Protein Oxidation Research Articles

Insulin oxidation and oxidative modifications alter glucose uptake, cell metabolism, and inflammatory secretion profiles

Insulin participates in glucose homeostasis in the body and regulates glucose, protein, and lipid metabolism. Chronic hyperglycemia triggers oxidative stress and the generation of reactive oxygen species (ROS), leading to oxidized insulin variants. Oxidative protein modifications can cause functional changes or altered immunogenicity as known from the context of autoimmune disorders. However, studies on the biological function of native and oxidized insulin on glucose homeostasis and cellular function are lacking. Native insulin showed heterogenous effects on metabolic activity, proliferation, glucose carrier transporter (GLUT) 4, and insulin receptor (INSR) expression, as well as glucose uptake in cell lines of five different human tissues. Diverse ROS compositions produced by different gas plasma approaches enabled the investigations of variously modified insulin (oxIns) with individual oxidative post-translational modification (oxPTM) patterns as identified using high-resolution mass spectrometric analysis. Specific oxIns variants promoted cellular metabolism and proliferation in several cell lines investigated, and nitrogen plasma emission lines could be linked to insulin nitration and elevated glucose uptake. In addition, insulin oxidation modified blood glucose levels in the chicken embryos (in ovo), underlining the importance of assessing protein oxidation and function in health and disease.

JAK inhibition with tofacitinib rapidly increases contractile force in human skeletal muscle.

Reduction in muscle contractile force associated with many clinical conditions incurs serious morbidity and increased mortality. Here, we report the first evidence that JAK inhibition impacts contractile force in normal human muscle. Muscle biopsies were taken from patients who were randomized to receive tofacitinib (n = 16) or placebo (n = 17) for 48 h. Single-fiber contractile force and molecular studies were carried out. The contractile force of individual diaphragm myofibers pooled from the tofacitinib group (n = 248 fibers) was significantly higher than those from the placebo group (n = 238 fibers), with a 15.7% greater mean maximum specific force (P = 0.0016). Tofacitinib treatment similarly increased fiber force in the serratus anterior muscle. The increased force was associated with reduced muscle protein oxidation and FoxO-ubiquitination-proteasome signaling, and increased levels of smooth muscle MYLK. Inhibition of MYLK attenuated the tofacitinib-dependent increase in fiber force. These data demonstrate that tofacitinib increases the contractile force of skeletal muscle and offers several underlying mechanisms. Inhibition of the JAK-STAT pathway is thus a potential new therapy for the muscle dysfunction that occurs in many clinical conditions.

Oxidative stress in the alveolar lavage fluid of children with Mycoplasma pneumoniae pneumonia.

To investigate the correlation between oxidative stress in the bronchoalveolar lavage fluid (BALF) of children with Mycoplasma pneumoniae pneumonia (MPP) and the clinical characteristics of severe MPP (SMPP) and refractory MPP (RMPP). Clinical and BALF-related data were collected from 83 patients with MPP, of which 29 had SMPP and 54 had general MPP (GMPP); 37 patients were in the RMPP group and 46 in the non-RMPP group. The levels of malondialdehyde (MDA) and advanced oxidation protein products (AOPP) as well as the activity levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) in BALF were detected. Logistic regression analyses were performed on MDA, AOPP, SOD, GSH-PX, gender, heat peak, neutrophil percentage, C-reactive protein, lactate dehydrogenase, d-dimer, lung consolidation, sputum embolus, and pleural effusion. The levels of MDA and AOPP in the BALF of the MPP group were significantly higher than those in the control group (p < .05), whereas SOD and GSH-PX levels were lower than those in the control group (p < .05). The BALF AOPP levels in the RMPP group were higher than those in the non-RMPP group, and the SOD and GSH-PX levels in the BALF were lower than those in the non-RMPP group; the difference was statistically significant (p < .05). The levels of MDA and AOPP in the BALF of children in the SMPP group were higher than those in the GMPP group, and the levels of SOD and GSH-PX were lower than those in the GMPP group, with statistically significant differences (p < .05). The C-index of the logistic regression model was 0.960 (95% confidence interval 0.958-0.963), which indicates that the model has good predictive ability. Advanced oxidation protein products may be a marker for predicting the conditions of SMPP and RMPP, and the prediction model can assess the risk of progression in children to RMPP, which is conducive to clinical diagnosis and treatment.

