Antioxidants最新文献

Xanthine oxidoreductase (XOR) is an enzyme involved in the oxidation of hypoxanthine and xanthine to uric acid. XOR has two isoforms: xanthine dehydrogenase and xanthine oxidase (XO). XO plays a major role in oxidative stress, causing the formation of reactive oxygen species. In the present study, we aimed to summarize the evidence on the association between XO and pregnancy complications. The PRISMA checklist guided the reporting of the data. We conducted systematic searches in the PubMed and Web of Science databases to identify all human studies investigating XO in pregnancy diseases up to June 2024. A total of 195 references have been identified and 14 studies were included. Most studies focused on women with PE and GD. Overall, all the included studies found a statistically significant increase in maternal, placental, and/or fetal XO levels, activity, or tissue expression in women with pregnancy complications, compared to those with uncomplicated pregnancies. Although promising, the quality and dimension of the included studies do not allow for a definitive answer to the question of whether XO may play a crucial role in pregnancy complications. Future studies are warranted to confirm if XO could represent a prognostic and therapeutic marker in pregnancy complications and their impact on long-term maternal and offspring cardiovascular health.

Psoriasis is characterized by excessive exfoliation of the epidermal layer due to enhanced pro-inflammatory signaling and hyperproliferation of keratinocytes, further modulated by UV-based anti-psoriatic treatments. Consequently, this study aimed to evaluate the impact of a lipid extract derived from the microalgae Nannochloropsis oceanica on the proteomic alterations induced by lipid derivatives in non-irradiated and UVB-irradiated keratinocytes from psoriatic skin lesions compared to keratinocytes from healthy individuals. The findings revealed that the microalgae extract diminished the viability of psoriatic keratinocytes without affecting the viability of these cells following UVB exposure. Notably, the microalgae extract led to an increased level of 4-HNE-protein adducts in non-irradiated cells and a reduction in 4-hydroxynonenal (4-HNE)-protein and 15-deoxy-12,14-prostaglandin J2 (15d-PGJ2)-protein adducts in UVB-exposed keratinocytes from psoriasis patients. In healthy skin cells, the extract decreased the UV-induced elevation of 4-HNE-protein and 15d-PGJ2-protein adducts. The antioxidant/anti-inflammatory attributes of the lipid extract from the Nannochloropsis oceanica suggest its potential as a protective agent for keratinocytes in healthy skin against UVB radiation's detrimental effects. Moreover, it could offer therapeutic benefits to skin cells afflicted with psoriatic lesions by mitigating their proliferation and inflammatory responses during UV radiation treatment.

Bioactive flavonoid epicatechin has been reported in the peel of litchi fruit but isolated from its hydroalcoholic extracts. This study isolated epicatechin with cellular glucose uptake modulatory and ROS production inhibitory properties from the ethyl acetate (EtOAc) extract using a bioassay-guided approach. The fruit peel was defatted with hexane and sequentially extracted using dichloromethane (DCM), EtOAc, methanol (MeOH) and water. In vitro phytochemical models, namely antioxidant (Fe³⁺ reducing, radical scavenging and anti-linoleic acid peroxidative) and glycaemic control (α-glucosidase and α-amylase inhibitory and glucose uptake modulatory), were employed for the bioassay-guided isolation, while the isolated compound was characterised using NMR and mass spectrometry and assessed for dose-dependent inhibition of α-glucosidase and lipopolysaccharide (LPS)-induced cellular ROS production, as well as modulation of cellular glucose uptake. Relative to the other extracts, the EtOAc extract had appreciable phenol and flavonoid contents, which perhaps influenced its potent anti-lipid peroxidative (65.0%) and α-glucosidase inhibitory (52.4%) effects. The α-glucosidase inhibitory potency of the fractions (1-8) from the EtOAc extracts correlated with their flavonoid contents, with fraction 5 outperforming other fractions. The fraction comprised a pool of fractions obtained from the DCM:MeOH:water (7:3:0.281 v/v/v) solvent system. LC-MS revealed the predominant presence of epicatechin in fraction 5, which was later isolated from one of the sub-fractions (sub-fraction 4) of fraction 5. This sub-fraction had stronger anti-lipid peroxidative (65.5%), α-glucosidase inhibitory (65.8%) and glucose uptake modulatory (38.2%) effects than the other sub-fractions from fraction 5, which could have been influenced by the isolated epicatechin. Moreover, the isolated epicatechin inhibited α-glucosidase (IC₅₀ = 35.3 µM), modulated cellular glucose uptake (EC₅₀ = 78.5 µM) and inhibited LPS-induced ROS production in RAW 264.7 macrophages in a dose-dependent fashion [IC₅₀ = 18.9 µM; statistically comparable (p > 0.05) to ascorbic acid, IC₅₀ = 9.57 µM]. Epicatechin from litchi peel EtOAc extract could potentiate glucose uptake modulatory, α-glucosidase inhibitory and ROS suppressive capacities, which could be influential in the use of litchi fruit peel for managing diabetes and associated oxidative damage.

