Lipid Oxidation Research Articles

Electrostatically-enhanced two-stage low-temperature tempering: Effects on the quality of frozen tan mutton

The two-stage low-temperature tempering (TLT) and TLT assisted by electrostatic fields (TLT-1500/2000/2500/3000) were developed to investigate their effects on the quality of frozen Tan mutton. The results demonstrated that both TLT and TLT-1500/2000/2500/3000 significantly (P < 0.05) enhanced the tempering rate compared to refrigerator tempering (4 °C, RT). The analysis of tempering, cooking, and centrifugal losses, along with the evaluation of electrical conductivity, pH, and TVB-N, showed that the water retention capacity and freshness of Tan mutton treated with TLT-2500 were closest to those of fresh Tan mutton. Scanning electron microscopy analysis demonstrated that TLT-2500 best maintained the tissue integrity of Tan mutton, while low-field nuclear magnetic resonance analysis revealed it contained the highest immobile water and least free water. Furthermore, Tan mutton treated with TLT-2000 and TLT-2500 exhibited minimal lipid oxidation and color change. In contrast, the most significant changes in all indicators were observed after RT.

Ferulic Acid Alleviates Lipid and Bile Acid Metabolism Disorders by Targeting FASN and CYP7A1 in Iron Overload-Treated Mice

Iron overload is a common complication in various chronic liver diseases, including non-alcoholic fatty liver disease (NAFLD). Lipid and bile acid metabolism disorders are regarded as crucial hallmarks of NAFLD. However, effects of iron accumulation on lipid and bile acid metabolism are not well understood. Ferulic acid (FA) can chelate iron and regulate lipid and bile acid metabolism, but its potential to alleviate lipid and bile acid metabolism disorders caused by iron overload remains unclear. Here, in vitro experiments, iron overload induced oxidative stress, apoptosis, genomic instability, and lipid deposition in AML12 cells. FA reduced lipid and bile acid synthesis while increasing fatty acid β-oxidation and bile acid export, as indicated by increased mRNA expression of PPARα, Acox1, Adipoq, Bsep, and Shp, and decreased mRNA expression of Fasn, Acc, and Cyp7a1. In vivo experiments, FA mitigated liver injury in mice caused by iron overload, as indicated by reduced AST and ALT activities, and decreased iron levels in both serum and liver. RNA-seq results showed that differentially expressed genes were enriched in biological processes related to lipid metabolism, lipid biosynthesis, lipid storage, and transport. Furthermore, FA decreased cholesterol and bile acid contents, downregulated lipogenesis protein FASN, and bile acid synthesis protein CYP7A1. In conclusion, FA can protect the liver from lipid and bile acid metabolism disorders caused by iron overload by targeting FASN and CYP7A1. Consequently, FA, as a dietary supplement, can potentially prevent and treat chronic liver diseases related to iron overload by regulating lipid and bile acid metabolism.

Ferroptotic cyanobacteria as biocontrol agent of the southern house mosquito Culex quinquefasciatus

Culex quinquefasciatus is a hematophagous mosquito, widely distributed around the world, that plays a crucial role in public and veterinary health. As an efficient vector of etiological agents, it exhibits a marked preference for urban environments and human blood. Despite advances in mosquito-borne disease control, managing mosquito populations remains an economically efficient and safe strategy to reduce the impact of epidemic outbreaks. However, achieving this goal requires ecologically acceptable tools that ensure sustainability and minimize adverse environmental impacts. In the present work, we investigated the effect of a non-toxigenic model cyanobacterium on Cx. quinquefasciatus larvae through regulated cell death. We observed that heat stress treatment of Synechocystis PCC 6803 inducing ferroptosis, results in larval lipid oxidation, leading to their death. This effect can be mitigated by rearing larvae in an environment containing canonical inhibitors of ferroptosis, such as ferrostatin 1, or antioxidants, like glutathione and ascorbic acid. Furthermore, larval cell death induced by ferroptotic cyanobacteria is closely linked to oxidative dysregulation and lipid peroxidation, both hallmarks of ferroptosis. Moreover, while ferroptotic Synechocystis significantly affects larval development, it does not influence oviposition site selection by gravid females.