Water-soluble chlorogenic acid-chitosan and polydatin-chitosan conjugates: antibacterial activity and inhibition of lipid and protein oxidation.

Chitosan (CS), an abundant alkaline polysaccharide, is valued for its biocompatibility, non-toxicity, and antibacterial properties. However, its limited solubility and modest antioxidant activity constrain its utility. Grafting polyphenols onto chitosan through the use of grafting reactions can enhance both the solubility and bioactivity of chitosan. Among the techniques employed, the free radical grafting method is favored for its simplicity, environmental sustainability, and its effectiveness in preserving biological activity. In this study, chlorogenic acid (CGA) and polydatin (PLD) were conjugated successfully to chitosan by a Vc/H2O2 redox system. Analytical techniques such as ultraviolet-visible (UV-visible) spectroscopy, fourier transform infrared (FTIR) spectroscopy, X-ray diffraction (XRD), and proton nuclear magnetic resonance (1H NMR) were employed to confirm the formation of covalent bonding between the polyphenol molecules and the chitosan backbone. The novel conjugates displayed superior antioxidant properties in comparison with pristine chitosan, as evidenced by their enhanced 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical, 2,2'-azinobis-(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS) radical, and hydroxyl radical scavenging capacities, and Fe2+ reducing power. Both CGA-CS and PLA-CS exhibited excellent lipid and protein oxidation inhibition capabilities. Furthermore, the conjugates were shown to have significant antibacterial effects against four common pathogenic bacteria: Pseudomonas fluorescens, Pseudomonas aeruginosa, Pseudomonas putida, and Staphylococcus aureus (P < 0.05). The newly synthesized water-soluble polyphenol-chitosan conjugates demonstrated remarkable biological activity, particularly CGA-CS. This study offers new insights and a strong theoretical foundation for developing natural food preservation materials with potential applications in the food industry. © 2024 Society of Chemical Industry.

Targeting BRD4-HK2 reverses the meta-inflammatory shift in perivascular adipose tissue and rescues cardiometabolic vascular dysfunction

Abstract Background/Introduction Reducing vascular inflammation is crucial to halt and reverse cardiometabolic damage. BRD4, an epigenetic pan-inflammatory activator whose inhibition has shown promising results in cancer, may play an important role in this context. However, its role in cardiometabolic disease remains unclear. Purpose To investigate BRD4-related transcriptional programmes and therapeutic modulation in translational models of cardiometabolic disease. Methods We dissected small arteries (100-300 μM) from visceral fat biopsies in healthy volunteers (n=16) and patients with obesity and hypertension (n=16), a highly prevalent cardiometabolic phenotype. We assessed the ex vivo effects of BRD4 inhibition on vascular function by pressure myography in the presence or absence of perivascular adipose tissue (PVAT), at baseline and after incubation with the BRD4 inhibitor RVX-208 or with anti-inflammatory/anti-metabolic drugs. We used a cardiometabolic mouse model (high-fat diet+L-NAME supplementation) that mirrored our human phenotype and orally administered RVX-208 (150 mg/kg) or vehicle for 5 days (n=6 per group) to confirm the in vivo effect of chronic BRD4 inhibition. Finally, we investigated the molecular pathways involved in the perivascular cross-talk in an in vitro model of human adipocytes (hADSCs) and endothelial cells (HAECs) using gene overexpression/silencing strategies. We assessed ROS and nitric oxide levels (confocal microscopy), protein and gene expressions (Western blot; qPCR), transcriptional (custom qPCR array; chromatin immunoprecipitation (ChIP)) and metabolic changes (metabolomics, lipidomics, mitochondrial swelling). Results Vascular inflammation, remodeling and function were altered in cardiometabolic patients/mice. RVX-208 attenuated ex vivo vascular dysfunction to a greater extent than anti-IL-1β, anti-IL-6 receptor and anti-TNF-α. In vessels with intact PVAT we observed a stronger effect, due to the restoration of healthy PVAT phenotype (Figure 1). In PVAT, Hexokinase-2 (Hk2) - a glycolytic enzyme implicated in mitochondrial dysfunction and inflammation - was the top downregulated gene by RVX-208 treatment; ChIP confirmed increased binding of BRD4 to the Hk2 promoter. In line, metabolomics and lipidomics assays revealed a PVAT glycolytic shift with increased fatty acid storage in disease states, which was reversed by BRD4 inhibition. The in vitro study showed that: i) healthy adipocytes overexpressing HK2 shift to an inflammatory phenotype; ii) their secretome induces an inflammatory phenotype in HAECs; iii) ex vivo PVAT-selective inhibition of HK2 ameliorates vascular dysfunction (Figure 2). Conclusions We identified BRD4-HK2 interaction at the PVAT level as a novel mediator of cardiometabolic damage. Its targeting rescues vascular dysfunction by reversing the PVAT meta-inflammatory shift. Epigenetic modulators of meta-inflammation may represent a promising strategy in patients with obesity and hypertension.

