides, the treatment stimulates immunogenic cell death through the cell surface exposure of calreticulin (CRT) and release of high-mobility group box 1 (HMGB1), which further stimulates dendric cell maturation, T cell infiltration, and macrophage polarization towards the M1 phenotype. Consequently, this strategy significantly inhibits postoperative tumor regrowth and extends overall survival. Our study indicates the potential of the combination of nanomedicine and microneedle to improve postoperative therapeutic efficiency.

Exogenous Nitric Oxide Induces Pathogenicity of Alternaria alternata on Huangguan Pear Fruit by Regulating Reactive Oxygen Species Metabolism and Cell Wall Modification.

Black spot caused by Alternaria alternata is one of the most common postharvest diseases in fruit and vegetables. A comprehensive investigation into its pathogenicity mechanism is imperative in order to propose a targeted and effective control strategy. The effect of nitric oxide (NO) on the pathogenicity of A. alternata and its underlying mechanism was studied. The results showed that treatment with 0.5 mM L-1 of sodium nitroprusside (SNP) (NO donor) increased the lesion diameter of A. alternata in vivo and in vitro, which was 22.8% and 13.2% higher than that of the control, respectively. Exogenous NO treatment also induced endogenous NO accumulation by activating nitric oxide synthase (NOS). In addition, NO triggered an increase in reactive oxygen species (ROS) levels. NO enhanced activities and gene expression levels of NADPH oxidase (NOX), superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase (APX), glutathione peroxidase (GPX), and glutathione reductase (GR). Moreover, NO stimulated cell wall degrading enzymes by activating the corresponding gene expression in vivo and in vitro. These results suggested that exogenous NO promoted the pathogenicity of A. alternata by inducing ROS accumulation and activating antioxidants and cell wall degrading enzymes. The present results could establish a theoretical foundation for the targeted control of the black spot disease in pear fruit.

Anti-fatigue effect of an enzymatically derived deer velvet extract through muscle damage recovery and improvement of antioxidant levels

Ethnopharmacological relevanceDeer velvet (DV) has been extensively used in traditional Oriental medicine to treat various diseases. Its pharmacological spectrum encompasses tonicity, longitudinal bone growth of adolescence, blood retention, hemopoiesis facilitation, enhancement of organ function, physical function improvement, and augmentation of physical vitality. Among its myriad effects, DV notably exhibits anti-fatigue properties; however, its specific mode of action is yet to be fully elucidated. Aim of the studyThis study was undertaken to investigate the anti-fatigue and exercise performance-enhancing effects of YC-1101(HENKIV®), an enzymatically derived DV extract, in C2C12 cell lines and forced swimming mouse models. Materials and methodsThe effect of YC-1101 on increasing cell growth and lowering lactate dehydrogenase (LDH) activity was assessed in C2C12. The antioxidative effects of YC-1101 and its mechanistic underpinnings were also evaluated in C2C12 cells. Moreover, mice were subjected to an exhaustive swimming test subsequent to 3 weeks of YC-1101 extract administration. Fatigue-associated biochemical parameters, such as LDH activity and lactate, superoxide dismutase, glutathione peroxidase, and malondialdehyde levels, were measured in serum and muscle tissues. ResultsYC-1101 significantly promoted myoblast growth and reduced LDH activity, indicative of a cell-proliferative effect. Notably, free radical scavenging assays and analysis of reactive oxygen species production and antioxidant-related mRNA expression corroborated the significant involvement of YC-1101 in antioxidation, an important mechanism in anti-fatigue processes. Furthermore, animal experiments demonstrated prolonged swimming endurance and inhibition of muscle LDH accumulation in forced swimming mouse models. Serum biochemical analysis further revealed significant modulation of the expression of anti-fatigue-related biomarkers. Various bioactive low-molecular-weight DV peptides were enriched in YC-1101 compared to YHC-BE-2038 (a DV extract without enzymatic digestion). The anti-fatigue effect of YC-1101 was significantly stronger than that of YHC-BE-2038. ConclusionsThese findings suggest the potential of YC-1101 as a nutraceutical adjunct in ameliorating fatigue, concurrently facilitating muscle damage recovery, and exerting antioxidant effects via the nuclear factor E2-related factor 2-Kelch-like ECH-associated protein-1 pathway. It can be assumed that the complex action of low-molecular-weight DV peptides produced during the enzymatic degradation process was effective, and the further research is needed.

