Thyroid disorders are increasingly prevalent globally and are considered metabolic-lifestyle diseases. While medications can manage thyroid dysfunction, they are usually lifelong, costly, and not always practical. Intermittent fasting (IF), a highly adaptable dietary regimen, has been shown to influence lifestyle, gut microbiome, and circadian rhythms. Our study hypothesized that IF, combined with vitamin supplementation, could reduce the risk of thyroid disorders due to their antioxidant effects. In this study, experimental animals were divided into five groups: Euthyroid, hypothyroidism control, IF + vitamin E, vitamin E, and IF. Hypothyroidism was induced using propylthiouracil (PTU) over 24 days, and IF and vitamin E (66 mg/ml) were administered based on the experimental group. The hypothyroid animals exhibited increased anxiety, weight gain, lipid peroxidation, and a significant reduction in thyroid hormone levels, locomotor activity, and antioxidant levels—clear signs of thyroid dysfunction’s impact on metabolism and overall health. Our proposed therapies IF and vitamin E effectively mitigated thyroid damage. Drawing inspiration from ancient Ayurveda and modern healthcare strategies, these cost-effective and practical regimens offer a promising solution to managing thyroid disorders globally.

Inflammation and oxidative stress contribute to the progression of chronic diseases, and the volume of research in this area is rapidly expanding. Various dietary indices have been developed to determine the overall inflammatory or oxidative stress potential of a diet; however, few have been validated in cardiometabolic disease populations. This review aimed to explore the association between dietary indices and biomarkers of inflammation and oxidative stress in adults with cardiometabolic conditions. Four databases were systematically searched for literature in any language (Embase, CINAHL, CENTRAL, and MEDLINE) with 12,177 deduplicated records identified. Seventeen studies of adults with metabolic syndrome, cardiovascular disease, type 2 diabetes, non-alcoholic fatty liver disease or chronic kidney disease were included. Fourteen studies were observational studies, one study was a clinical trial, and one was a randomised controlled trial. Four dietary indices were reported on with most studies (n=11) reporting on the dietary inflammatory index. The most reported biomarker was C-reactive protein. The findings were narratively synthesised. Results were inconclusive due to the heterogeneity of dietary indices and their use, disease states, and biomarkers reported. Only one study reporting on the dietary inflammatory index assessed all 45 parameters. Observational studies, particularly retrospective designs (n=7) are subject to recall and selection biases, potentially presenting overestimated results. Further research is required to determine the relationship between dietary indices and biomarkers of inflammation and oxidative stress in cardiometabolic disease populations. Future research should be rigorous, prospective, assess the full range of index parameters, and examine biomarkers the tool was developed for.

Green tea, a plant rich in bioactive compounds, has been highlighted for its beneficial effects. In the present systematic review and meta-analysis of randomised controlled trials (RCTs), the impact of green tea on inflammatory and oxidative markers is investigated. Using pre-defined keywords, online databases (PubMed, Scopus, Web of Science Core Collection, and Google Scholar) were searched for relevant articles, published from inception up to February 2024. The outcomes included C-reactive protein (CRP), tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1 beta (IL-1β), total antioxidant capacity (TAC), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPX). Analyses of subgroups, linear, and non-linear associations were also carried out. Out of 1264 records initially retrieved, 38 RCTs were included. Supplementation with green tea improved the following indicators: IL-1β (weighted mean difference (WMD): −0.10 pg/mL; 95% CI: −0.15, -0.06), MDA (WMD: −0.40 mcmol/L; 95 % CI: −0.63, −0.18), TAC (WMD: 0.09 mmol/L; 95% CI: 0.05, 0.13), SOD (WMD: 17.21 u/L; 95% CI: 3.24, 31.19), and GPX (WMD: 3.90 u/L; 95% CI: 1.85, 5.95); but failed to improve others, including CRP (WMD: 0.01 mg/L; 95% CI: −0.14, 0.15), IL-6 (WMD: −0.34 pg/mL; 95% CI:−0.94, 0.26), and TNF-α (WMD: −0.07 pg/mL; 95% CI: −0.42, 0.28). Supplementation with green tea can improve the body’s oxidative status. However, the results showed no significant effect of green tea on inflammatory markers, except for IL-1β. Further studies are needed to determine the effectiveness of green tea, particularly on inflammatory status.