Pnn deficiency alters expressions of calcium handling proteins and impairs nuclear envelope structure in cardiomyocytes

Abstract Pnn is a multi-functional protein playing roles in the regulation of gene transcription, mRNA alternative splicing, as well as cell-cell connection. Previous studies suggested an association between Pnn genetic defects and arrhythmogenic right ventricular cardiomyopathy (ARVC) in human. In this study, we applied an inducible cardiomyocyte-specific Pnn depletion mouse model (Myh6-CreERT2, Pnnflox/flox) to determine the impact of loss of Pnn on cardiac structure and function in mice. Six weeks after inducing Pnn gene disruption, electrocardiographic abnormalities, ventricular dilatation, and reduced left ventricular ejection fraction (LVEF) were observed in mice with loss of Pnn in cardiomyocytes. Histopathological examinations showed that the proliferation of cardiac fibroblasts and expression of α-smooth muscle actin were increased with Pnn depletion, while the cell-cell connection between cardiomyocytes were impaired. In addition to impaired intercalated discs, loss of Pnn also altered the distribution and expression of nuclear envelope proteins and the linker of nucleoskeleton and cytoskeleton (LINC) complex proteins, such as nuclear lamins, Emerin, and SUNs, in cardiomyocytes. Microarray analysis as well as subsequent RT-PCR and Western blots also indicated that loss of Pnn regulated myocardial expressions of genes responsible for calcium handling, such as RYR2, Atp2a2, Slc8a1, and Kcnj3. Furthermore, infiltrations of macrophages and neutrophiles were observed in the myocardium with Pnn depletion, while expression levels of oxidative stress-associated proteins were also significantly regulated by Pnn depletion. In conclusion, Pnn plays an essential role in the maintenance of intercalated disc integrity and nuclear envelope structure of cardiomyocytes, while cardiomyocyte-specific loss of Pnn impairs the calcium handling and leads to arrhythmogenic dilated cardiomyopathy in mice.Cardiac MRI of mice with Pnn depletionMyocardial expression of SUN2 and Emerin

Antioxidant and anticoagulant properties of myo-inositol determined in an ex vivo studies and gas chromatography analysis

Myo-inositol plays a key role in the vasculature and may be beneficial for preventing harmful environmental effects. In this study aortic rings were isolated from middle-aged (12-month-old) male Wistar rats and preincubated with myo-inositol (0.01–100 mg/L) for 2 h. A stable thromboxane A2 analog was added (0.1 nM, 2 h) to analyze vascular dysfunction. The concentration of myo-inositol in the organ baths was determined via gas chromatography. In another experiment, human blood plasma was subjected to pro-oxidant - hydrogen peroxide administration, and myo-inositol was added to analyze lipid and protein oxidation processes. The thromboplastin time, prothrombin time, and thrombin time were also studied. Myo-inositol administration protected thiol groups against oxidative stress, meanwhile decreased vascular contraction and potentiated vasodilation (concentrations 1–100 mg/L, but not ≤ 0.1 mg/L), and changed the level of 8-isoprostane (concentrations: 0.1–100 mg/L, but not 0.01 mg/L) in plasma treated with H2O2/Fe2+. A dose above 100 mg/L additionally protected lipids (measured as thiobarbituric acid reactive substances) and increased thrombin time. Moreover, significant differences in vascular relaxation were observed between the studied myo-inositol concentrations (1 vs. 10 vs. 100 mg/L), which was not detected under the 0.1 mg/L. The concentration of myo-inositol in the organ baths determined via gas chromatography revealed that this nutraceutical agent was not used by the aortic rings during the incubation period in physiological processes. A protective effect of myo-inositol against prooxidant damage to human plasma and rat thoracic arteries has been demonstrated.

