Antioxidants最新文献

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The current food systems are now unsustainable due to population growth, globalization, and climate change, contributing to environmental degradation and social inequalities [...].

Oxidative stress is a common event involved in cancer pathophysiology, frequently accompanied by unique lipid metabolic reprogramming phenomena. Oxidative stress is caused mainly by an imbalance between the production of reactive oxygen species (ROS) and the antioxidant system in cancer cells. Emerging evidence has reported that oxidative stress regulates the expression and activity of lipid metabolism-related enzymes, leading to the alteration of cellular lipid metabolism; this involves a significant increase in fatty acid synthesis and a shift in the way in which lipids are taken up and utilized. The dysregulation of lipid metabolism provides abundant intermediates to synthesize biological macromolecules for the rapid proliferation of cancer cells; moreover, it contributes to the maintenance of intracellular redox homeostasis by producing a variety of reducing agents. Moreover, lipid derivatives and metabolites play critical roles in signal transduction within cancer cells and in the tumor microenvironment that evades immune destruction and facilitates tumor invasion and metastasis. These findings suggest a close relationship between oxidative stress and lipid metabolism during the malignant progression of cancers. This review focuses on the crosstalk between the redox system and lipid metabolic reprogramming, which provides an in-depth insight into the modulation of ROS on lipid metabolic reprogramming in cancers and discusses potential strategies for targeting lipid metabolism for cancer therapy.

The interplay between oxidative stress and adipogenesis is a critical factor in the development of obesity and its associated metabolic disorders. Excessive reactive oxygen species (ROS) disrupt key transcription factors such as peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding protein alpha (C/EBPα), impairing lipid metabolism, promoting adipocyte dysfunction, and exacerbating inflammation and insulin resistance. Antioxidants, classified as endogenous (e.g., glutathione, superoxide dismutase, and catalase) and exogenous (e.g., polyphenols, flavonoids, and vitamins C and E), are pivotal in mitigating these effects by restoring redox balance and preserving adipocyte functionality. Endogenous antioxidants neutralize ROS and safeguard cellular structures; however, under heightened oxidative stress, these defenses are often insufficient, necessitating dietary supplementation. Exogenous antioxidants derived from plant-based sources, such as polyphenols and vitamins, act through direct ROS scavenging, upregulation of endogenous antioxidant enzymes, and modulation of key signaling pathways like nuclear factor kappa B (NF-κB) and PPARγ, reducing lipid peroxidation, inflammation, and adipocyte dysfunction. Furthermore, they influence epigenetic regulation and transcriptional networks to restore adipocyte differentiation and limit lipid accumulation. Antioxidant-rich diets, including the Mediterranean diet, are strongly associated with improved metabolic health, reduced obesity rates, and enhanced insulin sensitivity. Advances in personalized antioxidant therapies, guided by biomarkers of oxidative stress and supported by novel delivery systems, present promising avenues for optimizing therapeutic interventions. This review, "Crosstalk Between Antioxidants and Adipogenesis: Mechanistic Pathways and Their Role in Metabolic Health", highlights the mechanistic pathways by which antioxidants regulate oxidative stress and adipogenesis to enhance metabolic health.

Glutathione (GSH) is the most abundant antioxidant in the cell, and it is responsible for neutralizing reactive oxygen species (ROS). ROS can promote osteoclast differentiation and stimulate bone resorption and are some of the primary drivers of bone loss with aging and loss of sex steroids. Despite this, the role of GSH biosynthesis during osteoclastogenesis remains controversial. Here, we show that the requirements for GSH biosynthesis during osteoclastogenesis in vitro and in vivo are unique. Using a metabolomics approach, we discovered that both oxidative stress and GSH biosynthesis increase during osteoclastogenesis. Inhibiting GSH biosynthesis in vitro via the pharmacological or genetic inhibition of glutamate cysteine ligase (GCLC) prevented osteoclast differentiation. Conversely, the genetic ablation of GCLC in myeloid cells using LysMCre resulted in a decrease in bone mass in both male and female mice. The decreased bone mass of the LysMCre;Gclc^fl/fl mice was attributed to increased osteoclast numbers and elevated bone resorption. Collectively, our data provide strong genetic evidence that GSH biosynthesis is essential for the regulation of osteoclast differentiation and bone resorption in mice. Moreover, these findings highlight the necessity of complementing in vitro studies with in vivo genetic studies.

Polyphenols (PPs) are recognized as bioactive compounds and antimicrobial agents, playing a critical role in enhancing food safety, preservation, and extending shelf life. The antimicrobial effectiveness of PPs has different molecular and biological reasons, predominantly linked to their hydroxyl groups and electron delocalization, which interact with microbial cell membranes, proteins, and organelles. These interactions may reduce the efficiency of metabolic pathways, cause destructive damage to the cell membrane, or they may harm the proteins and nucleic acids of the foodborne bacteria. Moreover, PPs exhibit a distinctive ability to form complexes with metal ions, further amplifying their antimicrobial activity. This narrative review explores the complex and multifaceted interactions between PPs and foodborne pathogens, underlying the correlation of their chemical structures and mechanisms of action. Such insights shed light on the potential of PPs as innovative natural preservatives within food systems, presenting an eco-friendly and sustainable alternative to synthetic additives.