Supplementing exogenous xylanase improves the liver antioxidant capacity and immune response of Tibetan sheep fed wheat-based diets

Xylanase is a heteropolysaccharide found in the plant cell wall, which aids in the absorption and utilisation of nutrients. When embedded in animal feed, it enhances nutrient availability, leading to improved animal performance. The aim of this study was to explore the effect of xylanase supplementation in wheat-based feeds on the hepatic development, antioxidant capacity, and immune response in Tibetan sheep. Sixty healthy, weaned, non-neutered male lambs (19.35 ± 2.18 kg) were randomly assigned to two equal groups (n = 30 per group). Dietary treatments were: basal diet (H group), and basal diet with 0.2% xylanase supplementation (E group). After a 10–day adaptation period, the feeding trial was carried out for 90 days. The live weight, morphology, antioxidant capacity and immune response were measured. The differential genes in liver were identified by RNA-sequencing. Our results showed that the levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) were significantly higher in E group than in H group (p < 0.05). Enzyme-linked immunosorbent assay (ELISA) revealed that immunoglobulin A (IgA), IgM, and IgG were significantly higher in E group than in H group (p < 0.05). The hepatocytes of sheep fed xylanase diet showed arranged radially into hepatic plates cantered around the central vein, and the plates linked with each other to form a lost-like structure. A total of 4,509 differential genes (DEGs) were identified, among which 4,427 were up-regulated and 82 down-regulated. Additionally, the expression of antioxidant-related genes in cluding catalase (CAT), superoxide dismutase 1 (SOD1), oxidation resistance 1 (OXR1) and glutathione peroxidase 2 (GPX2), and immunity-related gene including mitogen-activated protein kinase 1 (MAPK1), signal transducer and activator of transcription 5B (STAT5B), janus kinase 3 (JAK3) and jun proto-oncogene (JUN) were verified using the quantitative reverse transcription polymerase chain reaction (qRT-PCR). Conclusion: In conclusion, dietary 0.2% xylanase supplementation promoted hepatic antioxidant capacity and immune response via modulating the expression of functional genes in Tibetan sheep.

Hypoxia activates FGF-23-ERK / MAPK signaling pathway in ischemia-reperfusion induced acute kidney injury.

Both hypoxia and fibroblast growth factor-23 (FGF-23) are key factors in ischemia-reperfusion (I/R)-induced acute kidney injury (AKI). This study aimed to explore the relationship between hypoxia and FGF-23 in AKI. An I/R-AKI animal model was established using male BALB/c mice. HK-2 cells, a part of the human proximal tubular epithelial cell line, were subjected to hypoxia/reoxygenation (H/R). qPCR was used to measure FGF-23 and HIF-1α, ELISA was used to measure inflammatory and oxidative stress cytokines. Western blotting used to measure the phosphorylation of ERK level. In I/R mice, the levels of interleukin-6 (IL-6), tumor necrosis factor (TNF-α), malondialdehyde (MDA), and the phosphorylation of extracellular signal-regulated kinase (ERK) were increased, whereas the levels of interleukin-10 (IL-10), superoxide dismutase (SOD), glutathione peroxidase (GPx), and klotho were decreased, compared to the sham operated mice. Silencing the FGF-23 expression in I/R mice normalized the levels of IL-6, IL-10, TNF-α, MDA, SOD, Gpx, and ERK phosphorylation (p-ERK). In HK-2 cells, hypoxia-reperfusion (H/R) elevated the levels of IL-6, TNF-α, MDA, and ERK phosphorylation, but reduced IL-10, SOD, GPx, and klotho levels. Hypoxia induced apoptosis in HK-2 cells but silencing of FGF-23 expression blocked the effects of hypoxia on cell apoptosis, proinflammatory factors levels, oxidative stress response, and p-ERK levels. FGF-23 is a key molecule in AKI, and hypoxia plays a crucial role in AKI by inducing cell apoptosis; however, its role is regulated by FGF-23. FGF-23 affects oxidative stress and the inflammatory response of kidney tissues by activating the ERK/mitogen-activated protein kinase (MAPK) signaling pathway.

