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 (SRD) to rats has proven to be a good model of systemic insulin resistance, the aim of our study was to analyze 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 a SRD causes a metabolic shift towards gluconeogenesis and fatty acid synthesis leading to an increase in triacilglyceride (TAG) levels in plasma and in the liver that were associated with a decrease in insulin sensitivity. Moreover, our results show that animals fed a SRD develop steatohepatitis characterized by the generation of oxidative stress, endoplasmic reticulum (ER) stress, inflammation, and apoptosis. Although no histological changes were observed after a two-week caloric restriction, key pathways associated with the progression of MASLD as inflammation, ER stress and apoptosis were slowed down. Notably, this two-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.

We searched PubMed, Web of Science, Embase, The Cochrane Library, China Biomedical Literature Database and other databases from inception to June 2023. The included studies were randomised controlled trials (RCT). The studies were screened by four authors, divided into two independent pairs. A total of eighteen studies were included, including 1362 patients, involving twelve intervention measures. The different nutrients had a significant effect on improving blood glucose, reducing inflammation levels and reducing oxidative stress compared with placebo (P < 0.05). Cumulative probability ranking showed that vitamin A + vitamin D + vitamin E ranked first in lowering fasting blood glucose (standardised mean difference (SMD) = 41.30, 95 % CI (2.07, 825.60)) and postprandial 2-h blood glucose (SMD = 15.19, 95 % CI (4.16, 55.53)). In terms of insulin resistance index, the first highest probability ranking is vitamin D (SMD = 5.12, 95 % CI (0.76, 34.54)). In terms of reducing the high-sensitivity C-reactive protein level, the first in probability ranking is VE (SMD = 2.58, 95 % CI (1.87,3.55)). The results of cumulative probability ranking showed that Mg + Zn + Ca + VD ranked first in reducing TNF-α (SMD = 1.90, 95% CI (0.40, 9.08)) and IL-6 (SMD = 1.83, 95 % CI (0.37, 9.12)). In terms of reducing malondialdehyde levels, the first ranked probability is VB1 (SMD = 4.99, 95 % CI (1.85, 13.46)). Cumulative probability ranking results showed that Ca + VD ranked first in reducing total antioxidant capacity (SMD = 0.66,95 % CI (0.38, 1.15)) and glutathione (SMD = 1.39, 95 % CI (0.43, 4.56)). In conclusion, nutritional interventions have significant effects on improving blood glucose, inflammatory levels and oxidative stress in patients with gestational diabetes. Due to the high uncertainty in the results and differences in the number and quality of studies included, the reliability of the conclusions still needs to be validated by conducting large-sample, high-quality RCT studies.

Clay minerals, such as layered double hydroxide (LDH) and montmorillonite (MMT), have attracted a great deal of attention for biological applications. Along with the rapid development of nanotechnology, public concern about the potential toxicity of nanoparticles is growing. In the present work, cytotoxicity of LDH and MMT was assessed in terms of inhibition of cell proliferation, generation of oxidative stress, and induction of inflammation response. Moreover, the biokinetics of LDH and MMT were evaluated; biokinetics provides information about in vivo absorption, distribution, and excretion kinetics. The results demonstrated that both LDH and MMT inhibited cell proliferation at relatively large concentrations and after long exposure time compared to other inorganic nanoparticles, although they generated reactive oxygen species (ROS). LDH induced pro-inflammatory cytokines in a size-dependent manner. Biokinetic study revealed that, after single-dose oral administration to mice, both LDH and MMT had extremely slow oral rates of absorption and did not accumulate in any specific organ. All the results suggest great potential of clay minerals for biological application at safe levels.

Non-alcoholic fatty liver disease (NAFLD) is a prevalent liver disorder, affecting approximately 25 % of the population. Coffee-drinking obese smokers exhibit lower body weights and decreased NAFLD rates, but the reasons behind this remain unclear. Additionally, the effect of nicotine, the main component of tobacco, on the development of NAFLD is still controversial. Our study aimed to explore the possible reasons that drinking coffee could alleviate NAFLD and gain weight and identify the real role of nicotine in NAFLD of obese smokers. A NAFLD model in mice was induced by administering nicotine and a high-fat diet (HFD). We recorded changes in body weight and daily food intake, measured the weights of the liver and visceral fat, and observed liver and adipose tissue histopathology. Lipid levels, liver function, liver malondialdehyde (MDA), superoxide dismutase (SOD), serum inflammatory cytokine levels and the expression of hepatic genes involved in lipid metabolism were determined. Our results demonstrated that nicotine exacerbated the development of NAFLD and caffeine had a hepatoprotective effect on NAFLD. The administration of caffeine could ameliorate nicotine-plus-HFD-induced NAFLD by reducing lipid accumulation, regulating hepatic lipid metabolism, alleviating oxidative stress, attenuating inflammatory response and restoring hepatic functions. These results might explain why obese smokers with high coffee consumption exhibit the lower incidence rate of NAFLD and tend to be leaner. It is essential to emphasise that the detrimental impact of smoking on health is multifaceted. Smoking cessation remains the sole practical and effective strategy for averting the tobacco-related complications and reducing the risk of mortality.

