Antioxidants最新文献

Postoperative delirium (POD) is a neurocognitive complication that commonly occurs after cardiac surgery. Despite the association of POD with increased morbidity and mortality, reliable perioperative biomarkers for predicting POD remain scarce. This retrospective observational study investigated whether temporal changes in perioperative redox balance are associated with POD development. Fifty adult patients who underwent elective cardiac surgery at Osaka University Hospital were included. Serum levels of derivatives of reactive oxygen metabolites (d-ROMs) and biological antioxidant potential (BAP) were measured preoperatively, immediately after intensive care unit admission, and on postoperative days 1-4. POD was assessed twice daily using the Intensive Care Delirium Screening Checklist (ICDSC), with an ICDSC score of ≥3 indicating delirium. POD occurred in 18 (36%) out of 50 patients. Compared with non-POD patients, those with POD exhibited higher preoperative d-ROMs levels, a lower BAP/d-ROMs ratio, a transient postoperative increase in BAP, and a relatively higher BAP/d-ROMs ratio during the early postoperative period. Preoperative d-ROMs levels showed a positive correlation with the maximum ICDSC score. In conclusion, perioperative redox dynamics are associated with POD risk and severity. Redox-related markers, particularly d-ROMs, may have potential as biomarkers for identifying patients at higher risk of POD after cardiac surgery, and their clinical utility warrants further prospective validation.

Dimethyl sulfoxide (DMSO) is widely utilized in the vitrification of oocytes, but DMSO exhibits concentration-dependent toxicity, which can compromise oocyte developmental potential by disrupting key cellular processes. This study reports the first successful use of cold shock protein B (CspB protein) as a substitute for DMSO in vitrification solutions for oocyte vitrification. Combining dynamics simulations and experimental validation, we demonstrated CspB's ability to inhibit ice crystallization and recrystallization by stabilizing its position at the ice-water interface and reducing ice formation rates. Recombinant CspB was successfully expressed and shown to bind to the oolemma. In vitrification solutions, CspB (1-2 mg/mL) effectively reduced ice crystal size and enabled a significant reduction or complete replacement of DMSO. This strategy markedly improved the post-thaw survival rates of both mouse and bovine metaphase II (MII) oocytes. Furthermore, oocytes vitrified with an optimized formulation (15% ethylene glycol + 2 mg/mL CspB) exhibited developmental competence (cleavage and blastocyst rates), oxidative stress markers (ROS, GSH), mitochondrial function (membrane potential and content), and apoptosis levels (Caspase-3/9) comparable to those treated with a standard DMSO-containing system. Transcriptomic analysis revealed that CspB's cryoprotection involves the modulation of the mTOR signaling pathway. This role was functionally confirmed, as activation of mTOR abolished CspB's beneficial effects, reinstating oxidative damage, mitochondrial dysfunction, and apoptosis. Thus, the CspB protein replaces DMSO with direct ice crystal formation suppression and mTOR-mediated oxidative stress regulation. This study offers a protein-based alternative to conventional permeable cryoprotectants. This approach holds promise for improving reproductive biotechnologies across species.

Curcumin, a natural polyphenol derived from turmeric, functions as a potent exogenous antioxidant and exhibits a range of benefits in the prevention and management of metabolic diseases. Despite its extremely low systemic bioavailability, curcumin demonstrates significant bioactivity in vivo, a phenomenon likely attributable to its accumulation in the intestines and subsequent modulation of systemic oxidative stress and inflammation. This article systematically reviews the comprehensive regulatory effects of curcumin on systemic metabolic networks-including glucose metabolism, amino acid metabolism, lipid metabolism, and mitochondrial metabolism-and explores their molecular basis, particularly how curcumin facilitates systemic metabolic improvements by alleviating oxidative stress and interacting with inflammation. Preclinical studies indicate that curcumin accumulates in the intestines, where it remodels the microbiota through prebiotic effects, enhances barrier integrity, and reduces endotoxin influx-all of which are critical drivers of systemic oxidative stress and inflammation. Consequently, curcumin improves insulin resistance, hyperglycemia, and dyslipidemia across multiple organs (liver, muscle, adipose) by activating antioxidant defense systems (e.g., Nrf2), enhancing mitochondrial respiratory function (via PGC-1α/AMPK), and suppressing pro-inflammatory pathways (e.g., NF-κB). Clinical trials have corroborated these effects, demonstrating that curcumin supplementation significantly enhances glycemic control, lipid profiles, adipokine levels, and markers of oxidative stress and inflammation in patients with obesity, type 2 diabetes, and non-alcoholic fatty liver disease. Therefore, curcumin emerges as a promising multi-target therapeutic agent against metabolic diseases through its systemic antioxidant and anti-inflammatory networks. Future research should prioritize addressing its bioavailability limitations and validating its efficacy through large-scale trials to translate this natural antioxidant into a precision medicine strategy for metabolic disorders.