PSAT1 is upregulated by METTL3 to attenuate high glucose-induced retinal pigment epithelial cell apoptosis and oxidative stress

BackgroundDiabetic retinopathy (DR) is a major ocular complication of diabetes mellitus, and a significant cause of visual impairment and blindness in adults. Phosphoserine aminotransferase 1 (PSAT1) is an enzyme participating in serine synthesis, which might improve insulin signaling and insulin sensitivity. Furthermore, it has been reported that the m6A methylation in mRNA controls gene expression under many physiological and pathological conditions. Nevertheless, the influences of m6A methylation on PSAT1 expression and DR progression at the molecular level have not been reported.MethodsHigh-glucose (HG) was used to treat human retinal pigment epithelial cells (ARPE-19) to construct a cell injury model. PSAT1 and Methyltransferase-like 3 (METTL3) levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). PSAT1, B-cell lymphoma-2 (Bcl-2), Bcl-2 related X protein (Bax), and METTL3 protein levels were examined by western blot assay. Cell viability and apoptosis were detected by Cell Counting Kit-8 (CCK-8) and TUNEL assays. Reactive oxygen species (ROS), malondialdehyde (MDA), and Glutathione peroxidase (GSH-Px) levels were examined using special assay kits. Interaction between METTL3 and PSAT1 was verified using methylated RNA immunoprecipitation (MeRIP) and dual-luciferase reporter assay.ResultsPSAT1 and METTL3 levels were decreased in DR patients and HG-treated ARPE-19 cells. Upregulation of PSAT1 might attenuate HG-induced cell viability inhibition and apoptosis and oxidative stress promotion in ARPE-19 cells. Moreover, PSAT1 was identified as a downstream target of METTL3-mediated m6A modification. METTL3 might improve the stability of PSAT1 mRNA via m6A methylation.ConclusionMETTL3 might mitigate HG-induced ARPE-19 cell damage partly by regulating the stability of PSAT1 mRNA, providing a promising therapeutic target for DR.

Oxidative damage biomarkers and antioxidant enzymes in saliva of patients with peri-implant diseases

Objectives8-hydroxydeoxyguanosine (8-OHdG) and Malondialdehyde (MDA) are commonly used as markers to evaluate oxidative DNA and Lipid damage in disorders including chronic inflammatory diseases. Superoxide dismutase (SOD) and glutathione peroxidase (GPx) protect tissues against oxidative injury from free oxygen radicals generated by various metabolic processes. The aim of this study was to evaluate 8-OHdG and MDA levels, and SOD and GPx activities in whole saliva of patients with peri-implant diseases.Materials and methodsA cross-sectional study was conducted on a sum of 60 age gender balanced; peri-implantitis (n = 20), peri-mucositis (n = 20) and healthy (n = 20) individuals. Unstimulated whole saliva samples were collected and to determine the clinical condition of each subject; the plaque index (PI), gingival index (GI), peri-implant probing pocket depth (PIPD), peri-implant presence of bleeding on probing (BOP) (with/without suppuration) and radiographic signs of crestal bone loss (BL) were measured. The salivary 8-OHdG level was measured using the ELISA method. SOD, GPx activities and MDA levels were determined spectrophotometrically.ResultsA total of 60 individuals had evaluations of 318 implants. In comparison to the peri-mucositis and peri-implantitis groups, the healthy group had significantly lower PI and GI scores (p < 0.001). The PIPD value differed amongst the groups, with the peri-implantitis group having the highest value (p < 0.001). Compared to the peri-mucositis and control groups, the peri-implantitis group had a significantly higher BL score (p < 0.001 and p < 0.001, respectively). The peri-implantitis group showed a significantly higher 8-OHdG level (p < 0.001; p < 0.001 respectively) than the peri-mucositis and control groups. Compared to the peri-mucositis and control groups, the peri-implantitis group had a significantly higher MDA level (p < 0.001 and p < 0.001, respectively). The peri-implantitis group had a significantly higher SOD level (p < 0.001 and p < 0.001, respectively) in comparison to the peri-mucositis and control groups. There was no significant difference in GPx levels between the peri-mucositis and control groups (p > 0.05), while the peri-implantitis group had significantly lower GPx levels than the peri-mucositis and control groups (p < 0.001 and p < 0.001, respectively).ConclusionsElevated levels of oxidative stress in saliva may indicate the onset of pathological bone loss surrounding the implant and may be an indication of peri-implantitis.Clinical relevanceIn peri-implant diseases, changes may occur in the levels of 8-OHdG, MDA, SOD and GPx in saliva, which may lead to a deterioration in the oxidant/antioxidant balance.

