Antioxidants最新文献

Nuclear factor erythroid 2-related factor 2 (Nrf2) is a master regulator of the cellular antioxidant response, modulating redox homeostasis, detoxification, and cytoprotective pathways. Impaired Nrf2 signaling has been associated with a wide range of cutaneous pathologies, including photoaging, autoimmune disorders, and inflammation. In this review, we highlight roles of Nrf2 in the physiological and pathological mechanisms underlying oxidative stress, autoimmunity-associated skin damage, and fibrotic diseases, with a particular emphasis on photoaging, psoriasis, vitiligo, and autoimmune-associated skin fibrosis. Furthermore, we elucidate several natural bioactive compounds, their therapeutic applications, and delivery platforms for mitigating oxidative stress-mediated skin damage through the modulation of Nrf2 signaling, aiming to translate basic insights into clinical interventions for oxidative stress-driven skin disorders.

Chemotherapy causes primordial follicle apoptosis, resulting in premature ovarian insufficiency (POI) and infertility. In this study, we found that intraperitoneal injection of retinoic acid (RA) and calcitriol partially reversed the cyclophosphamide and doxorubicin treatment-induced decrease in primordial follicles in neonatal mouse ovaries. Furthermore, RA and calcitriol co-treatment reversed cyclophosphamide treatment-induced PI3K/Akt activity and FOXO3a nuclear export in the oocytes within primordial follicles, suggesting that the oocyte transcriptional activity was decreased, which in turn reduced the binding of chemotherapeutic drugs to DNA. Consistent with these findings, RA and calcitriol co-treatment reversed cyclophosphamide treatment-induced changes in reactive oxygen species (ROS), DNA damage response proteins (γH2AX, p-CHK2, p-p53, PUMA, BAX, Cleaved Caspase-3, and cPARP), and antioxidant proteins (NRF2, HO-1, and GPX4). Moreover, RA and calcitriol co-treatment preserved fertility in cyclophosphamide-treated mice without impairing cyclophosphamide's antitumor efficacy in MCF-7 tumor-bearing mice. Thus, RA and calcitriol protect mouse primordial follicles from cyclophosphamide treatment-induced apoptosis by inhibiting cyclophosphamide treatment-induced oocyte transcriptional activity and enhancing antioxidant capacity. Our results suggest a potential strategy for preserving ovarian reserve during chemotherapy in female cancer patients.

This narrative review aims to systematize the current knowledge on the dual role of reactive oxygen species and reactive nitrogen species in cancer processes, from their physiological function in redox signaling to their pathological impact in oxidative distress. The mechanisms of biomolecule damage, particularly DNA, and deregulation of signaling pathways induced by excessive ROS/RNS concentrations, which promote neoplastic transformation, are presented. The importance of diet and endogenous antioxidants in cancer prevention is also discussed, emphasizing the role of natural antioxidants in prevention and adjunctive therapy. In this context, oleanolic acid emerges as a promising compound with dual action modulating oxidative stress, capable of balancing cellular redox responses. We discuss the most important antioxidant mechanisms of oleanolic acid, the interconnection of oxidative stress with carcinogenesis-related pathways, anticancer mechanisms mediated by oxidative stress modulation, and structural modifications and modern application techniques that improve its bioavailability, as well as future perspectives on oleanolic acid research in the context of its antioxidant and anticancer activity. Overall, available experimental and preclinical data indicate that oleanolic acid, through pleiotropic modulation of oxidative stress and signaling networks, holds promise as an adjuvant agent in cancer prevention and therapy.