Oxidative Phosphorylation as a Predictive Biomarker of Oxaliplatin Response in Colorectal Cancer

Oxaliplatin is successfully used on advanced colorectal cancer to eradicate micro-metastasis, whereas its benefits in the early stages of colorectal cancer remains controversial since approximately 30% of patients experience unexpected relapses. Herein, we evaluate the efficacy of oxidative phosphorylation as a predictive biomarker of oxaliplatin response in colorectal cancer. We found that non-responding patients exhibit low oxidative phosphorylation activity, suggesting a poor prognosis. To reach this conclusion, we analyzed patient samples of individuals treated with oxaliplatin from the GSE83129 dataset, and a set of datasets validated using ROCplotter, selecting them based on their response to the drug. By analyzing multiple oxaliplatin-resistant and -sensitive cell lines, we identified oxidative phosphorylation KEGG pathways as a valuable predictive biomarker of oxaliplatin response with a high area under the curve (AUC = 0.843). Additionally, some oxidative phosphorylation-related biomarkers were validated in primary- and metastatic-derived tumorspheres, confirming the results obtained in silico. The low expression of these biomarkers is clinically relevant, indicating poor prognosis with decreased overall and relapse-free survival. This study proposes using oxidative phosphorylation-related protein expression levels as a predictor of responses to oxaliplatin-based treatments to prevent relapse and enable a more personalized therapy approach. Our results underscore the value of oxidative phosphorylation as a reliable marker for predicting the response to oxaliplatin treatment in colorectal cancer.

Evaluation of fenugreek (Trigonella foenum-graecum L.) powder supplementation on metabolic syndrome, oxidative stress and inflammation in high fat diet fed rats

As an anti-diabetic medicinal plant, fenugreek seed (FG) (Trigonella foenum-graecum L.) has long been utilized and has many therapeutic uses. The current investigation sought to ascertain the effects of FG powder supplementation on insulin resistance, dyslipidemia, and oxidative stress in rats given a high-fat (HF) diet. Measurements of biochemical and antioxidant indicators were made in animal blood and tissue samples, including malondialdehyde (MDA), nitric oxide (NO), advanced oxidation protein product (AOPP), reduced glutathione (GSH), superoxide dismutase (SOD), triglycerides (TG), and catalase (CAT). Furthermore, the tissues of the kidney, heart, and liver were stained histologically. HF diet feeding in rats declined in antioxidant enzyme activities, along with a rise in MDA and other indicators of oxidative stress, which were mitigated by the supplementation of FG. Additionally, FG supplementation enhanced the expression of genes corresponding to antioxidants in the liver of rats given HF diet. FG supplements in HF diet-fed rats displayed altered gene expression in the livers that metabolized fat. Histological staining of the liver demonstrated that FG supplementation reduced necrosis and the accumulation of fat droplets in the liver of rats given HF diets. In conclusion, this finding showed that FG supplementation in HF diet fed rats reduced the plasma lipids, decreased oxidative stress and raised antioxidant enzyme activities. FG may therefore aid in reducing the chronic complications linked to the HF diet in experimental rats.

Effect of Litsea cubeba and Cinnamon Essential Oil Nanoemulsion Coatings on the Preservation of Plant-Based Meat Analogs

Plant-based meat analogs (PBMAs) are promising sustainable food sources. However, their high moisture and protein contents make them prone to microbial deterioration, limiting their shelf life and sensory appeal. This study explored enhancing PBMAs’ shelf life using nanoemulsions of Litsea cubeba and cinnamon essential oils, emulsified with chitosan and Tween 80. The composite nanoemulsion, produced through high-pressure homogenization, exhibited a droplet size of 4.99 ± 0.03 nm, a polydispersity index (PDI) of 0.221 ± 0.008, and a zeta potential of 95.13 ± 2.67 mV, indicating remarkable stability (p &lt; 0.05). Applied to PBMAs stored at 4 °C, it significantly improved color and pH balance and reduced thiobarbituric acid reactive substances and cooking loss. Most notably, it inhibited the growth of Escherichia coli and Staphylococcus aureus, curbing spoilage and protein oxidation, thereby extending the products’ shelf life and preserving sensory quality. As shown above, the encapsulation of LCEO/CEO in nanoemulsions effectively inhibits spoilage and deterioration in PBMAs, improving flavor and quality more than direct addition. Future studies should explore using various essential oils and emulsifiers, as well as alternative encapsulation techniques like microcapsules and nanoparticles, to further prevent PBMA deterioration.