The role of rice husk in Oreochromis niloticus safety enhancement by bio-adsorbing copper oxide nanoparticles following its green synthesis: an endeavor to advance environmental sustainability

Lowering nanoparticles (NPs) toxicity before discharge into aquatic environments and employing agricultural waste materials for environmental sustainability are necessary nowadays. Since this has never been done, this work examines how green CuO NPs treated with rice husk (RH) as a bio-adsorbent may be safer for Nile tilapia (Oreochromis niloticus) than chemically manufactured ones. So, five groups of fish were randomly placed in glass aquaria. One group was a control, and four groups received 50 mg/L green and chemically produced CuO NPs (GS and CS) with and without RH for 24, 48, and 96 h. RH was collected from all groups, and the results showed GS-CuO NPs had a greater adsorptive capacity than CS-CuO NPs after all time intervals. After analyzing fish indicators in all groups compared to the control, higher Cu bioaccumulation was exhibited in the liver and gills. The liver and gills showed elevated levels of glutathione peroxidase (GPx), catalase (CAT), and thiobarbituric acid reactive substances (TBARS), while the levels of glutathione reduced (GSH) were significantly lower. In addition, Cu exposure impaired liver and gill histology. Finally, our results indicated that using RH as an adsorbent for CuO NPs after their green synthesis instead of chemical synthesis before they enter the aquatic environment can enhance the overall health of fish and environmental sustainability.

Toxicodynamics of cadmium in the green mussel Perna viridis (Linnaeus, 1758) using bioenergetic and physiological biomarkers.

This study evaluated the toxicity of cadmium (Cd) on the green mussel Perna viridis, aiming to identify toxicological endpoints and investigate its responses across physiological, bioenergetic, and biochemical parameters. The 96-hour LC50 value for Cd in P. viridis was 3.03 ± 0.12 mg L-1, with a 95% confidence interval of 2.35-3.91 mg L-1. Chronic toxicity tests revealed a No Observable Effect Concentration (NOEC), Lowest Observable Effect Concentration (LOEC), and chronic toxicity values of 0.20, 0.37, and 0.29 mg L-1, respectively. Cadmium accumulation in treated mussels increased 46- to 215-fold compared to the control group. Superoxide dismutase, catalase, glutathione S-transferase, and glutathione peroxidase levels in exposed mussels exhibited a significant increase compared to the control group. The redox index ratio, acetylcholinesterase activity, and lysosomal membrane stability decreased with increasing exposure concentrations. Levels of reduced and oxidized glutathione, glutathione reductase, lipid peroxidation, and metallothionein-like proteins increased in exposed mussels. Clearance rate, respiration rate, and excretion rate decreased in a dose-dependent manner. Protein, carbohydrate, and lipid levels decreased with increasing exposure concentration (p < 0.001). Mitochondrial electron transport system activity increased, while cellular energy allocation (p < 0.001) and scope for growth decreased in a dose-dependent manner (p < 0.01). The significant increase in antioxidants suggests heightened oxidative stress in mussels under Cd exposure. The physiological activities of the mussels were severely affected, ultimately leading to a reduced scope for growth. The toxicological data generated in this study contribute to the development of seawater quality criteria for the metal Cd.

Evaluating the effectiveness of Toxfin and Novasil as dietary aflatoxin-binding agents in broilers for sustaining hepatic antioxidant capacity and intestinal health status during aflatoxin B1 exposure.