Antimutagenic and anticoagulant therapeutic effects of Ag/Ag2O nanoparticles from Olea europaea leaf extract: mitigating metribuzin-induced hepato-and nephrotoxicity.

Silver nanoparticles (Ag/Ag₂O NPs) have garnered attention for their potent antioxidant, antimicrobial, and anti-inflammatory properties, showing promise for therapeutic applications, particularly in mitigating chemical-induced toxicity. This study aimed to synthesize Ag/Ag₂O NPs using Olea europaea (olive) leaf extract as a green, eco-friendly reducing agent and evaluate their protective effects against metribuzin-induced toxicity in Wistar rats, focusing on oxidative stress, hematological parameters, and lipid profiles, with specific dose optimization. Ag/Ag₂O NPs were synthesized using Olea europaea leaf extract, and their properties were confirmed via XRD, FTIR, SEM, EDS, and UV-visible spectroscopy. Wistar rats exposed to metribuzin (110mg/kg/day) were treated with two doses of Ag/Ag₂O NPs (0.062mg/kg and 0.125mg/kg). Hematological and biochemical markers were assessed to evaluate the NPs' protective effects. Physicochemical characterization confirmed the successful formation of Ag/Ag₂O NPs loaded with phytochemicals, exhibiting crystallite sizes of 23nm and 19nm, a particle size of 25nm, and significant peaks in XRD, FTIR, and UV-Vis spectra indicating the formation of Ag/Ag₂O. Metribuzin exposure led to significant hematological disruptions (elevated WBC, reduced RBC and hemoglobin) and worsened lipid profiles (increased cholesterol, LDL, and triglycerides). The lower NP dose (0.062mg/kg) improved WBC, RBC, hemoglobin, and platelet counts, normalized lipid levels, and positively influenced biochemical markers such as serum creatinine and uric acid. In contrast, the higher NP dose (0.125mg/kg) showed mixed results, with some improvements but an increase in triglycerides and continued elevation of ASAT and ALAT enzyme levels. Ag/Ag₂O NPs synthesized via green methods using olive leaf extract effectively mitigated metribuzin-induced toxicity, especially at lower doses, by improving oxidative stress markers and hematological and biochemical profiles. Dose optimization is crucial to maximize therapeutic benefits and minimize adverse effects, underscoring their potential in treating chemical-induced toxicity.

Long-term enzyme replacement therapy in Fabry patients protects against oxidative and inflammatory process.

Fabry disease (FD) is an X-linked recessive lysosomal storage disorder, characterized by a deficiency of α-galactosidase, which causes the progressive accumulation of glycosphingolipids, especially globotriaosylsphingosine (Gb3), in lysosomes across multiple organs. Substrate deposition, associated with tissue damage in FD, also contributes to the emergence of a pro-inflammatory state presented by some patients. We investigated pro- and anti-inflammatory cytokines, and the expression of inflammation-associated genes in treated FD patients, as well as oxidative parameters. We found a decrease in the production of cytokines IL-1β, IL-6, IL-10, and TNF-α in male FD patients and a normalization of redox status in male and female FD patients, once the levels of protein, lipid oxidation, and nitrite and nitrate content were like healthy individuals. Our results suggest that long-term ERT in men with FD contributes to the reduction of a pro-inflammatory scenario and a decrease of oxidative damage in patients, reflecting greater control throughout the disease and in the multisystemic changes characteristic of this disorder. These findings lead us to believe that long-term ERT can improve the redox status and protect these individuals against oxidative and nitrative stress, as well as the inflammatory process.