Machine Learning Assisted Stroke Prediction in Mechanical Circulatory Support: Predictive Role of Systemic Mitochondrial Dysfunction.

Stroke continues to be a major adverse event in advanced congestive heart failure (CHF) patients after continuous-flow left ventricular assist device (CF-LVAD) implantation. Abnormalities in mitochondrial oxidative phosphorylation (OxPhos) have been critically implicated in the pathogenesis of neurodegenerative diseases and cerebral ischemia. We hypothesize that prior stroke may be associated with systemic mitochondrial OxPhos abnormalities, and impaired more in post-CF-LVAD patients with risk of developing new stroke. We studied 50 CF-LVAD patients (25 with prior stroke, 25 without); OxPhos complex proteins (complex I [C.I]-complex V [C.V]) were measured in blood leukocytes. Both at baseline (pre-CF-LVAD) and postoperatively (post-CF-LVAD), the prior-stroke group had significantly lower C.I, complex II (C.II), complex IV (C.IV), and C.V proteins when compared to the no-prior-stroke group. Oxidative phosphorylation proteins were significantly decreased in prior-stroke group at post-CF-LVAD compared to pre-CF-LVAD. Machine learning Least Absolute Shrinkage and Selection Operator (LASSO) and Random Forest modeling identified six prognostic factors that predicted postoperative stroke with an area under the receiver operating characteristic (ROC) curve (AUC) of 0.93. Oxidative phosphorylation protein reduction appeared to be associated with the new stroke after implantation. Our study found for the first time the existence of mitochondrial dysfunction at the peripheral level in CHF patients with prior ischemic stroke even before CF-LVAD implantation. The changes in OxPhos protein expression could serve as biomarkers in predicting new post-CF-LVAD strokes.

Stability of the Glycated Amino Acid 6-(2-Formyl-5-hydroxymethyl-1-pyrrolyl)-l-norleucine (Pyrraline) During Oxidation.

Food proteins may be modified during processing and storage through reactions with reducing sugars (Maillard reaction, glycation) or by reactive oxygen species (protein oxidation). Little is known about particular reactions at the interface of glycation and oxidation. In the present study, the glycated amino acid pyrraline (6-(2-formyl-5-hydroxymethyl-1-pyrrolyl)-l-norleucine) and the proteinogenic amino acids tyrosine and tryptophan were subjected to different types of oxidation. The stability of the amino acids was assessed by HPLC with UV detection, whereas oxidation products were assigned by HPLC with triple quadrupole or time-of-flight mass spectrometric detection. Conditions that lead to oxidation of aromatic proteinogenic amino acids can also lead to oxidation of pyrraline. Pyrraline was particularly unstable in the presence of permanganate, hypochlorite, and under hydroxyl radical-generating conditions (iron, ethylenediaminetetraacetic acid, ascorbic acid). Evidence obtained by high-resolution mass spectrometry revealed the oxidation of pyrraline to 6-(2,5-diformyl-1-pyrrolyl)-l-norleucine, 6-(2-carboxy-5-hydroxymethyl-1-pyrrolyl)-l-norleucine, 6-(2-formyl-5-carboxy-1-pyrrolyl)-l-norleucine, and 6-(2,5-dicarboxy-1-pyrrolyl)-l-norleucine in the presence of potassium permanganate. The latter product was isolated by semipreparative HPLC and characterized by NMR. Under hydroxyl radical-generating conditions, pyrraline is hydroxylated at the ring under formation of 6-(2-formyl-4-hydroxy-5-hydroxymethyl-1-pyrrolyl)-l-norleucine or 6-(2-formyl-3-hydroxy-5-hydroxymethyl-1-pyrrolyl)-l-norleucine. This study shows that the so-called "advanced glycation end products" are no end products of the Maillard reaction, but may undergo further chemical degradation reactions.

Effect of Shikimic Acid on Oxidation of Myofibrillar Protein of Duck Meat During Heat Treatment.