The primary causes of female mortality often involve diseases related to oxidative stress. Dietary total antioxidant capacity (TAC) evaluates its antioxidant content and potential health effects. This study, registered with PROSPERO (ID: CRD42024427784), explores the association between dietary TAC and women’s health outcomes, including endocrine conditions with gynaecological implications, obstetric outcomes, gynaecological conditions and oncological diseases related to the female reproductive system. We conducted a systematic search in MEDLINE (via PubMed), EMBASE, LILACS and CINAHL for observational studies published up to February 2024 that explored the relationship between dietary TAC and these health conditions. Data were analysed using RevMan 5·4 software. Nineteen studies met the eligibility criteria (sample sizes: 64–3209 women) and examined various conditions, including neoplasms (breast, endometrial and ovarian), bacterial vaginosis, menopause, polycystic ovary syndrome (PCOS), pre-eclampsia (PE), gestational diabetes mellitus (GDM), miscarriage, infertility and inflammation and oxidative stress markers. The meta-analysis identified a significant association between dietary TAC, measured in vitamin C equivalents, and breast cancer, revealing that women with the disease had a lower dietary TAC due to reduced antioxidant intake. Mixed results were found for endometrial cancer, while higher TAC levels were associated with a lower risk of PCOS and infertility. Among postmenopausal women, higher TAC correlated with fewer symptoms such as sleep issues and anxiety. In gestational conditions, higher dietary TAC was linked to a lower risk of miscarriage, GDM and PE. Twelve of the nineteen studies demonstrated significant associations between dietary TAC and the outcomes of interest.

Current evidence points to a research-practice gap in mental health. There is a specific unmet need to identify novel strategies to improve diagnostic criteria, especially when clinical manifestations overlap as in the case of bipolar (BD) and major depressive disorder (MDD). Based on the rapidly evolving notion that affective disorders are characterized by disrupted brain-body communication, current efforts of neuropsychiatric research are converging towards the identification of specific clusters of peripheral interconnected biomarkers. We argue that these can capture the complexity of the disease as they are linked to the fundamental pathophysiological mechanisms underlying BD or MDD, and can thus deliver an unbiased biosignature. Here we provide a critical viewpoint on the promises and challenges of biomarkers to identify reliable biosignatures of affective disorders. Novel methodological insight and relevant biomarkers are discussed with a main focus on immunometabolic derangements and disrupted redox balance. Major advancements are reviewed taking into consideration that an unbiased diagnosis can only derive from a deep understanding of how biological, psychological, and social factors interact ultimately affecting the clinical manifestation of affective disorders.

The therapeutic effects of probiotics in patients with traumatic brain injury (TBI) remain unclear. This study aimed to investigate the effects of probiotic supplementation on cell adhesion molecules, oxidative stress, and antioxidant parameters in TBI patients. This randomized, double-blind, placebo-controlled trial included 46 TBI patients who were randomly assigned to receive either a probiotic supplement (n = 23) or a placebo (n = 23) for 14 days. The probiotic capsule contained four strains of Lactobacillus (L. casei, L. bulgaricus, L. rhamnosus, L. acidophilus), two strains of Bifidobacterium (B. longum, B. breve), and Streptococcus thermophilus. Serum levels of intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, pro-oxidant antioxidant balance (PAB), malondialdehyde (MDA), nitric oxide (NO), total antioxidant capacity (TAC), and arylesterase (ARE) activity were measured at the beginning and end of the trial. Dietary intakes of patients were also recorded at the beginning and end of the trial. At the end of the study, there were no significant changes in ICAM-1, VCAM-1, PAB, MDA, NO, TAC, and ARE levels. However, patients who received probiotic supplements had significantly increased dietary intakes of energy, macronutrients, vitamin E, zinc, copper, and selenium compared with the placebo group. This study provides evidence that probiotic supplementation for 14 days in TBI patients has beneficial effects on dietary intake. However, it did not affect serum levels of cell adhesion molecules, oxidative stress, or antioxidant parameters. These findings should be considered preliminary, and further research is needed to evaluate long-term and clinical outcomes.