Corrective role of endophytic exopolysaccharides from Clerodendrum infortunatum L. on arsenic-induced ovarian steroidogenic dysfunction and associated inflammatory responses

The present investigation aimed to evaluate the therapeutic potential of exopolysaccharides (EPSs) derived from endophytic fungi against arsenic [As(III)]-mediated metabolic and reproductive ailments. Two endophytic fungi, Diaporthe arengae (CleR1) and Fusarium proliferatum (CleR3), were isolated from Clerodendrum infortunatum (Cle), and used for the extraction of two types of EPSs. GC–MS analysis confirmed the presence of hydroxymethyl furfural (HMF) and α-d-glucopyranose in the EPS1 (CleR1) and EPS2 (CleR3), respectively. FTIR analysis revealed the potential As(III)-chelation properties of both EPSs. EPS1 and EPS2 significantly mitigated As(III)-induced oxidative stress and lipid peroxidation by restoring the activities of antioxidative enzymes. EPSs successfully corrected the gonadotropin imbalance and steroidogenic alterations. The downregulation of proinflammatory (NF-κB and TNF-α) and proapoptotic (BAX) mediators and the upregulation of antiapoptotic (Bcl-2) markers were also detected following the treatment with EPSs. Histomorphological restoration of reproductive and metabolic organs was also observed in both the EPS groups. Moreover, the As(III)-induced increase in the immunoreactivity of the androgen receptor (AR) was successfully reversed by these EPSs. Molecular docking predicted that HMF and α-d-glucopyranose of EPS1 and EPS2 interact with the active site of AR by limiting its activity. Hence, EPS could be effective for developing new therapeutic strategies for managing As(III) toxicity.

Multiplex antimicrobial activities of the self-assembled amphiphilic polypeptide β nanofiber KF-5 against vaginal pathogens

BackgroundVaginal infections caused by multidrug-resistant pathogens such as Candida albicans and Gardnerella spp. represent a significant health challenge. Current treatments often fail because of resistance and toxicity. This study aimed to synthesize and characterize a novel amphiphilic polypeptide, KF-5, and evaluate its antibacterial and antifungal activities, biocompatibility, and potential mechanisms of action.ResultsThe KF-5 peptide was synthesized via solid-phase peptide synthesis and self-assembled into nanostructures with filamentous and hydrogel-like configurations. Characterization by scanning electron microscopy (SEM), transmission electron microscopy (TEM), and atomic force microscopy (AFM) confirmed the unique nanostructural properties of KF-5. KF-5 (125, 250, or 500 µg/ml) demonstrated potent antibacterial and antifungal activities, with significant inhibitory effects on drug-resistant Candida albicans and Gardnerella spp. (P < 0.05). In vitro assays revealed that 500 µg/ml KF-5 disrupted microbial cell membranes, increased membrane permeability, and induced lipid oxidation, leading to cell death (P < 0.05). Cytotoxicity tests revealed minimal toxicity in human vaginal epithelial cells, keratinocytes, and macrophages, with over 95% viability at high concentrations. Molecular dynamics simulations indicated that KF-5 interacts with phospholipid bilayers through electrostatic interactions, causing membrane disruption. In vivo studies using a mouse model of vaginal infection revealed that 0.5, 1, and 2 mg/ml KF-5 significantly reduced fungal burden and inflammation, and histological analysis confirmed the restoration of vaginal mucosal integrity (P < 0.01). Compared with conventional antifungal treatments such as miconazole, KF-5 exhibited superior efficacy (P < 0.01).ConclusionsKF-5 demonstrates significant potential as a safe and effective antimicrobial agent for treating vaginal infections. Its ability to disrupt microbial membranes while maintaining biocompatibility with human cells highlights its potential for clinical application. These findings provide a foundation for further development of KF-5 as a therapeutic option for combating drug-resistant infections.

Oxidative Stress-mediated Lipid Peroxidation-derived Lipid Aldehydes in the Pathophysiology of Neurodegenerative Diseases.