To assess the efficacy of Toxfin and Novasil as aflatoxin-binding agents in broilers exposed to aflatoxin B1 (AFB1) from 11 to 30days, 288 mixed-sex Ross 308 broiler chickens were randomly allocated to four dietary groups: control feed, control feed + 0.25mg/kg AFB1, AFB1 feed + 0.3% Toxfin, and AFB1 feed + 0.3% Novasil. The evaluation encompassed growth performance for the grower (11-20days), finisher (21-30days), and overall (11-30days) phases, carcass characteristics, serum biochemical components, liver function enzymes, hepatic antioxidant capacity, AFB1 residue in the liver and kidney, and ileal morphology at 30days, and apparent nutrient digestibility during 29-30days. Exposure to AFB1 significantly resulted in reduced growth efficiency, lowered carcass yields, liver hypertrophy, impaired metabolic and hepatic functions, liver oxidative stress, disrupted ileum architecture, diminished nutrient digestibility, and accumulated AFB1 in the liver and kidney. Conversely, supplementation of Toxfin or Novasil significantly augmented body weight gain (BWG) and reduced feed conversion ratio (FCR) during the finisher and overall phases, elevated BWG in the grower phase, heightened levels of glucose, hepatic protein, and glutathione peroxidase, declined malondialdehyde content, improved apparent metabolizable energy, and lowered AFB1 residues in the liver and kidney. Furthermore, Toxfin inclusion significantly reduced FCR during the grower phase, enhanced European production efficiency factor during the grower and overall phases, augmented dressing percentage, declined proportional liver weight, elevated concentrations of total protein, albumin, and total antioxidant capacity, heightened villus surface area, and boosted crude protein digestibility. To conclude, incorporating 0.3% Toxfin into broilers' feeds confers a more effectual safeguard than Novasil against the deleterious consequences of AFB1 exposure.

Impacts of dietary Ajwain (Trachyspermum ammi L.) on growth, antioxidative capacity, immune responses, and intestinal histology of grey mullet (Liza ramada)

This study investigated the impacts of dietary supplements with ajwain seed extract (ASE) on the growth, biochemical parameters, digestive enzymes, antioxidant activity, immunity, and intestine histology of Liza ramada. Juveniles (N = 450) with an initial weight of 40.12 ± 0.14 g were fed six experimental diets enriched with ASE at 0 (control), 0.2, 0.4, 0.6, 0.8, and 1.0 g/kg diet for 60 days. Results revealed that fish-fed diets containing ASE at levels of 0.6 g/kg or higher exhibited significantly improved growth parameters including final weight, weight gain percentage, and specific growth rate, along with enhanced feed conversion efficiency compared to lower ASE levels and the control diet. Survival rates remained similar across all experimental groups. Digestive enzyme activity, particularly lipase, was highest in groups fed higher ASE levels (≥ 0.4 g/kg diet). Histomorphological analysis of the intestine showed improved villi structures with increasing ASE supplementation, reaching an optimal appearance at 0.8 g/kg. Blood biochemical analysis indicated higher total protein and globulin concentrations, and lower total cholesterol levels in groups with higher ASE intake (≥ 0.4 g/kg diet). Immune parameters increased with increasing ASE concentrations, including lysozyme activity, bactericidal percentage, and nitroblue tetrazolium levels. Antioxidant status, measured through superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and malondialdehyde (MDA) levels, showed significant improvements with ASE supplementation, with optimal dietary ASE levels for maximizing SOD (0.73 g/kg), CAT (0.74 g/kg), GPx (0.83 g/kg), and minimizing MDA (0.73 g/kg) identified through polynomial regression analysis. These findings suggest that ASE supplementation (0.6–0.8 g/kg) positively influences the growth performance, digestive function, gut health, immunity, and antioxidant status of L. ramada, highlighting its potential as a beneficial dietary additive in aquaculture.