Acetaminophen (APAP) overdose is a major cause of acute liver failure and can be fatal, often without early symptoms. Protein deficiency, arising from illness or inadequate diet, impairs growth, immunity, and tissue repair. Both conditions can harm the kidneys, yet the impact of energy imbalance on renal physiology remains unclear. In this study, APAP toxicity and a low-protein diet induced behavioral suppression and tissue damage, as evidenced by reduced whole-body, liver, and kidney weights in rats. In kidney mitochondria of rats exposed to only toxic APAP doses, ATP levels declined sharply while ADP and AMP increased. AMP deaminase and ATPases' activities rose about twofold and 1.5-fold, respectively, whereas cytosolic 5'-nucleotidase activity fell nearly threefold, suggesting compensatory responses to disrupted energy balance. The strongest reductions in ATP and the greatest increases in AMP and ATPase activity occurred in APAP-intoxicated rats fed a low-protein diet. This combination also intensified lipid peroxidation and oxidative protein damage, evidenced by elevated TBARS, reduced protein SH-groups, and increased protein carbonyls. Overall, APAP intoxication with protein deficiency disrupts renal energy metabolism, leading to mitochondrial dysfunction and structural kidney injury. Nutritional status therefore critically influences drug-induced nephrotoxicity, and antioxidant strategies may help prevent damage under metabolic stress.

Cancer remains one of the most common causes of death worldwide and imposes enormous social and economic burdens. Human tumor-associated NADH oxidase (ENOX2, also known as tNOX) is a cancer cell-specialized NADH oxidase that is expressed on the membranes of cancer cells. In this study, we investigated the potential role of ENOX2 in regulating stemness properties in oral cancer through a combination of in vitro, in vivo, and bioinformatics approaches. We found that ENOX2 physically interacted with the stem cell transcription factor, SOX2, in co-immunoprecipitation experiments. The expression and activity of ENOX2 were elevated in p53-functional SAS and p53-mutated HSC-3 oral cancer cell spheroids compared with their monolayer counterparts. Consistently, SIRT1, a downstream effector modulated by ENOX2 through NAD⁺ generation, was also upregulated in spheroid cultures. Functional studies further established that ENOX2 overexpression significantly enhanced spheroid formation, self-renewal properties, stem cell marker expression, and PKCδ expression, whereas ENOX2 knockdown produced the opposite effects. In xenograft models, ENOX2-overexpressing oral cancer cell spheroids exhibited enhanced tumorigenicity, while ENOX2-silenced spheroids formed significantly smaller tumors. Complementary analyses of public transcriptomic and proteomic datasets revealed elevated ENOX2 expression in human head and neck tumor tissues compared with adjacent normal tissues. Based on these findings and literature-supported correlations, we propose a putative ENOX2-SIRT1-SOX2 regulatory framework that may contribute to the acquisition and maintenance of stem-like properties of oral cancer cells. While the ENOX2-SOX2 interaction was experimentally validated, the roles of SIRT1 and other downstream components are inferred from bioinformatic analyses and prior studies; thus, this axis represents a hypothetical model that warrants further mechanistic investigation. Collectively, our results identify ENOX2 as a potential regulator of oral cancer stemness and provide a conceptual foundation for future studies aimed at elucidating its downstream pathways and clinical relevance in head and neck tumors.

This study included the nectar of nine standard apple (Malus × domestica) cultivars ('Red Aroma', 'Discovery', 'Summerred', 'Rubinstep', 'Elstar', 'Asfari', 'Eden', 'Fryd', and 'Katja') and two crab apple (Malus sylvestris) cultivars ('Dolgo' and 'Professor Sprenger'). The aim was to determine the diversity of chemical compounds in the floral nectar of the two different apple species and their cultivars. Chemical analysis identified five sugars, two sugar alcohols, two organic acids, forty phenolic compounds, and five phenylamides. The crab apples 'Dolgo' and 'Professor Sprenger', along with the commercial cultivar 'Rubinstep', had the highest levels of all three main sugars (glucose, sucrose, and fructose). The cultivar's 'Katja' nectar had the highest level of total phenolic content (60.7 mg/100 g GAE), the nectar sample from 'Dolgo' exhibited the greatest ability to neutralise DPPH radicals (83.4 mg/100 g TE), and the 'Dolgo' (100.6 mg/100 g TE FW) and 'Katja' (72.1 mg/100 g TE FW) nectars proved to be the best reducing agents. Floral nectar from 'Eden' and 'Fryd' showed very high levels of isorhamnetin, 49.04 mg/kg and 50.83 mg/kg, respectively, while nectar from 'Katja' had the highest level of gentisic acid at 39.06 mg/kg. Besides being vital for insects, apple floral nectar is a significant reservoir of phenolic compounds and can be considered a "superfood" for the human diet.