The myofibrillar protein (MP) of duck meat is prone to excessive oxidation during thermal processing, resulting in a decline in its overall quality. In this paper, the effect of shikimic acid on the oxidative structure of duck muscle fibrin was studied. The findings showed that, at a mass ratio of 1:50,000 (g/g) between shikimic acid and MP, the carbonyl content of MP was reduced by 74.20%, while the sulfhydryl content was increased by 73.56%. MP demonstrated the highest denaturation temperature, whereas its thermal absorption was the lowest. The percentage of α-helixes and β-sheets increased by 16.72% and 24.74%, respectively, while the percentage of irregular structures decreased by 56.23%. In addition, the surface hydrophobicity index of MP exhibited a significant decrease (p < 0.05), while there was a significant increase in its free radical-scavenging ability (p < 0.05). Molecular fluorescence spectrum analysis showed that shikimic acid could bind to MP, altering the internal environment of MP and enhancing its thermal stability. FTIR analysis showed that shikimic acid could enhance the distribution of protein particle sizes by reducing irregular structures, the proportion of β-rotation, and the degree of protein aggregation. It is hoped that this research can offer scientific support for improving meat processing technology.

Mesenchymal Stem Cell Therapy Mitigates Acute and Chronic Lung Damages of Sulfur Mustard Analog Exposure

Sulfur mustard (SM) is an established chemical weapon that can result in severe damage to parts of the body. Currently, there are no effective treatments available for SM-caused damage. We aimed to investigate the therapeutic potential of adipose-derived mesenchymal stromal cells (AD-MSCs) and conditioned medium (CM-MSCs) in acute and chronic pulmonary mouse models caused by 2-chloroethyl ethyl sulfide (CEES), an SM analog. The mice were divided into 4 experimental groups:(1) CEES+AD-MSCs, (2) CEES+CM-MSCs, (3) CEES, and (4) control. The model observation time was divided into 7 days for the short and 6 months for the long term. AD-MSCs were injected into mice via intraperitoneal injection 24 hours after CEES exposure. The therapeutic effects of AD-MSCs on pulmonary tissue damage were assessed using a histopathologic assay, measuring the neutrophil count, and bronchial alveolar lavage fluid (BALF) protein level. The levels of inflammatory and anti-inflammatory cytokines were evaluated using the enzyme-linked immunosorbent assay as the outcomes of interest. Lung damage progression was reduced by AD-MSC treatment in mice after CEES injection into the peritoneum. The proportion of CD11b+F4/80+ macrophages in the peritoneum was significantly lowered by AD-MSC treatment following CEES exposure. AD-MSC administration also reduced the level of pro-inflammatory cytokines, BALF protein, and nitric oxide levels in the peritoneal cavity. By reducing inflammation and enhancing tissue healing, AD-MSCs and CM-MSC help prevent acute lung damage caused by CEES. The current study supports the use of a mouse model as a solid experimental foundation and indicates potential use for future cell treatment.

Emodin-based Regulation and Control of Serum Complement C5a, Oxidative Stress, and Inflammatory Responses in Rats with Urosepsis via AMPK/SIRT1

Emodin, derived from Rheum officinale and aloe, is known for its diverse benefits such as anti-inflammatory, antioxidant, and antibacterial properties. Currently, the impact of emodin on urosepsis is unclear. This study aims to investigate the mechanism of action of emodin in urosepsis. Peripheral blood mononuclear cells (PBMCs) were purchased from Cloud-Clone Animal Inc. and treated with emodin. Cell viability and the lactate dehydrogenase (LDH) level were then assessed. In a separate experiment, a urosepsis model was established in Sprague Dawley rats which were subsequently treated with emodin. The levels of oxidative stress-related factors, serum complements and inflammatory factors were measured using commercial kits. Blood urea nitrogen and serum creatinine levels were determined using a fully automatic biochemical analyzer. The levels of pro-inflammatory proteins and AMP-activated protein kinase (AMPK)/Sirtuin 1 (SIRT1) pathway-related proteins were evaluated via Western blot. PBMCs were unaffected by emodin concentrations below 60 μg/mL, and minimal LDH levels were detected in the cells. Emodin attenuated the effects of Escherichia coli and diminished the production of serum complements, oxidative stress-related proteins, and inflammatory factors in PBMCs. Notably, the effects of emodin were lessened by an AMPK pathway inhibitor. Additionally, emodin alleviated oxidative stress, complement system activation, inflammation, and kidney injury in urosepsis rats through the AMPK/SIRT1 signaling pathway. Emodin improved kidney damage in urosepsis rats by activating the AMPK/SIRT1 signaling pathway, which reduced oxidative stress, inflammation, and complement system activation.