Preparation and characterization of cysteine-rich collagen peptide and its antagonistic effect on microplastic induced damage to HK-2 cells

Cysteine (Cys) plays a significant role in the stability and antioxidant capacity of peptide. This study was to prepare Cys-rich collagen peptide and evaluate its preventive effect on microparticle (MPs)-induced HK-2 cell damage. The results showed that the Cys-rich peptides (AMP-C) were successfully prepared from collagen hydrolysate by plastein reaction in the presence of exogenous Cys. The scavenging activities of 2,2-Diphenyl-1-picrylhydrazyl and hydroxyl radical of AMP-C were significantly higher than those of original peptides without Cys. The fraction with molecular weight < 3 kDa (AMP-CA) significantly improved MPs-induced damage and apoptosis of HK-2 cells. Compared with the same fractions lacking Cys (AMP-A), AMP-CA showed better performance in reducing reactive oxygen species and increasing the total superoxide dismutase and glutathione peroxidase levels, which may be related to its down-regulation of Kelch-like ECH-associated protein 1 (Keap1) expression. In addition, AMP-CA showed strong effects on inhibiting interleukin-6, tumor necrosis factor-α, monocyte chemoattractant protein-1, kidney injury molecule-1, and nuclear factor kappa-B levels. Finally, 330 Cys-containing peptides were isolated from AMP-CA, among which Leucine-Glycine-Asparagine-Glycine-Cysteine-Proline (LGNGCP) showed the lowest binding energy with Keap1 protein. In conclusion, the Cys-rich collagen peptide with higher antioxidant activity was successfully prepared by plastein reaction, which alleviated the HK-2 cells damage induced by MPs through antioxidant and anti-inflammatory. Our findings suggested that Cys-rich collagen peptide might be used as a functional food to mitigate health hazards associated with MPs accumulation.

Insights for possible association and impact of thyroidectomy to osteoarthritis

Background and aim of studyThyroidectomy and osteoarthritis have drawn more attention in last decades due to increase various local and systemic risk factors. This study is aimed to determine the association and impact between thyroidectomy and osteoarthritis by serological measurement of most specific related markers.ResultsMeasurement of thyroid markers showed the level of thyroid-stimulating hormone (TSH) was significantly increased, while parathyroid hormone (PTH), triiodothyronine (T3), and thyroxine (T4) levels were decreased in osteoarthritis subjected to thyroidectomy group (OTG) when compared to hyperthyroidism subjected to thyroidectomy group (TG), osteoarthritis group (OG), and healthy control group (CG). Detection the activity of bone markers showed the level of R-factor was significantly elevated concomitant with significant reduction in Dickkopf related protein 1 (DKK1), human hyaluronan-binding protein 2 (HABP2), osteocalcin (OC) in OG and OTG groups, while osteopontin (OPN) and procollagen I C-terminal propeptide (PICP) were significantly increased and decreased in TG and OTG. Furthermore, the level of S100 Calcium binding protein (S100CBP) showed significant decreased in patient’s groups, while TG with OTG groups exhibited significant reduction in sclerostin (SOST) concentration. Regarding the inflammatory markers, the levels of interleukin-1 (IL-1) was increased in the OTG, while the level of interleukin-10 (IL-10) was increased in OG and TG groups, and reduced in OTG. While, the level of transforming growth factor-beta (TGF-β) was decreased in OG and TG associated with significant increases in tumor necrosis factor-alpha level (TNF-α) in OTG. Measurement of oxidant and antioxidant activity markers showed the levels of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) were significantly reduced in all patient’s groups compared to control, except the level of CAT in TG, whereas, malondialdehyde (MDA) level was increased in OG and OTG patients. Furthermore, the levels of Alkaline phosphatase (ALP), C-Reactive protein (CRP), and erythrocyte sedimentation rate (ESR) were increased in all patient groups compared to control, while fatty acid-binding protein (FABP) level was increased in OTG only.ConclusionThis unique study in Iraq is identified the interaction effect and impact of thyroidectomy to osteoarthritis according to the results that showed various changes and degree of correlation of study biomarkers in all patient groups, however more depth of specific quantitative and qualitative studies are required to support this association and the impact claim at molecular level.