Trichinellosis is a widespread food-borne zoonosis, causing mild to severe illness in humans with potential fatality. Its treatment remains challenging due to the side effects and limited efficacy of specific drugs. Therefore, the current study was conducted to assess the therapeutic effects of ellagic acid (EA) alone and combined with albendazole against trichinellosis and its biochemical and pathological alterations in mice. Mice were divided into two main groups: G1 and G2 for the intestinal and muscular phases, respectively. Then each group was subdivided into five subgroups: (a) non-infected control, (b) infected control non-treated, (c) infected and treated with EA, (d) infected and treated with albendazole, and (e) infected and treated with a combination of both. Parasitological, biochemical, and histopathological studies were used to evaluate the therapeutic outcomes. Treatment with EA resulted in a significant reduction of the mean counts of intestinal adult worms and muscular larvae compared to the infected control. EA improved oxidative stress as it reduced nitric oxide and increased catalase activities in intestinal and muscular tissues. Additionally, it alleviated the inflammatory response, as evidenced by downregulating IL-6 and increasing IL-10 expressions in tissues. Furthermore, it improved liver functions and ameliorated the pathological alterations induced by trichinellosis. The best results were detected in combination treatments that indicated synergistic effects between EA and albendazole. In conclusion, EA can be used as an anti-inflammatory and antioxidant with a promising anti-parasitic impact against trichinellosis.

Spontaneous abortion (SA) is considered one of the most prevalent adverse outcomes of pregnancy. SA may occur due to genetic susceptibility and various maternal factors such as nutritional status. The aim of this study was to assess how dietary carotenoids and the FTO gene are related to SA. This case–control study included 192 women with a history of SA as the case group and 347 healthy women without history of SA as the control group. To evaluate carotenoid intake, a valid 168-item food frequency questionnaire (FFQ) was used. The FTO gene was genotyped for the presence of the rs9939609 polymorphism using the tetra-primer amplification refractory mutation system-polymerase chain (ARMS-PCR). The results indicated a significant negative association between dietary intake of β-cryptoxanthin and SA in carriers of the TT genotype of the FTO rs9939609 polymorphism after adjustment for age, BMI, physical activity, smoking, alcohol drinking, and calorie intake (β = −0.28, P = 0.02). No association was found between SA with dietary intake of beta-carotene, alpha-carotene, lutein, and lycopene among carriers of different FTO genotypes. The FTO genotype may have an effect on the association between SA and carotenoid intake. Dietary intake of β-cryptoxanthin may act as a protective factor against SA only in carriers of the TT genotype of the FTO rs9939609 polymorphism.

Oxidative stress may be involved in the progression of hypothyroidism in patients with Hashimoto thyroiditis (HT). Vitamin C is a well-known powerful antioxidant. To our knowledge, whether vitamin C intake relates to hypothyroidism in patients with HT remains unclear. In this cross-sectional study based on the National Health and Nutrition Examination Survey, 2007–2012, we aimed to explore the relationship between total vitamin C intake and hypothyroidism in patients with HT, using multivariate logistic regression models and restricted cubic spline analyses. Our results showed a significant negative linear association between total vitamin C intake (log10-transformed data) and hypothyroidism in HT. Compared with those with the lowest quartile of total vitamin C intake (log10-transformed), participants with the highest quartile were at lower odds of having hypothyroidism (adjusted OR 0·40, 95 % CI: 0·18, 0·88, Ptrend = 0·027). This association was consistent in subgroups stratified by sex (Pfor interaction = 0·084) and age (≥ 60 years and < 60 years, Pfor interaction = 0·330). This study revealed that total vitamin C intake was inversely associated with hypothyroidism among individuals with HT, indicating that higher vitamin C intakes (4·57–1258·9 mg/d) may be associated with a lower likelihood of hypothyroidism among HT participants.