Oxidative stress contributes to brain aging processes and is implicated in related functional decline. Developing strategies to mitigate oxidative stress is therefore of significant interest. In this study, a neutral polysaccharide (GBPN) was isolated from ginseng berry. Structural analysis revealed that GBPN (molecular weight 1.52 × 10⁴ Da) is primarily composed of glucose (53.18%), arabinose (24.3%), and galactose (16.75%). Glucose exists in the forms of →4)-Glcp-(1→ (32.95%), →6)-Glcp-(1→ (13.81%), and →4,6)-Glcp-(1→ (3.70%), while arabinose exists as →1)-Araf (9.73%), →1)-Arap (5.82%), →2)-Arap-(1→ (0.66%), →5)-Araf-(1→ (7.62%), and →3,5)-Araf-(1→ (1.69%) forms, while galactose exists in the forms of →1)-Galp (3.58%), →3)-Galp-(1→ (1.59%), and →3,6)-Galp-(1→ (12.67%). GBPN adopts a triple-helix conformation and exhibits a curled lamellar appearance. Functionally, GBPN exhibited strong 2,2-diphenyl-1-picrylhydrazyl radical, hydroxyl radical scavenging activity, and iron ion chelation capacity. It can activate the antioxidant system in D-galactose-induced aging-like mice, and simultaneously enhance their learning and memory abilities. Mechanistic analysis revealed that these effects are associated with the kelch-like ECH-associated protein 1/nuclear factor erythroid 2-related factor 2 pathway. These findings suggest that ginseng berry polysaccharides like GBPN hold promise as potential agents for alleviating oxidative stress and cognitive deficits in aging-related contexts.

Melatonin, an ancient and evolutionarily conserved indolamine, has long attracted attention for its multifunctional roles in redox homeostasis. More recently, it has been studied in relation to immune regulation and cancer biology. Beyond its well-known circadian function, melatonin modulates oxidative stress by directly scavenging reactive oxygen and nitrogen species and by upregulating antioxidant enzymes, including superoxide dismutase, catalase, and glutathione peroxidase. At the same time, it exerts wide-ranging immunomodulatory functions by influencing both innate and adaptive immune responses. All these actions converge within the tumor microenvironment, where oxidative stress and immune suppression drive cancer progression. Although the antitumoral effects of melatonin have traditionally been interpreted through its actions on T cells and NK cells, recent studies identify macrophages as an underappreciated and pivotal target. Notably, melatonin influences macrophage polarization, favoring antitumor M1 phenotypes over pro-tumoral M2 states, while attenuating chronic inflammation and restoring mitochondrial function. This review summarizes current knowledge on melatonin's antioxidant and immunoregulatory mechanisms, highlighting its impact on the tumor immune microenvironment, with a particular focus on the growing recognition of macrophages as a compelling new axis through which melatonin may exert anticancer effects.

Emerging evidence suggests that viral infections may contribute to the onset and progression of Alzheimer's disease (AD) and other forms of dementia. Understanding the mechanism of viral involvement in the pathogenesis of AD and related dementia (ADRD) could contribute to reducing the burden caused by these conditions, which affect a large portion of the aging population. Some studies indicate the link between AD and viral infections, notably coronaviruses and herpesviruses. In AD, excessive production of reactive oxygen species (ROS) results in the modifications of lipids, proteins, and nucleic acids, contributing to synaptic dysfunction and cognitive impairments. Experimental evidence suggests that viral infections linked to ADRD induce the cellular production of ROS, possibly contributing to the pathogenesis of these conditions. Despite significant advances in defining the roles of ROS in neurological disorders and viral infections, the specific roles of ROS in virus-associated ADRD have not been thoroughly investigated. The main objective of this review article is to comprehensively provide information on the experimental evidence for the production of ROS by viruses to help the readers investigate the role of ROS in the relationship between viral infections with ADRD.

Acute lung injury (ALI) is characterized by acute respiratory insufficiency, including tachypnea, cyanosis refractory to oxygen, decreased lung compliance, and diffuse alveolar infiltrates, which is a condition associated with high morbidity and mortality that usually results in the development of multiple organ dysfunction. Acute lung injury in humans is histopathologically characterized by neutrophilic alveolitis, injury of the alveolar epithelium and endothelium, hyaline membrane formation, and microvascular thrombi. Different animal models of experimental lung injury have been used to investigate mechanisms of lung injury, such as LPS-induced ALI, hyperoxia-induced ALI, and ventilator-induced lung injury (VILI). Here we will show selected preclinical mice models used as proof of concept to test new drugs in vivo with anti-inflammatory properties, discussing their particularities and clarifying the context of use.