Acyl-quinic acids (AQAs), present in various plants with many health benefits, are regarded as therapeutic agents in the prevention and treatment of chronic and cardiovascular diseases. The molecular network-guided identification of ten AQA compounds, two new (5 and 7) and eight known compounds, were isolated from V. rotundifolia L. f. by using a newly applied extraction method. Their structures were determined through spectroscopic means, reaction mixtures, and modified Mosher and PGME techniques. These compounds were assessed for their anti-inflammatory and antioxidant capabilities. Notably, compounds 1, 3, 4, 6, 8, and 9 exhibited notable DPPH radical scavenging activity. In LPS-induced HT-29 cells, compounds 2-7 significantly inhibited IL-8 production. Furthermore, compounds 3-5 and 7 markedly suppressed NO production, while compounds 1-10 effectively inhibited IL-6 production in LPS-induced RAW264.7 cells. Western blot analyses revealed that compounds 3-5, and 7 reduced iNOS and COX-2 expression, and compounds 2-5, 7, and 8 also diminished the expression levels of p38 MAPK phosphorylation. Docking studies demonstrated the active compounds' binding affinity with the IL-8, iNOS, COX-2, and p38 MAPK proteins through interactions with essential amino acids within the binding pockets of complexes. The findings suggest that compounds 1, 3, 4, 6, 8, and 9, and compounds 3-5, and 7, hold promise as potential therapeutic agents for treating antioxidative and inflammatory diseases, respectively.

Reactive oxygen and nitrogen species (ROS and RNS) include two families of molecules that, in recent years, have been shown to be involved in a wide range of biological functions, such as seed and pollen germination, the development and regulation of root architecture, stomatal movement, senescence, flowering, and fruit formation and ripening [...].

Concerns over the safety of ethoxyquin (EQ) highlight the need for safer, more effective feed antioxidants. This study investigated a healthier antioxidant compound (AC) as a potential alternative to EQ in broilers. A total of 351 one-day-old Arbor Acres Plus male broilers were randomly assigned to three treatments for 21 days: control (CON), EQ group (200 g/ton EQ at 60% purity), and AC group (200 g/ton AC containing 18% butylated hydroxytoluene, 3% citric acid, and 1% tertiary butylhydroquinone). AC supplementation reduced the acid value, peroxide value, and malondialdehyde content in stored feed, decreased feed intake and the feed conversion ratio without affecting body weight gain, and enhanced antioxidant capacity (liver total antioxidant capacity and superoxide dismutase; intestinal catalase and glutathione peroxidase 7). It improved intestinal morphology and decreased barrier permeability (lower diamine oxidase and D-lactate), potentially by promoting ZO-1, Occludin, and Mucin2 expression. The AC also upregulated NF-κB p50 and its inhibitor (NF-κB p105), enhancing immune regulation. Additionally, the AC tended to increase beneficial gut microbiota, including Lactobacillus, and reduced Bacteroides, Corprococcus, and Anaeroplasma. Compared to EQ, the AC further enhanced feed oxidative stability, the feed conversion ratio, intestinal morphology and barrier functions, and inflammatory status, suggesting its potential as a superior alternative to EQ for broiler diets.

Patients with Alzheimer's disease and related dementia (ADRD) are faced with a formidable challenge of focal amyloid deposits and cerebral amyloid angiopathy (CAA). The treatment of amyloid deposits in ADRD by targeting only oxidative stress, inflammation and hyperlipidemia has not yielded significant positive clinical outcomes. The chronic high-fat diet (HFD), or gut dysbiosis, is one of the major contributors of ADRD in part by disrupted transport, epigenetic DNMT1 and the folate 1-carbon metabolism (FOCM) cycle, i.e., rhythmic methylation/de-methylation on DNA, an active part of epigenetic memory during genes turning off and on by the gene writer (DNMT1) and eraser (TET2/FTO) and the transsulfuration pathway by mitochondrial 3-mercaptopyruvate sulfur transferase (3MST)-producing H₂S. The repeat CAG expansion and m⁶A disorder causes senescence and AD. We aim to target the paradigm-shift pathway of the gut-brain microbiome axis that selectively inhibits amyloid deposits and increases mitochondrial transsulfuration and H₂S. We have observed an increase in DNMT1 and decreased FTO levels in the cortex of the brain of AD mice. Interestingly, we also observed that probiotic lactobacillus-producing post-biotic folate and lactone/ketone effectively prevented FOCM-associated gut dysbiosis and amyloid deposits. The s-adenosine-methionine (SAM) transporter (SLC25A) was increased by hyperhomocysteinemia (HHcy). Thus, we hypothesize that chronic gut dysbiosis induces SLC25A, the gene writer, and HHcy, and decreases the gene eraser, leading to a decrease in SLC7A and mitochondrial transsulfuration H₂S production and bioenergetics. Lactobacillus engulfs lipids/cholesterol and a tri-directional post-biotic, folic acid (an antioxidant and inhibitor of beta amyloid deposits; reduces Hcy levels), and the lactate ketone body (fuel for mitochondria) producer increases SLC7A and H₂S (an antioxidant, potent vasodilator and neurotransmitter gas) production and inhibits amyloid deposits. Therefore, it is important to discuss whether lactobacillus downregulates SLC25A and DNMT1 and upregulates TET2/FTO, inhibiting β-amyloid deposits by lowering homocysteine. It is also important to discuss whether lactobacillus upregulates SLC7A and inhibits β-amyloid deposits by increasing the mitochondrial transsulfuration of H₂S production.