Trichinellosis is a re-emerging worldwide foodborne zoonosis. Oxidative stress is one of the most common detrimental effects caused by trichinellosis. In addition, Trichinella infection poses an infinite and major challenge to the host’s immune system. Resistance and side effects limit the efficiency of the existing anti-trichinella medication. Given that concern, this work aimed to investigate the anti-helminthic, antioxidant, anti-inflammatory and immunomodulatory effects of resveratrol and zinc during both phases of Trichinella spiralis infection. Sixty-four Swiss albino mice were divided into four equal groups: non-infected control, infected control, infected and treated with resveratrol, and infected and treated with zinc. Animals were sacrificed on the 7th and 35th days post-infection for intestinal and muscular phase assessments. Drug efficacy was assessed by biochemical, parasitological, histopathological, immunological, and immunohistochemical assays. Resveratrol and zinc can be promising antiparasitic, antioxidant, anti-inflammatory, and immunomodulatory agents, as evidenced by the significant decrease in parasite burden, the significant improvement of liver and kidney function parameters, the increase in total antioxidant capacity (TAC), the reduction of malondialdehyde (MDA) level, the increase in nuclear factor (erythroid-derived 2)-like-2 factor expression, and the improvement in histopathological findings. Moreover, both drugs enhanced the immune system and restored the disturbed immune balance by increasing the interleukin 12 (IL-12) level. In conclusion, resveratrol and zinc provide protection for the host against oxidative harm and the detrimental effects produced by the host’s defense response during Trichinella spiralis infection, making them promising natural alternatives for the treatment of trichinellosis.

Kisspeptin is characterized as a neuropeptide with a pivotal function in female and male infertility, and its antioxidant properties have been demonstrated. In this study, the effects of kisspeptin on the improvement of the vitrification and thawing results of human ovarian tissues were investigated. In this work, 12 ovaries from patients who underwent hysterectomy were collected laparoscopically, and then 32 samples from each of their tissues were taken. Haematoxylin and eosin (H&E) staining was performed to check the normality of the ovarian tissue and, subsequently, the samples were allocated randomly into four groups, including: (1) fresh (control), (2) vitrification, (3) vitrified + 1 μM kisspeptin, and (4) vitrified + 10 μM kisspeptin groups. After vitrification, thawing, and tissue culture processes, H&E staining for tissue quality assessment, terminal deoxynucleotidyl transferase dUTP nick end labelling assay for apoptosis evaluation, and malondialdehyde (MDA), superoxide dismutase (SOD), and ferric reducing ability of plasma tests for oxidative stress appraisal were carried out. Our histological results showed incoherency of ovarian tissue morphology in the vitrification group compared with other groups. Other findings implicated increased apoptosis rate and MDA concentration and reduced SOD activity and total antioxidant capacity (TAC) in the vitrification group compared with the control group (P < 0.05). Moreover, decreased apoptosis rate and MDA concentration, and increased TAC and SOD function were observed in the vitrification with kisspeptin groups (1 μM and 10 μM) compared with the vitrified group (P < 0.05). Our reports express that kisspeptin is an effective agent to overcome the negative effects of vitrification by regulating reactive oxygen species-related apoptotic processes.

Obeticholic acid (OCA), a farnesoid X receptor (FXR) agonist, has been demonstrated to ameliorate the histopathological characteristics of liver damage. Nonetheless, the systemic safety profile of OCA with regard to reproduction and development remains poorly understood. In the present study, we conducted a dose–response experiment by administering OCA at doses of 5 mg/kg, 10 mg/kg, or 20 mg/kg through tube feeding to investigate its effect on reproductive development and fertilization rate in both male and female mice. Furthermore, we evaluated the levels of protein and mitochondrial function in the placenta through western blot, qPCR, and scanning electron microscopy. The results showed that 10 mg/kg and 20 mg/kg OCA doses significantly reduced the rate of placental implantation (P < 0.05). Also, OCA increased maternal body weight. In addition, OCA increased levels of FXR and TGR5 and produced changes in oxidative stress levels (P < 0.05). Mitochondrial activity result found that 10 mg/kg and 20 mg/kg of OCA significantly reduced the mitophagy autosomes/nucleus compared with the normal control group (P < 0.05). What is more, there was no significant difference in sperm count after OCA intervention in either C57BL/10 mice or BALB/c mice. Overall, we demonstrated that OCA treatment protected against placental implantation by suppressing placental oxidative stress and mitochondrial activity.