Nitric Oxide-Dependent Regulation of Oxygen-Related Processes in a Rat Model of Lead Neurotoxicity: Influence of the Hypoxia Resistance Factor

Background/Aims: Lead exposure is known to induce oxidative stress and neurotoxicity. Nitric oxide (NO) plays an important role in modulating oxidative stress, with L-arginine as a precursor of NO and Nω-nitro-L-arginine (L-NNA) as an inhibitor of NO synthase, an enzyme that catalyses the production of nitric oxide (NO) from L-arginine. Methods: This study investigated the differential effects of L-arginine and L-NNA on markers of oxidative stress and biochemical changes in brain tissue from rats with different levels of resistance to hypoxia exposed to lead nitrate. Rats with either low or high resistance to hypoxia were exposed to lead nitrate (oral 3.6 mg lead nitrate/kg b.w. per day for 30 days) and treated with L-arginine (600 mg/kg b.w., i.p., 30 min before and after exposure to lead nitrate) or L-NNA (35 mg/kg b.w., i.p., 30 min before and after exposure to lead nitrate). Brain tissue samples were analysed for lipid peroxidation, oxidative modification of proteins, and activity of antioxidant enzymes, including superoxide dismutase, catalase, glutathione reductase, and peroxidase, and total antioxidant status (TAS). We also examined the biomarkers of biochemical pathways involving the activity of alanine and aspartate aminotransferases, succinate dehydrogenase (SDH), and α-ketoglutarate dehydrogenase (KGDH). In addition, the trend observed was supported by assessments of the acetylcholine levels and acetylcholinesterase activity (ACh-AChE system) in brain tissue. Results: In rats with low resistance to hypoxia, the L-arginine treatment significantly reduced lipid peroxidation and oxidative protein modification but increased antioxidant enzyme activity, suggesting a protective effect against lead-induced oxidative stress. Conversely, in rats with high resistance to hypoxia, L-NNA had a protective effect, reducing lead-induced oxidative damage and decreasing lipid peroxidation, whereas L-arginine exacerbated oxidative stress and impaired antioxidant defences. These findings were supported by corresponding changes in the acetylcholine-acetylcholinesterase system, reflecting the observed patterns of lead-induced oxidative stress and neurotoxicity. The study shows that L-arginine exerts a protective effect by reducing lead-induced oxidative damage via an improvement in TAS. Our study shows that lead nitrate exposure significantly increases ala-nine and aspartate aminotransferase activity in brain tissue, with L-arginine exacerbating and L-NNA reversing this effect. The lead nitrate exposure also affected the activities of SDH and KGDH, which are important for cellular energy production and hypoxia resistance, with L-arginine altering SDH activity depending on the level of resistance and L-NNA enhancing both SDH and KGDH activities. These trends were further validated by alterations in the ACh-AChE system, highlighting the differential role of NO-dependent mechanisms in modulating lead-induced neurotoxicity based on hypoxia resistance. Conclusion: These findings suggest potential targeted therapeutic strategies based on the oxidative stress profile and highlight the potential of nitric oxide system modulators in counteracting lead-induced biochemical alterations and the dynamics of the ACh-AChE system depending on the individual physiological reactivity of organisms.

Research Progress on the Effect and Mechanism of Superchilling Preservation Technology on Meat Quality Control.

During storage and transportation, meat is susceptible to the effects of microorganisms, endogenous enzymes, and oxygen, leading to issues such as moisture loss, spoilage, and deterioration. Superchilling, as a preservation method that combines the benefits of refrigeration and freezing, can effectively slow the growth and reproduction of microorganisms, control protein and lipid oxidation, reduce water loss, and maintain the quality and sensory properties of meat. This paper reviews the current application status of superchilling technology in meat preservation, focusing on the mechanisms of ice crystal formation, water retention, tenderness preservation, protein and fat oxidation control, and microbial growth inhibition under superchilling conditions. Additionally, it summarizes the research progress on the combined application of superchilling with emerging technologies such as electric fields, magnetic fields, and electron beams in meat preservation and explores its potential and future prospects for improving meat quality. The aim is to provide scientific evidence and technical support for the application of superchilling technology in enhancing meat quality.

Genotype-Dependent Variations in Oxidative Stress Markers and Bioactive Proteins in Hereford Bulls: Associations with DGAT1, LEP, and SCD1 Genes.