Aging is a general biological process inherent in all living organisms. It is characterized by progressive cellular dysfunction. For many years, aging has been widely recognized as a highly effective mechanism for suppressing the progression of malignant neoplasms. However, in recent years, increasing evidence suggests a "double-edged" role of aging in cancer development. According to these data, aging is not only a tumor suppressor that leads to cell cycle arrest in neoplastic cells, but also a cancer promoter that ensures a chronic proinflammatory and immunosuppressive microenvironment. In this regard, in our review, we discuss recent data on the destructive role of senescent cells in the pathogenesis of cancer. We also identify for the first time correlations between the modulation of the senescence-associated secretory phenotype and the antitumor effects of naturally occurring molecules.

Chenopodium formosanum (djulis), well known for its vivid color variation during diverse senescence stages, has attracted attention for its perceived health benefits and antioxidant capacity. Djulis leaves, often discarded as biowaste after harvesting, were evaluated for their potential as a source of antioxidant compounds. The current study analyzes the physicochemical and antioxidant activities of red, green, and yellow djulis leaf extracts across various senescence stages to probe their prospective utility in cosmeceuticals. Various plant compounds including total carbohydrates, phenolics and flavonoids, chlorophyll a and b, and betaxanthins and betacyanins were measured using spectrophotometric techniques. Antioxidant potential was assessed using DPPH, FRAP, CUPRAC, TEAC, and DMPD assays. Green djulis leaves displayed elevated total carbohydrate and chlorophyll levels, whereas red djulis leaves exhibited heightened phenolic, flavonoid, betaxanthin, and betacyanin content, indicating its suitability for cosmeceutical applications. Antioxidant evaluations revealed substantial disparities among the extracts, with red djulis leaf extract demonstrating superior antioxidant activity in most assays. These findings revealed the distinct antioxidant profiles of djulis leaf extracts influenced by color and senescence stage. These findings advance our understanding of the bioactive attributes of djulis leaves and their potential for incorporation into functional products.

Chronic stress poses threats to the physical and psychological well-being of dogs. Resveratrol (Res) is a polyphenol with antidepressant properties and has rarely been studied in dogs. This study aimed to investigate the stress-relieving effects and underlying mechanism of Res in dogs. Dogs were fed a basal diet supplemented with Res for 35 days. The fecal microbiota of the dogs was cultured with Res in vitro. The results show that Res improved the stress-related behaviors and increased the serum levels of 5-hydroxytryptamine (5-HT), brain-derived neurotrophic factor (BDNF), immunoglobulin A, and antioxidant capacity in dogs. Res downregulated the hormones of the hypothalamic-pituitary-adrenal axis. The abundance of butyric-producing bacteria, like Blautia, increased, while the growth of Fusobacterium related to gut inflammation was inhibited in the Res group. A higher content of fecal butyric acid was observed in the Res group. The metabolome indicated that Res increased the fecal and serum levels of tryptophan (Trp) and decreased the consumption of Trp by microorganisms. A chronic unpredictable mild stress mouse model was established, and Res was administered for 35 days. The results show that Res ameliorated the stress-related behavior and increased the levels of Trp and 5-HT in the whole brains of mice. The relative mRNA expression of genes associated with the tight junction protein, aryl hydrocarbon receptor, and Trp transporters in the colon were upregulated. In conclusion, Res could ameliorate canine stress by increasing 5-HT, BDNF, and the antioxidant capacity and improving the immune function and stress response, which was attributed to the role of Res in the restructuring of gut microbiota and the modulation of tryptophan metabolism.

Environmental stressors such as nitrogen and phosphorus play a critical role in regulating the growth and physiological functions of Litopenaeus vannamei, a key species in aquaculture. This study investigates the effects of nitrogen and phosphorus stress on shrimp growth, oxidative stress, tissue damage, and molecular mechanisms. Exposure to increasing concentrations of nitrogen and phosphorus significantly reduced growth rates. Oxidative stress markers, including superoxide dismutase (SOD), catalase (CAT), total antioxidant capacity (T-AOC), and malondialdehyde (MDA), indicated heightened oxidative damage under both stress conditions, with nitrogen stress causing more severe responses than phosphorus stress. Histopathological analysis revealed substantial damage to the gills and hepatopancreas, organs essential for respiration and metabolism. Transcriptomic analysis identified differentially expressed genes (DEGs) enriched in apoptosis, lysosome, sphingolipid metabolism, and phagosome pathways, suggesting shared molecular responses to nitrogen and phosphorus stress. The results demonstrate that L. vannamei initiates oxidative and immune responses to cope with environmental stressors, but the adaptive capacity remains limited. These findings provide a foundation for understanding the stress tolerance mechanisms in shrimp and inform future strategies for breeding high-resistance strains in aquaculture.