Neurodegenerative diseases such as Alzheimer's, Parkinson's, and amyotrophic lateral sclerosis cause damage and gradual loss of neurons affecting the central nervous system. Neurodegenerative diseases are most commonly seen in the ageing process. Ageing causes increased reactive oxygen species and decreased mitochondrial ATP generation, resulting in redox imbalance and oxidative stress. Oxidative stress-generated free radicals cause damage to membrane lipids containing polyunsaturated fatty acids, leading to the formation of toxic lipid aldehyde products such as 4- hydroxynonenal and malondialdehyde. Several studies have shown that lipid peroxidation-derived aldehyde products form adducts with cellular proteins, altering their structure and function. Thus, these lipid aldehydes could act as secondary signaling intermediates, modifying important metabolic pathways, and contributing to the pathophysiology of several human diseases, including neurodegenerative disorders. Additionally, they could serve as biomarkers for disease progression. This narrative review article discusses the biological and clinical significance of oxidative stress-mediated lipid peroxidation-derived lipid aldehydes in the pathophysiology of various neurodegenerative diseases.

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.

Hemp cellulose-based aerogels and cryogels: From waste biomass to sustainable absorbent pads for food preservation

This study presents a circular economy approach utilizing hemp stems and rice straw, typically perceived as low-value agricultural waste, to develop a sustainable alternative to traditional plastic absorbent pads for food packaging. The development of an active material was achieved through the utilization of hemp cellulose and a bioactive extract isolated from rice straw. In addition to reducing plastic pollution, this material demonstrates the potential to enhance food preservation. This research provides evidence of the benefits of repurposing agricultural by-products to create valuable and environmentally-friendly products. Hemp cellulose was extracted, characterized, and processed to develop stable aerogels and cryogels through supercritical CO2 drying and freeze-drying. The water stability and internal structure of the materials were guided via TEMPO-mediated oxidation and high-pressure homogenization. Both materials showed versatile physicochemical and mechanical properties. Nevertheless, with higher water sorption (2.20 mL/g), minimal dimensional changes, and lower shrinkage, cryogels were suitable for meat absorbent pad application. To enhance the cryogels functionality, they were impregnated with a rice straw bioactive extract in two different concentrations. The incorporation of the extract did not affect the structure of the cryogels, improved their mechanical properties and the antioxidant activity remained stable after drying (63.89–78.96 %). Finally, the performance of the developed materials was compared to commercial plastic pads and pristine meat preservation challenge test during 9 days at refrigeration conditions. The incorporation of rice straw extract improved meat color preservation. While moderate extract concentrations (75 mg/g) showed a protective effect against lipid oxidation, higher levels (187.5 mg/g) induced pro-oxidant reactions. This research highlights the potential of hemp cellulose-based cryogels as sustainable and functional packaging materials for meat products.

The contributory role of GSK3β in hypertension exacerbating atherosclerosis by regulating the OMA1/PGC1α pathway.

Atherosclerosis is closely related to endothelial dysfunction and hypertension. GSK3β is a critical regulator in atherosclerosis. This study was carried out to investigate the effects of GSK3β on hypertension exacerbating atherosclerosis in vitro and in vivo. L-NAME + HFD-ApoE-/- mice were used for this study for 12 weeks, and their endothelial dysfunction and inflammation were analyzed. Oil red O and H&E staining revealed that treatment with LiCl, an inhibitor of GSK3β, reduced atherosclerotic lesions and lipid accumulation. The levels of lipid homeostasis and oxidation stress were attenuated following LiCl administration. LiCl-treated ApoE-/- mice showed lowered blood pressure. LiCl also suppressed the expressions of Drp1, Bax, ICAM1, VCAM1 and TNF-α compared to HFD + L-NAME induced mice and oxLDL + L-NAME-treated Human aorta endothelial cell line(HAECs). LiCl treatment increased the expressions of MFN2 and Bcl2. Mitotracker-red, MitoSOX and JC-1 staining indicated that LiCl treatment reduced mitochondrial division and ROS production, increased mitochondrial ΔΨm compared to oxLDL + L-NAME-treated HAECs. The expression of OMA1 was decreased by LiCl treatment, while PGC1α expression was increased. In HAECs, we found that OMA1 knockdown increased mitochondrial function and the expression of PGC1α. We also demonstrated LiCl increased OMA1 ubiquitination compared with the Control group, thus decreased OMA1 expression. Furthermore, siOMA1 antagonized the increased protein expressions of ICAM1, VCAM1, TNF-α, Bax and Drp1, decreased the protein expressions of Bcl2 and MFN2 by siPGC1α. Taken together, we demonstrated that GSK3β could play a contributory role in hypertension exacerbating atherosclerosis by regulating the OMA1/PGC1α pathway and inhibiting mitochondrial function.