Maternal undernutrition remains a major modifiable risk factor for adverse pregnancy outcomes. Dietary supplements are widely used to bridge nutritional gaps, but their efficacy, safety, and quality control remain controversial. This review critically evaluates the mechanisms, clinical evidence, and quality assurance of key supplements (folic acid, iron, vitamin D, calcium, iodine, omega-3 PUFA, choline, and multiple micronutrients) specifically in pregnant and postpartum women. We highlight that while folic acid (400-800 µg/d) and iron supplementation reduce neural tube defects by >70% and maternal anaemia by 30-50%, respectively, high-dose antioxidant cocktails (vitamins C + E) have shown no benefit and potential harm in large RCTs. Up to 18-40% of commercially available prenatal supplements contain undeclared pharmaceuticals, heavy metals, or incorrect dosages, underscoring the urgent need for advanced analytical methods (LC-MS/MS, HRMS, NMR). We propose the GAPSS (Genotype-Analytics-Physiology-Safety-Sustainability) framework for future personalised maternal nutrition. Rigorous, pregnancy-specific quality control combined with biomarker-guided supplementation is essential to maximise benefits and minimise risks.

Chronic stress impairs cognition through gut-brain axis dysregulation and metabolic imbalance. This study applied untargeted fecal metabolomics to investigate the cognitive and metabolic effects of Bacopa monnieri (L.) Wettst (Brahmi), mixed Thai berry, and their combined extracts in rats exposed to chronic unpredictable mild stress. Cognitive performance was evaluated using the novel object recognition test. Fecal metabolites were profiled using LC-ESI-QTOF-MS, followed by data preprocessing and multivariate statistical analysis. Orthogonal partial least squares regression was applied to identify metabolites associated with the recognition index, and pathway enrichment analysis was subsequently performed to interpret biological relevance. All interventions were associated with improved recognition performance and treatment-related metabolic modulation. Biosynthesis of unsaturated fatty acids was consistently enriched across treatment groups, indicating a shared involvement of lipid remodeling. Treatment-specific responses were also observed: Brahmi was associated with linoleic and alpha-linolenic acid metabolism; mixed Thai berry extract demonstrated dose-dependent modulation of lipid metabolism, with low-dose supplementation additionally yielding amino-acid-derived metabolites; and bile acid-related signaling was uniquely detected in the low-dose combined extract group. These findings demonstrate that fecal metabolomics can capture distinct metabolic signatures associated with herbal extract-induced cognitive improvement and highlight lipid remodeling as a shared metabolic feature across interventions under chronic stress.

The consumption of virgin olive oil has been associated with a broad spectrum of beneficial effects. These health outcomes are attributed not only to its high monounsaturated fatty acid content but also to its bioactive components. Nowadays, the flavoring of olive oil has gained popularity to improve its antioxidant properties, modify its sensory characteristics, and enhance its oxidative stability. This study explores spectrofluorometry as a fast, non-destructive, and eco-friendly tool to monitor oxidation and predict shelf life in virgin olive oils (VOOs). Both unflavored and flavored rosemary and basil samples were studied. Over nine months of storage, monthly autofluorescence measurements at 330 nm excitation revealed dynamic spectral changes. These changes were mapped into three distinct emission zones (I, II, and III), providing a spectral fingerprint of oil freshness and stability. Autofluorescence analysis revealed that oxidation-related emission increased while pigment-related emission decreased over time, especially within the first five months. Rosemary and basil flavoring slowed degradation due to antioxidant migration from the herbs. It is proposed that a ratio between the fluorescence intensity of Zone III/Zone II of the spectrum of less than 0.6 indicates oils stored for more than three months.