Cellular damage is a direct consequence of inherent instability. Oxygen-containing free radical reactive oxygen species are the most well-recognized examples. Free radical-induced harm is countered by the body's production of endogenous antioxidants, including superoxide dismutase, catalase, glutathione, and melatonin. Foods containing vitamins A, B, C, E, coenzyme Q-10, selenium, flavonoids, lipoic acid, carotenoids, and lycopene demonstrate antioxidant properties, as explored within the field of nutraceuticals. A crucial area of study centers on how reactive oxygen species, exogenous antioxidants, and the gut microbiota interact, and how this interaction can enhance protection against the peroxidation of macromolecules such as proteins and lipids. The maintenance of a dynamic balance within the microbial community is key to this process. Through a scoping review, we intend to map the scientific literature addressing oxidative stress related to oral microbiota and the utilization of natural antioxidants for counteraction, to ascertain the quantity, type, qualities, and characteristics of existing studies, and to suggest potential research gaps.
Recently, green microalgae have gained significance because of their nutritional and bioactive constituents, which makes them some of the most promising and innovative functional food options. This study sought to assess the chemical composition and in vitro antioxidant, antimicrobial, and antimutagenic properties of an aqueous extract from the green microalgae Ettlia pseudoalveolaris, sourced from freshwater lakes in the Ecuadorian Andes. To ascertain the microalga's capacity to mitigate endothelial damage induced by hydrogen peroxide-mediated oxidative stress, human microvascular endothelial cells (HMEC-1) were employed. In addition, the eukaryotic model organism Saccharomyces cerevisiae was employed to investigate the possible cytotoxic, mutagenic, and antimutagenic effects exhibited by E. pseudoalveolaris. A pronounced antioxidant capability was evident in the extract, combined with a moderate antibacterial effect, primarily because of the high concentration of polyphenolic compounds. The extract's antioxidant compounds are a probable contributor to the observed reduction in endothelial damage within HMEC-1 cells. An antimutagenic effect, resulting from a direct antioxidant mechanism, was also observed. In vitro studies revealed *E. pseudoalveolaris* to be an excellent source of bioactive compounds, showcasing antioxidant, antibacterial, and antimutagenic activities, suggesting its potential as a functional food.
Several stimuli, including ultraviolet radiation and air pollutants, can activate cellular senescence. In this study, the protective role of the marine algae compound 3-bromo-4,5-dihydroxybenzaldehyde (3-BDB) on PM2.5-induced skin cell damage was investigated using both in vitro and in vivo approaches. The HaCaT keratinocyte, human in origin, was first treated with 3-BDB, followed by exposure to PM25. The consequence of PM25 exposure, including reactive oxygen species (ROS) generation, lipid peroxidation, mitochondrial dysfunction, DNA damage, cell cycle arrest, apoptotic protein expression, and cellular senescence, was examined using confocal microscopy, flow cytometry, and Western blot. Reactive oxygen species, DNA damage, inflammation, and senescence were found to be outcomes of PM2.5 exposure in the current study. check details However, the application of 3-BDB lessened the PM2.5-catalyzed creation of reactive oxygen species, mitochondrial breakdown, and DNA injury. vaccines and immunization Likewise, 3-BDB's impact included reversing PM2.5-induced cell cycle arrest and apoptosis, decreasing cellular inflammation and cellular senescence both in vitro and in vivo studies. In addition, the PM25-activated mitogen-activated protein kinase signaling pathway and activator protein 1 were effectively inhibited by 3-BDB. Therefore, PM25-induced skin injury was lessened by the presence of 3-BDB.
Tea, a globally-grown beverage, thrives in diverse geographical and climatic conditions, notably in China, India, the Far East, and Africa. Conversely, the practice of growing tea has expanded to include numerous European regions, leading to the successful production of high-quality, chemical-free, organic, single-estate teas. Thus, this study had the objective of characterizing the health-promoting qualities, particularly the antioxidant potential, in traditional hot and cold brewing processes for black, green, and white teas from throughout Europe, through a collection of antioxidant assays. Measurements of total polyphenol/flavonoid content and metal chelating activity were also performed. Interface bioreactor By means of ultraviolet-visible (UV-Vis) spectroscopy and ultra-high performance liquid chromatography coupled with high-resolution mass spectrometry, the distinctive characteristics of the various tea brews were ascertained. European teas, surprisingly, exhibit impressive quality, with significant levels of health-promoting polyphenols and flavonoids, and comparable antioxidant capacity to teas from other parts of the world, as demonstrated by our research for the first time. Crucially important for defining European teas, this research offers essential knowledge for both European tea farmers and consumers. It acts as a helpful guide to selecting teas from the old continent and optimal brewing methods for gaining the maximum health benefits from tea.