Hosta plantaginea (Lam.) Aschers flower modulates inflammation and amino acid metabolism by inhibiting NF-κB/MAPK/JAK-STAT/PI3K-Akt and AMPK pathways to alleviate benign prostatic hyperplasia in rats

Benign prostatic hyperplasia (BPH) is the most common urogenital disease in men with no definitive treatment. Inflammation, androgen imbalance, and oxidative stress play crucial roles in the pathogenesis of BPH. The flower of Hosta plantaginea (Lam.) Ascher is a pivotal medicinal plant in China, used to treat BPH. However, its effect and mechanism against BPH have not been clear. Our aim was to decipher the pharmacodynamics and mechanisms of H. plantaginea flower against BPH. The extract yields and HPLC-based chemoprofile of ethanolic extract (HP) and total flavonoid (TF) of H. plantaginea flowers were used as reference standard to ensure their quality. The testosterone propionate-induced BPH rat model was used to assess the effects of HP and TF. Protein expression, metabolomics, and network pharmacology analyses were performed. Twenty constituents were identified in both HP and TF, with four quantitatively analyzed using the HPLC method. HP and TF demonstrated significant therapeutic effects on BPH, including reduced prostate size and prostatic index, improved pathological injury of prostate, as well as increased levels of testosterone, superoxide dismutase, glutathione, and glutathione peroxidase, along with decreased levels of dihydrotestosterone, 5 alpha-reductase, epidermal growth factor, TNF-α, IL-1β, IL-6, and malondialdehyde. Western blotting assay indicated that HP and TF prominently inhibited the protein expression of phosphorylated p65, IκBα, JNK, p38, Erk1/2, JAK1, STAT3, PI3K, Akt, and AMPKα1 in a dose-dependent manner. Integrating metabolomics and network pharmacology analyses revealed that HP and TF observably regulated 30 differential metabolites and 11 hub genes across the aforementioned pathways, which are closely associated with amino acid metabolism. The proposed comprehensive strategy of in vivo experiments, metabolomics, and network pharmacology studies has demonstrated that HP and TF could alleviate BPH injury in rats by suppressing inflammation, androgen imbalance, oxidative stress, and amino acid metabolism through the inhibition of NF-κB, MAPK, JAK-STAT, PI3K-Akt, and AMPK pathways, which provides novel insights into the potential of H. plantaginea flower as a treatment for BPH.

A Modified Self-micro Emulsifying Liposome for Bioavailability Enhancement of Quercetin and its biological effects

Quercetin (QT) is a chief dietary flavonoid with a myriad of health benefits, however, its poor solubility and low bioavailability restrict its food application. Thus, the present study aimed at enhancing its solubility using a modified self-micro emulsifying system (QT-TPGS-QS). The stability of liposome was assessed via monitoring of its particle indexes (size, zeta potential, PDI, stability towards in-vitro digestion, drug release, and encapsulation efficiency). Further, antibacterial and cellular antioxidant potential of liposomes were determined. QT-TPGS-QS exhibited good optical clarity with a loading ratio of 2.1%. The liposome showed uniform spherical and regular shape (< 100 nm) with a QT release rate of 85.61% ± 0.32% in simulated in-vitro digestion. QT-TPGS-QS demonstrated superior antibacterial activity compared to QT alone against Escherichia coli, Staphylococcus aureus, and Salmonella. In-vitro antioxidant evaluation confirmed that the QT-TPGS-QS exhibited a significantly higher free radical scavenging ability than QT alone. Cellular assay confirmed that QT-TPGS-QS (15 μg/mL) exhibited a good protection effect on oxidative stress induced by H2O2. Catalase (CAT) and glutathione peroxidase (GSH-Px) levels were significantly upregulated, concurrent with a reduction of malondialdehyde (MDA) suggesting that QT-TPGS-QS might be effective in inhibiting the production of intracellular reactive oxygen species (ROS), and to be considered as food additive or in nutraceuticals.

Evaluation of Glutathione Peroxidase (GPx) and Superoxide Dismutase (SOD) salivary levels in Oral Lichen Planus patients, Diabetics, and Diabetics with Oral Lichen Planus

Evaluation of Glutathione Peroxidase (GPx) and Superoxide Dismutase (SOD) salivary levels in Oral Lichen Planus patients, Diabetics, and Diabetics with Oral Lichen Planus