The objective of this study is to assess the influence of genetic polymorphisms in DGAT1, LEP, and SCD1 on the oxidative stress biomarkers and bioactive protein levels in Hereford bulls. A total of sixty-eight bulls were analyzed at 22 months of age to assess growth metrics and carcass quality, with a focus on polymorphisms in these genes. The key markers of oxidative stress, including malondialdehyde (MDA), and the activities of antioxidant enzymes such as glutathione reductase (GluRed), glutathione peroxidase (GPx), and superoxide dismutase (SOD) were measured, alongside bioactive compounds like taurine, carnosine, and anserine. The results show that the TT genotype of DGAT1 is linked to significantly higher MDA levels, reflecting increased lipid peroxidation, but is also associated with higher GluRed and GPx activities and elevated levels of taurine, carnosine, and anserine, suggesting an adaptive response to oxidative stress. The LEP gene analysis revealed that the CC genotype had the highest MDA levels but also exhibited increased GPx and SOD activities, with the CT genotype showing the highest SOD activity and the TT genotype the highest total antioxidant status (TAS). The SCD1 AA genotype displayed the highest activities of GluRed, GPx, and SOD, indicating a more effective antioxidant defence, while the VA genotype had the highest MDA levels and the VV genotype showed lower MDA levels, suggesting protective effects against oxidative damage. These findings highlight genotype specific variations in the oxidative stress markers and bioactive compound levels, providing insights into the genetic regulation of oxidative stress and antioxidant defences, which could inform breeding strategies for improving oxidative stress resistance in livestock and managing related conditions.

Research Progress on the Mechanism of the Impact of Myofibrillar Protein Oxidation on the Flavor of Meat Products.

Myofibrillar proteins primarily consist of myosin, actin, myogenin, and actomyosin. These proteins form complex networks within muscle fibers and are crucial to the physical and chemical properties of meat. Additionally, myofibrillar proteins serve as significant substrates for the adsorption of volatile flavor compounds, including aldehydes, alcohols, ketones, and sulfur and nitrogen compounds, which contribute to the overall flavor profile of meat products. A series of chemical reactions occur during the processing, storage, and transportation of meat products. Oxidation is one of the most significant reactions. Oxidative modification can alter the physical and chemical properties of proteins, ultimately impacting the sensory quality of meat products, including flavor, taste, and color. In recent years, considerable attention has been focused on the effects of protein oxidation on meat quality and its regulation. This study investigates the impact of myofibrillar protein oxidation on the sensory attributes of meat products by analyzing the oxidation processes and the factors that initiate myofibrillar protein oxidation. Additionally, it explores the control of myofibrillar protein oxidation and its implications on the sensory properties of meat products, providing theoretical insights relevant to meat processing methods and quality control procedures.

Melatonin Mediates Cardiac Tissue Damage under Septic Conditions Induced by Lipopolysaccharide.

Lipopolysaccharide (LPS) is known to induce oxidative stress and inflammation, leading to significant damage in cardiac tissues. This study investigates the protective effects of melatonin (MLT) against LPS-induced oxidative damage, inflammation, and apoptosis in rat heart tissue. Rats were divided into four groups (n = 6 per group): control, melatonin-treated, LPS-treated, and LPS + melatonin-treated. Oxidative stress markers, including thiobarbituric acid-reactive substances (TBARSs) and advanced oxidation protein products (AOPPs), were measured. Additionally, inflammatory markers, such as interleukin-6 (IL-6) levels, inducible nitric oxide synthase (iNOS) and nitric oxide (NO) content, and apoptotic markers, caspase-3, caspase-9, and acidic DNase activity, were evaluated. LPS treatment significantly increased TBARS, AOPP, and IL-6 levels, as well as the activity of caspase-3, acidic DNase and iNOS and NO content compared to the control group. Co-treatment with melatonin significantly reduced the levels of TBARS and AOPP levels, and caspase-3 and acidic DNase activities nearly matched those of the control group, while caspse-9 was still slightly increased. Interestingly, IL-6, iNOS and NO levels were significantly decreased but did not fully match the values in the control group. Melatonin mitigates LPS-induced oxidative stress, inflammation, and apoptosis in rat heart tissue by affecting all studied parameters, demonstrating its potential as a therapeutic agent for conditions characterized by oxidative stress and inflammation. Further research is warranted to explore the clinical applications of melatonin in cardiovascular diseases.