Classified as an alpha-coronavirus, PEDV, or Porcine Epidemic Diarrhea Virus, can trigger severe diarrhea and dehydration in piglets at birth. Due to the central role of hepatic lipid peroxides in mediating both cellular proliferation and death, a comprehensive understanding of the role and regulation of endogenous lipid peroxide metabolism during coronavirus infection is essential. PEDV piglet livers experienced a considerable decrease in the enzymatic activities of SOD, CAT, mitochondrial complex I, complex III, and complex V, and a concomitant reduction in glutathione and ATP levels. While other markers remained stable, malondialdehyde and reactive oxygen species, associated with lipid peroxidation, demonstrated a significant elevation. Through transcriptomic analysis, we identified that PEDV infection caused a reduction in peroxisome metabolic function. Quantitative real-time PCR and immunoblotting assays were utilized to confirm the further down-regulation of anti-oxidative genes, encompassing GPX4, CAT, SOD1, SOD2, GCLC, and SLC7A11. The ROR-dependent MVA pathway is critical for LPO. Further research suggests ROR also actively regulates the peroxisome-involved genes CAT and GPX4, a phenomenon observed in PEDV piglets. Using ChIP-seq and ChIP-qPCR, our findings indicated that ROR directly binds these two genes. This binding was significantly diminished by the presence of PEDV. Significant reductions were observed in the occupancies of histone active marks, such as H3K9/27ac and H3K4me1/2, alongside the active co-factor p300 and polymerase II, at the CAT and GPX4 locus. Critically, the PEDV infection's influence on the physical connection between ROR and NRF2 contributed to a decrease in the transcriptional regulation of CAT and GPX4. In PEDV piglet livers, ROR, interacting with NRF2 and histone modifications, could be a contributing factor to variations in CAT and GPX4 gene expression.
Systemic lupus erythematosus (SLE), a chronic immune-inflammatory disorder, is noted for its affectation of multiple organs and a deficiency in self-tolerance mechanisms. Epigenetic changes are characterized as holding a pivotal position in the pathophysiology of SLE. A murine pristane-induced SLE model's diet is supplemented with oleacein (OLA), a major extra virgin olive oil secoiridoid, in this study, aiming to assess its effects. The study involved administering pristane injections to 12-week-old female BALB/c mice, which were subsequently fed an OLA-enriched diet at a concentration of 0.01% (w/w) for 24 weeks. The evaluation of immune complex presence relied on both immunohistochemistry and immunofluorescence techniques. Researchers studied thoracic aortas with a view to understanding endothelial dysfunction. Signaling pathways and oxidative-inflammatory mediators were characterized using the Western blotting technique. Moreover, we conducted an examination of epigenetic modifications, including the impact of DNA methyltransferase (DNMT-1) and micro(mi)RNA expression, in renal tissue. Nutritional treatment with OLA reduced kidney damage by lessening the accumulation of immune complexes. Protective effects might be related to adjustments in mitogen-activated protein kinase pathways, the Janus kinase/signal transducer and activator of transcription signaling cascade, nuclear factor kappa B modulation, nuclear factor erythroid 2-related factor 2 activity, modifications in inflammasome signaling pathways, and the regulation of miRNAs (miRNA-126, miRNA-146a, miRNA-24-3p, miRNA-123) along with DNA methyltransferase 1 (DNMT-1) expression. The diet incorporating OLA returned the levels of endothelial nitric oxide synthase and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-1 to normal. These preliminary outcomes propose a diet supplemented with OLA as a novel nutraceutical therapy for SLE, supporting its role as a novel epigenetic modulator of the immunoinflammatory process.
Cellular subtypes are susceptible to pathological damage when subjected to hypoxic environments. The lens, interestingly, is a naturally hypoxic tissue, with glycolysis providing its primary energy source. To ensure both long-term lens clarity and the absence of nuclear cataracts, hypoxia is a critical element. The present work explores the sophisticated adaptations exhibited by lens epithelial cells to adapt to oxygen-deficient conditions while maintaining normal growth and metabolic activity. Our data indicate a substantial increase in the glycolysis pathway's activity in human lens epithelial (HLE) cells subjected to hypoxia. Glycolysis's inhibition in hypoxic environments stimulated endoplasmic reticulum (ER) stress and reactive oxygen species (ROS) production within HLE cells, causing apoptosis. Despite the restoration of ATP, the cellular damage failed to completely resolve, with the presence of ER stress, the creation of reactive oxygen species, and the occurrence of cellular apoptosis.