A positive association has been demonstrated between consumption of sucrose-sweetened beverages and the prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD). Since the administration of 30 % sucrose in the drinking water (sucrose-rich diet (SRD)) to rats has proven to be a good model of systemic insulin resistance, the aim of our study was to analyse the effect of caloric restriction applied on SRD-treated rats by switching back to a standard diet, on liver morphology, function and metabolism. Consumption of an SRD causes a metabolic shift towards gluconeogenesis and fatty acid synthesis leading to an increase in TAG levels in plasma and in the liver that were associated with a decrease in insulin sensitivity. Moreover, our results show that animals fed an SRD develop steatohepatitis characterised by the generation of oxidative stress, endoplasmic reticulum (ER) stress, inflammation and apoptosis. Although no histological changes were observed after a 2-week caloric restriction, key pathways associated with the progression of MASLD as inflammation, ER stress and apoptosis were slowed down. Notably, this 2-week intervention also increased liver insulin sensitivity (evaluated by AKT activity in this tissue) and drove the lipid metabolic profile towards oxidation, thus lowering circulating TAG levels. In summary, the present study uncovers underlying mechanisms affected, and their metabolic consequences, during the first stages of the phenotypic reversal of steatohepatitis by switching back to a standard diet after receiving sucrose-sweetened water for several weeks.

This study evaluated the effect of green tea extract and metformin and its interaction on markers of oxidative stress and inflammation in overweight women with insulin resistance. After screening, 120 women were randomly allocated in 4 groups: Placebo (PC): 1g of microcrystalline cellulose/day; Green tea (GT): 1 g (558 mg polyphenols) of standardized dry extract of green tea/day and 1 g of placebo/day; Metformin (MF): 1 g of metformin/day and 1 g of placebo/day; Green Tea and Metformin (GTMF): 1 g (558 mg polyphenols) and 1 g of metformin/day. All groups were followed-up for 12 weeks with assessment of oxidative damage to lipids and proteins, specific activity of antioxidant enzymes and inflammatory cytokine serum levels. The association of green tea with metformin significantly reduced IL-6 (GTMF: –29.7((–62.6)–20.2))(p = 0.004). Green tea and metformin isolated reduced TNF-α (GT: –12.1((–18.0)–(–3.5)); MF: –24.5((–38.60)–(–4.4)) compared to placebo (PB: 13.8 (1.2–29.2))(P < 0.001). Also, isolated metformin reduced TGF-β (MF: –25.1((–64.4)–0.04)) in comparison to placebo (PB: 6.3((–1.0)–16.3))(p = 0.038). However, when combined, their effects were nullified either for TNF-α (GTMF: 6.0((–5.7)–23.9) and for TGF-β (GTMF: –1.8((–32.1)–8.5). This study showed that there is a drug-nutrient interaction between green tea and metformin that is dependent on the cytokine analyzed.

Hydrogen sulfide (H2S) has been shown to play a significant role in oxidative stress across various tissues and cells; however, its role in sperm function remains poorly understood. This study aimed to investigate the protective effect of GYY4137, a slow-releasing H2S compound, on sperm damage induced by H2O2. We assessed the effects of GYY4137 on motility, viability, lipid peroxidation and caspase-3 activity in human spermatozoa in vitro following oxidative damage mediated by H2O2. Spermatozoa from 25 healthy men were selected using a density gradient centrifugation method and cultured in the presence or absence of 10 μM H2O2, followed by incubation with varying concentrations of GYY4137 (0.625–2.5 μM). After 24 h of incubation, sperm motility, viability, lipid peroxidation, and caspase-3 activity were evaluated. The results indicated that H2O2 adversely affected sperm parameters, reducing motility and viability, while increasing oxidative stress, as evidenced by elevated lipid peroxidation and caspase-3 activity. GYY4137 provided dose-dependent protection against H2O2-induced oxidative stress (OS). We concluded that supplementation with GYY4137 may offer antioxidant protection during in vitro sperm preparation for assisted reproductive technology.