Fortification of yogurt with cloves extract: Quality characteristics, sensory attributes, and antioxidant evaluation

The purpose of the current study was to evaluate the impact of different concentrations of clove extract (CE: 0%, 0.5%, 1.0%, and 2.0%) on the viscoelasticity, viscosity, syneresis, texture, sensory quality, and antioxidant properties of set yogurt up to 21 days in cold storage. The addition of CE enlarged the total suspended solids (TSS) and mineral contents while reducing whey separation. On the other hand, CE existence dropped the consistency index (k) and elastic modulus (G’) of yogurt gels and further lessening was observed with prolonged storage period. Moreover, the textural firmness remained unaffected whereas gels that are more cohesive were attained with integration of CE. Similarly, total phenolics and free radical scavenging activity increased significantly (p &lt; 0.05) by CE supplementation, and amplified lipid oxidation was observed with increased storage time. Addition of CE lowered the lightness (L*) index and manipulated the organoleptic properties whereas the sample with 1% CE showed improvement in texture and flavor; however, the overall acceptability reduced for samples with higher concentration of CE.

Novel method to improve oxidative stability of safflower oil: An artificial oil body loaded with curcumin coupled rosmarinic acid

Safflower oil is easily oxidized; therefore, its oxidative stability can be improved using artificial oil bodies (AOBs). AOBs were assembled using safflower oil, phospholipids, and a conjugate comprising safflower caleosin (Ctcaleosin) and rosmarinic acid. AOBs coupled with rosmarinic acid exhibited better physical and thermal stability. The conjugate comprising safflower caleosin and rosmarinic acid was obtained by forming stable C-N covalent bonds. Circular dichroism spectroscopy analysis revealed that α-helix levels increased in safflower caleosin in the conjugate, which could be ascribed to the improvement in the stability and flexibility of safflower caleosin anchored by rosmarinic acid. Rosmarinic acid covering the surface of the AOBs and curcumin (Cur) located in the core of the artificial oil bodies significantly improved the physical and lipid oxidation stabilities of the artificial oil bodies. In vitro, release assay confirmed that curcumin in safflower caleosin-rosmarinic acid conjugate-modified AOBs loaded with curcumin (RAOBC) had a slower release efficiency than the free curcumin solution. The hemolysis assay confirmed the biological safety of RAOBC. The assembly of RAOBC can prevent the oxidation and deterioration of safflower oil, broadening its application in industry.

Using Celery Powder in a Semi-Dry Fermented Sausage 'Heat-Treated Sucuk': Nitrosamine Formation, Lipid Oxidation, and Volatile Compounds.

This study investigated the effect of using celery powder (CP) as source of pre-converted nitrite (treatments: A: 150 mg/kg NaNO2, B: 100 mg/kg NaNO2 + CP as 50 mg/kg NaNO2 equivalent, C: 50 mg/kg NaNO2 + CP as 100 mg/kg NaNO2 equivalent, D: CP as 150 mg/kg NaNO2 equivalent) on the physicochemical and microbiological properties in heat-treated sucuk (HTS), a kind of semi-dry fermented sausage. The influence of cooking time (CT) on the nitrosamine formation in HTS with and without CP was also determined. The results indicated that the use of CP increased the pH value and decreased the aw value. Micrococcus/Staphylococcus and residual nitrite were not affected by the use of CP. TBARS value varied from 0.78 to 0.90 mg MDA/kg. CP did not affect the abundance of hexanal in HTS, however, it increased the abundance of camphene. The results of PCA showed that treatments A, B, and C had similar volatile compound profiles. CP did not affect both N-nitrosodimethylamine and N-nitrosodiethylamine, but their levels increased as the CT increased. Increased CT also resulted in increased N-nitrosopiperidine (NPIP) in all treatments, but the cooking for 1 min did not cause a significant increase in treatments A, B, and C. CP leads to a significant increase in NPIP content, especially after 3 and 5 min of cooking in HTS.