This study investigates the effects of oil quality and trace mineral source on the growth performance, antioxidant activity, and meat quality of growing-finishing pigs. A total of 180 crossbred pigs (Duroc × Landrace × Large White [64.4 ± 1.95]) were randomly allocated five dietary treatments based on body weight (BW) and sex in a 30 d trial. Pigs were fed five diets: (i) fresh soy oil + inorganic trace minerals (ITMs) + inorganic selenium (FISI), (ii) oxidized soy oil + ITMs + inorganic selenium (OISI), (iii) fresh soy oil + ITMs + selenium yeast (FISY), (iv) oxidized soy oil + ITMs + selenium yeast (OISY), and (v) oxidized soy oil + organic trace minerals (OTMs) + selenium yeast (OOSY). Each dietary treatment included six replicates and six pigs per replicate (three barrows and three gilts). Feeding OISI resulted in lower average daily gain (ADG) and dressing percentage (p < 0.05). The OOSY group had a higher dressing percentage and activities of serum CAT and GSH-Px in growing-finishing pigs (p < 0.05). In addition, the relative abundance of Campylobacterota in the colonic digesta varied with the quality of soy oil and source of trace minerals (p < 0.05), but no significant differences in short-chain fatty acid concentrations were observed among all dietary groups. In conclusion, adding oxidized soy oil to the diet negatively impacted the ADG and dressing percentage of growing-finishing pigs, and replacing ITMs with OTMs and SY alleviated these negative impacts. A combination of OTMs and SY can support antioxidant capacity to mitigate the negative impacts of oxidized oil on the growth performance and dressing percentage of growing-finishing pigs.

Although the precise molecular mechanisms responsible for neuronal death and motor dysfunction in late-onset Parkinson's disease (PD) are unknown, evidence suggests that mitochondrial dysfunction and neuroinflammation occur early, leading to a collective increase in reactive oxygen species (ROS) production and oxidative stress. However, the lack of methods for tracking oxidative stress in the living brain has precluded its use as a potential biomarker. The goal of the current study is to address this need through the evaluation of the first superoxide (O₂^•-)-sensitive radioactive tracer, [¹⁸F]ROStrace, in a model of late-onset PD. To achieve this goal, MitoPark mice with a dopaminergic (DA) neuron-specific deletion of transcription factor A mitochondrial (Tfam) were imaged with [¹⁸F]ROStrace from the prodromal phase to the end-stage of PD-like disease. Our data demonstrate [¹⁸F]ROStrace was sensitive to increased oxidative stress during the early stages of PD-like pathology in MitoPark mice, which persisted throughout the disease course. Similarly to PD patients, MitoPark males had the most severe parkinsonian symptoms and metabolic impairment. [¹⁸F]ROStrace retention was also highest in MitoPark males, suggesting oxidative stress as a potential mechanism underlying the male sex bias of PD. Furthermore, [¹⁸F]ROStrace may provide a method to identify patients at risk of Parkinson's before irreparable neurodegeneration occurs and enhance clinical trial design by identifying patients most likely to benefit from antioxidant therapies.

Alpha-lipoic acid (ALA) is a bioactive molecule with significant health effects. The biological action of ALA has been ascribed to the characteristic antioxidant properties of the oxidized form (ALA) and its reduced counterpart the dihydrolipoic acid (DHLA) system. The ALA/DHLA combination represents an ideal antioxidant since it can quench radicals, is able to chelate metals, is amphiphilic, and has no major adverse effects. This unique system is able to scavenge reactive oxygen species, exerting a major effect on tissue levels of reduced forms of other antioxidants, including glutathione. For this reason, ALA is also known as the "antioxidant of antioxidants". This review analyzes the antioxidant, anti-inflammatory, and neuroprotective effects of ALA and discusses its applications as an ameliorative tool for chronic diseases and those associated with oxidative stress. Results from in vitro and in vivo studies demonstrated that ALA modulates various oxidative stress pathways suggesting its application, alone or in combination with other functional substances, as a useful support in numerous conditions, in which the balance oxidant-antioxidant is disrupted, such as neurodegenerative disorders. Based on several successful clinical studies, it has been also established that oral ALA supplements are clinically useful in relieving the complications of diabetes and other disorders including cardiovascular diseases and nerve discomforts suggesting that ALA can be considered a useful approach to improving our health.