This study investigated the impact of diallyl disulfide (DADS) on oxidative stress induced by hydrogen peroxide (H2O2) in ovine rumen epithelial cells (RECs). Initially, the effects of DADS were evaluated on cellular reactive oxygen species (ROS) levels, antioxidant capacity in RECs were estimated. Then, RNA-seq analysis was conducted in DADS-treated and untreated cells to analyze the differential gene expression, as well as Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Finally, the effects of DADS on Kelch-like ECH associated protein 1/the nuclear factor erythroid 2-related factor 2 (Keap1/Nrf2) signaling pathway in RECs were evaluated. Results showed that DADS remarkably enhanced superoxide dismutase (SOD) activity and total antioxidant capacity (T-AOC) (P < 0.05) while reducing ROS and malonaldehyde production (P < 0.05) in H2O2-treated RECs. Transcriptomic analysis revealed that DADS might influence glutathione synthesis through cysteine and methionine metabolism, thereby affecting the transcription of genes involved in immunity and oxidative stress. The DADS treatment resulted in increased nuclear translocation of Nrf2 and upregulation of mRNA and protein levels of quinone oxidoreductase 1, heme oxygenase 1, and Nrf2. The Nrf2-specific inhibitor nullified the protective effects of DADS on malonaldehyde formation induced by H2O2 and decreased T-AOC and SOD activities. In conclusion, DADS demonstrated the ability to alleviate oxidative stress in RECs by promoting antioxidative capacity through the Keap1/Nrf2 signaling pathway.

Obesity is a multifactorial pathophysiological condition with an imbalance in biochemical, immunochemical, redox status and genetic parameters values. We aimed to estimate the connection between relative leucocyte telomere lengths (rLTL) – biomarker of cellular ageing with metabolic and redox status biomarkers values in a group of obese and lean children. The study includes 110 obese and 42 lean children and adolescents, both sexes. The results suggested that rLTL are significantly shorter in obese, compared with lean group (P < 0·01). Negative correlation of rLTL with total oxidant status (TOS) (Spearman’s ρ = –0·365, P < 0·001) as well as with C-reactive protein (Spearman’s ρ = –0·363, P < 0·001) were observed. Principal component analysis (PCA) extracted three distinct factors (i.e. principal components) entitled as: prooxidant factor with 35 % of total variability; antioxidant factor with 30 % of total variability and lipid antioxidant – biological ageing factor with 12 % of the total variability. The most important predictor of BMI > 30 kg/m2 according to logistic regression analysis was PCA-derived antioxidant factor’s score (OR: 1·66, 95th Cl 1·05–2·6, P = 0·029). PCA analysis confirmed that oxidative stress importance in biological ageing is caused by obesity and its multiple consequences related to prooxidants augmentation and antioxidants exhaustion and gave us clear signs of disturbed cellular homoeostasis deepness, even before any overt disease occurrence.