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.

Nanotechnology strategy for inhibition of PARP1 and IL-17A-associated with neurotoxicity in rats exposed to hospital wastewater.

Hospital wastewater (HWW) poses a serious hazard to human health security concerning its high susceptibility to neurodegeneration. Water sources and ecosystems are exposed to a complicated pollution load from a variety of refractory organics and pharmaceutical active composites. This study evaluates the treated newly developed nanocomposite (NiFe2O4) HWW on the neural injury induced by HWW action in rats. Three groups of male Wistar rats were distributed, with eight rats in each: group I: tap water served as a control; group II: HWW; and group III: nano-HWW. Each group was intragastrical administrated with each type of water (2.5 ml/100 g b.wt/6 h) for 28 consecutive days. The open field test and Morris Water Maze assessed behavioral activity and spatial learning 2 days before the last day. The research demonstrated that HWW treated with nanocomposite (NiFe2O4) may exert decreased risks of the neural impairment effect of HWW. This improvement was achieved by reducing the neurotoxicity by lowering nitric oxide contents, lipid peroxidation, acetylcholinesterase, interleukin-17A (IL-17A), and poly(ADP-ribose) polymerase1(PARP1) while restoring the antioxidant biomarkers and neurotransmitter levels (β-endorphin, norepinephrine, dopamine, and serotonin) of the treated groups in the cortex and brainstem and enhancement of the histopathology of the cortex as well. In conclusion, this study introduced a newly developed nanotechnology application for treating HWW to protect from neural injury. The findings of this research have significant value for policymakers, Ministry of Health management, and environmental organizations in their selection of suitable techniques and procedures to optimize hospital wastewater treatment efficiency.

Research progress of sea buckthorn (Hippophae rhamnoides L.) in prevention and treatment of cardiovascular disease.

Sea buckthorn (Hippophae rhamnoides L.) contains a variety of biologically active compounds, including flavonoids, terpenoids, polysaccharides, organic acids, volatile oils, and vitamins. It has been demonstrated to be effective in the treatment of cardiovascular disorders. In this paper, we evaluated the pharmacological effects of sea buckthorn in cardiovascular diseases through preclinical studies, and revealed the mechanism of action of the active components in sea buckthorn in cardiovascular diseases, including anti-inflammatory, lipid oxidation regulation, antioxidant, vascular function modulation, anti-platelet aggregation, autophagy, intestinal microorganism regulation, and cell apoptosis reduction. In clinical trials, sea buckthorn was proven to be effective in managing lipid metabolism, blood pressure, and blood glucose levels in patients. We also extensively reviewed the safety of sea buckthorn medicine and its toxicity to numerous organs. To summarize, sea buckthorn has a beneficial effect on cardiovascular disease and may give a novel strategy for clinical intervention and therapy. This paper summarizes the phytochemistry, pharmacology, clinical applications, safety, and toxicity of sea buckthorn in order to better understand the mechanism of action of the various bioactive components in sea buckthorn, investigate its medicinal potential, and provide more options for the treatment of cardiovascular diseases.

Effects of Wheat Bran-Derived Alkylresorcinols on the Physical and Oxidative Stability of Oil-in-Water Emulsions as related to pH

Alkylresorcinols (ARs), a homolog series of phenolipids naturally occurring in many by-products, can meet the high demand of the food industry for natural antioxidants. In this study, ARs (C17–C25) were isolated from wheat bran, and their antioxidant activity was tested in oil-in-water emulsions at pH 3.5 and pH 7.0 at two concentrations (15 and 30 mg/L of emulsion) during 14 days of storage at 35 °C. Results revealed that lipid oxidation was affected by both ARs concentration and pH of the emulsion. Indeed, when ARs were added, a significant suppression of hydroperoxides and aldehydes (hexanal and nonanal) formation with a consequent prolongation of their lag phases (5-fold) was observed at pH 3.5, while at pH 7.0 the lag phases were doubled. No influence of ARs on emulsion particle size was found. The present work demonstrated how ARs could represent sustainable and innovative natural antioxidants for emulsion-based food.