Particulate matter (PM) is a significant contributor to air pollution-associated negative health effects, and cardiovascular disease patients are more susceptible to air pollution-mediated damage of the heart and vessels. The present study investigated the protective effects against PM-induced cardiovascular damage by classic cardiovascular drugs, as used for the standard therapy of cardiovascular disease patients. Male C57BL/6J mice were exposed to ambient PM_2.5 (<2.5 µm) for 3 days with or without treatment with the cholesterol-lowering drug atorvastatin (20 mg/kg/d) or the angiotensin-converting enzyme (ACE) inhibitor captopril (50 mg/kg/d). Both drugs mitigated PM_2.5-induced systolic blood pressure increases and partially prevented endothelial dysfunction, as reflected by a mixed effect on endothelial nitric oxide synthase phosphorylation. Both drugs ameliorated reactive oxygen species (ROS) formation and phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX-2) expression in the vasculature of PM_2.5-exposed mice. Pulmonary ROS levels showed a minor improvement by the treatments, whereas Nox2 mRNA expression was not diminished. Only captopril showed some anti-inflammatory effects in the heart and lung of PM_2.5-exposed mice, whereas both drugs failed to reduce systemic inflammation measured in plasma. These findings offer new insights into potential mitigation strategies for PM_2.5-induced cardiovascular complications, particularly for patients at higher cardiovascular risk, like those with coronary artery or ischemic heart disease or hypertension.

Antioxidants have acquired a central position in modern nutrition and preventive medicine, and honey bee products are increasingly recognized as complex natural matrices that provide a rich and diverse source of these compounds [...].

Background: Agri-food by-products are increasingly recognized as valuable sources of tannins, whose antioxidant properties represent the primary driver of their biological activity across human and animal health. The strong redox-modulating capacity of condensed and hydrolysable tannins provides a unifying mechanistic explanation for their effects on inflammation, metabolism, gut integrity and neuroprotection. Methods: This narrative review synthesizes evidence obtained through a structured literature search across major databases, selecting studies that investigated antioxidant mechanisms of tannin-rich matrices from plant- and processing-derived residues. Results: Condensed tannins, particularly proanthocyanidins, consistently display potent antioxidant activity through radical scavenging, metal chelation and activation of endogenous defenses, thereby underpinning their anti-inflammatory, anti-ischemic, neuroprotective and metabolic actions. Hydrolysable tannins similarly exert strong antioxidative effects that support antimicrobial activity, enzyme modulation and protection against neuroinflammation. In animals, the antioxidant capacity of tannins translates into improved oxidative balance, enhanced immune status, reduced tissue damage, better feed efficiency and mitigation of oxidative stress-linked methane emission pathways. Conclusions: Antioxidant activity emerges as the central, cross-species mechanism through which tannins mediate diverse health benefits. Tannin-rich agri-food by-products therefore represent promising sustainable antioxidant resources, although their efficacy remains influenced by tannin class, degree of polymerization and dosage, warranting further mechanistic and translational research.

Ponicidin, a bioactive diterpenoid derived from Rabdosia rubescens, has been shown to exhibit antitumor activity across a range of cancer types. Despite its potential therapeutic applications, the precise effects and underlying molecular mechanisms of ponicidin in the context of lung cancer remain insufficiently characterized. This study aims to investigate the antitumor effects of ponicidin in lung cancer, focusing on its impact on cell growth and cellular oxidative stress. Our findings demonstrate that ponicidin significantly inhibits the viability of lung cancer cells while exhibiting minimal cytotoxicity to normal lung cells. Notably, ponicidin induces cell death in lung cancer cells via the induction of oxidative stress, a process likely mediated by the depletion of sulfhydryl antioxidants and the downregulation of thioredoxin reductase (TrxR), both of which play critical roles in maintaining cellular redox homeostasis. Moreover, ponicidin was found to concurrently activate endoplasmic reticulum stress, induce mitochondrial dysfunction, and promote DNA damage, further contributing to its antitumor effects. In vivo, the efficacy of ponicidin was confirmed in tumor-bearing mouse models, where ponicidin treatment led to a significant reduction in tumor growth without significant toxicity or adverse effects on the animals. These findings suggest that ponicidin holds significant promise as a safe and effective therapeutic agent for lung cancer, warranting further investigation into its clinical applicability.