Oxidative stress is a risk factor for mammary health, resulting in decreased milk yield and milk quality. Application of exogenous bioactive compounds has been a research focus of antioxidation of animals in the mammary gland. Quercetin is a flavonoid extracted from vegetables, fruits and tea and has been shown to have a variety of biological activities, but the effect of quercetin on redox imbalance in mammary epithelial cells is unclear. In this study, cells of HC11, a mouse mammary epithelial cell line, were treated with quercetin, and the effects and molecular mechanisms of quercetin protection on hydrogen peroxide-induced oxidative stress were studied. Results showed that 20 μΜ quercetin attenuated hydrogen peroxide-induced lactate dehydrogenase release and reactive oxygen species (ROS) accumulation and alleviated the reduction of cell viability and antioxidant capacity. Quercetin significantly restored the activation of mitogen-activated protein kinase (MAPK) and nuclear factor E2-related factor 2 (Nrf2) pathways induced by hydrogen peroxide. Importantly, the inhibitors of p38 MAPK and extracellular regulated protein pathways affected the activation of Nrf2 pathway. All inhibitors of MAPK and Nrf2 pathways reduced the protective effects of quercetin on cell proliferation, the activity of catalase and the expression of glutamate-cysteine ligase modifier subunit. Meanwhile, the effects of quercetin on the production of ROS and expression of glutamate/cystine reverse transporter light chain were mainly dependent on Nrf2 pathway. In summary, the protective effect of quercetin in mammary epithelial cells was mediated via MAPK and Nrf2 pathways.

The purpose of this study was to investigate the effect of an egg white hydrolysate (EWH) to protect white adipose tissue damage from cardiometabolic changes induced by severe hypertension. Male Wistar rats were uninephrectomised and divided: SHAM (weekly subcutaneous vehicle (mineral oil + propylene glycol, 1:1)), SHAM + EWH (subcutaneous vehicle plus EWH via gavage, 1 g/kg per day), DOCA (deoxycorticosterone acetate diluted in vehicle subcutaneously weekly in subsequent doses of 20 mg/kg -1st week, 12 mg/kg - 2–3th week, and 6 mg/kg -4–8th week, respectively, plus 1 % NaCl and 0·2 % KCl in drinking water), and DOCA + EWH. Body weight gain, food and water intake, glucose and lipid metabolism were evaluated. Oxidative stress was assessed by biochemical assay and immunofluorescence for NOX-1, nuclear factor kappa B (NFκB), and caspase-3 in retroperitoneal white adipose tissue (rtWAT). Proinflammatory cytokines (IL-6 and 1β), CD163+ macrophage infiltration, and immunohistochemistry for TNFα and uncoupling protein-1 were evaluated, as well as histological analysis on rtWAT. Glutathione peroxidase and reductase were also determined in plasma. EWH showed hypocholesterolemic, antioxidant, anti-inflammatory, and anti-apoptotic properties in the arterial hypertension DOCA-salt model. The results demonstrated the presence of functional changes in adipose tissue function by a decrease in macrophage infiltration and in the fluorescence intensity of NFκB, NOX-1, and caspase-3. A reduction of proinflammatory cytokines and restoration of antioxidant enzymatic activity and mitochondrial oxidative damage by reducing uncoupling protein-1 fluorescence intensity were also observed. EWH could be used as a potential alternative therapeutic strategy in the treatment of cardiometabolic complications associated with malignant secondary arterial hypertension.

Maternal obesity may trigger long-term neurodevelopmental disorders in offspring. Considering the benefits of the Brazil nut (Bertholletia excelsa H.B.K.), a rich source of nutrients such as selenium, this study aimed to evaluate its effect on the behavior of obese rat offspring and its relationship with oxidative stress. From 60 days of age until weaning, female Wistar rats were fed a high-fat diet (mHF) or an HF diet supplemented with 5% Brazil nut (mHF/BN), while control mothers (mCTL) were fed a standard diet or a standard diet supplemented with 5% Brazil nut (mBN). Male pups received a standard diet throughout life and, at 30 and 90 days old, were subjected to behavioral tasks to evaluate anxiety and cognition. Biochemical evaluations were performed at 90 days of age. No alterations were observed in the anxiety behavior of the offspring. However, the offspring of the mHF group (oHF) exhibited impaired short-term memory at 30 and 90 days of age and impaired long-term memory at 30 days. Short-term memory impairment was prevented by Brazil nuts in young rats (30 days). While the serum selenium concentration was reduced in the oHF group, the serum catalase concentration was reduced in all groups, without changes in lipid peroxidation or protein carbonylation. Brazil nut maternal diet supplementation prevented short- and long-term cognitive impairment in the offspring, which may be related to the selenium levels.