Modern views on the etiology and role of microbial persistence in the development of inflammatory processes in the periodontal complex (review)

Alveolar tissue diseases cause the appearance of dentition defects, thereby reducing the patients' work capacity and quality of life. The purpose of this research was to investigate, modern views on the etiology of periodontitis and the role of microbial persistence in the development of inflammatory processes of periodontal complex basing on a review of literary sources. Literature review was conducted using PubMed, Web of Science, Scopus, Google Scholar from 2018 to March 2024. There were no restrictions on the date of publication or the language of scientific sources. Searches were conducted according to MeSH (Medical Subject Headings) with using the following search terms: "periodontitis", "oral mucosa", "gums", "dental plaque", "periodontium", "traumatic occlusion", "microorganisms". In total, during the initial analysis 82 literary sources were selected and processed, after further systematization of the selected information using general scientific methods, 70 of them remained. Used methods: bibliographic and analytical. Generalized perio­dontitis is a chronic inflammatory-dystrophic process that occurs as a result of various factors. In the pathogenesis of this disease, the key role is played by the inflammatory process, which is a complex interaction of microcirculatory, he­matological and connective tissue reactions to the lesion. Local (exogenic) and general (endogenic) causative factors are distinguished. The main factors that cause pathological changes in periodontium are bacterial biofilm, traumatic occlusion and various anatomical anomalies. Dental plaque occupies a special and main place among the causes of periodontitis. At present, leading pathogenetic links in the development of the inflammation in the periodontium, in par­ticular, the disruption of free radical oxidation, the processes of peroxide oxidation of lipids and proteins, the disorder of the functional state of the antioxidant system, the formation of oxidative stress, as well as the humoral link of adaptive immune protection and cytokinesis, have not been sufficiently studied. There is no doubt about the role of the microbial factor in the etiology of periodontal diseases, but the penetration of microbes into the periodontium does not always lead to the development of the disease, because the organism has a number of protective mechanisms that counteract the development of inflammation.

Polydatin Prevents Electron Transport Chain Dysfunction and ROS Overproduction Paralleled by an Improvement in Lipid Peroxidation and Cardiolipin Levels in Iron-Overloaded Rat Liver Mitochondria.

Increased intramitochondrial free iron is a key feature of various liver diseases, leading to oxidative stress, mitochondrial dysfunction, and liver damage. Polydatin is a polyphenol with a hepatoprotective effect, which has been attributed to its ability to enhance mitochondrial oxidative metabolism and antioxidant defenses, thereby inhibiting reactive oxygen species (ROS) dependent cellular damage processes and liver diseases. However, it has not been explored whether polydatin is able to exert its effects by protecting the phospholipid cardiolipin against damage from excess iron. Cardiolipin maintains the integrity and function of electron transport chain (ETC) complexes and keeps cytochrome c bound to mitochondria, avoiding uncontrolled apoptosis. Therefore, the effect of polydatin on oxidative lipid damage, ETC activity, cytochrome levels, and ROS production was explored in iron-exposed rat liver mitochondria. Fe2+ increased lipid peroxidation, decreased cardiolipin and cytochromes c + c1 and aa3 levels, inhibited ETC complex activities, and dramatically increased ROS production. Preincubation with polydatin prevented all these effects to a variable degree. These results suggest that the hepatoprotective mechanism of polydatin involves the attenuation of free radical production by iron, which enhances cardiolipin levels by counteracting membrane lipid peroxidation. This prevents the loss of cytochromes, improves ETC function, and decreases mitochondrial ROS production.