The objective was to evaluate the use of resveratrol conjugated with silica nanoparticles during the in vitro maturation of bovine oocytes. The oocytes were divided into the following treatment groups during the maturation process: control (n = 159), resveratrol 0.5 μM (n = 158), resveratrol 1 μM (n = 155), nanoparticles conjugated with 0.5 μM resveratrol (n = 159), and nanoparticles conjugated with 1 μM resveratrol (n = 158). Several parameters were assessed, including cumulus oophorus size, reactive oxygen species (ROS) production, oocyte nuclear maturation, cell apoptosis, cleavage rates, and blastocyst production rates. Statistical analysis was conducted using Sigma Plot software (version 11) and SAS Studio, with statistical significance defined as P ≤ 0.05 for the main effects and interactions. The results indicated that the cumulus oophorus size was smaller in the resveratrol 1 μM treatment group, and the oocyte size was reduced in the nanoparticle 1 μM treatment group. No significant differences were detected between the treatment groups in terms of ROS production, oocyte maturation, or cell apoptosis. However, the resveratrol 1 μM treatment group exhibited decreased rates of cleavage and blastocyst formation. In contrast, the nanoparticles 0.5 μM and 1.0 μM treatments showed improved cleavage and blastocyst rates compared with the resveratrol 1.0 μM treatment group. In summary, while resveratrol alone at 1 μM concentration had a negative impact on cleavage and blastocyst rates, the use of silica nanoparticles conjugated with resveratrol (both 0.5 μM and 1 μM) enhanced these outcomes, suggesting a potential advantage in using nanoparticle-conjugated resveratrol for the in vitro maturation of bovine oocytes.

Manganese (Mn) is a crucial trace element that actively participates in a diverse array of physiological processes. Mn is maintained at appropriate levels in the body by absorption and excretion by the body. Dysregulation of Mn homeostasis can lead to a variety of diseases, especially the accumulation of Mn in the brain, resulting in toxic side effects. We reviewed the metabolism and distribution of Mn at multiple levels, including organ, cellular and sub-cell levels. Mitochondria are the main sites of Mn metabolism and energy conversion in cells. Enhanced Mn superoxide dismutase activity reduces mitochondrial oxidative stress and inhibits cancer development. In addition, Mn enhances anti-cancer immune responses through the cGAS–STING pathway. We introduced various delivery vectors for Mn delivery to cancer sites for Mn supplementation and anti-cancer immunity. This review aims to provide new research perspectives for the application of Mn in the prevention and treatment of human diseases, especially by enhancing anti-cancer immune responses to inhibit cancer progression.

Curcumin, a natural bioactive compound, is known to exert therapeutic effects on cancer and dysplasia. However, less is known about its effects on DNA damage and repair in obesity. Therefore, this study was to examine the novel role of curcumin in regulating DNA repair signalling using a high-fat diet (HFD)-induced obesity in mice. Male C57BL/6 mice were fed either a 60 % HFD or standard chow with curcumin (2·5 g/kg diet) for 8 weeks. We observed that curcumin alleviated weight gain, preserved glucose balance and enhanced liver fat accumulation and lipid profile in mice with obesity induced by an HFD. Curcumin enhanced the adipocyte-derived mesenchymal stem cell (ADMSC) population (Sca-1 + CD45-) and expression of phosphorylated checkpoint kinase1 (pCHK1), a DNA repair gene, in adipocytes isolated from adipose tissues of HFD-induced obesity in mice. Moreover, in human preadipocytes, treatment with 10 μM curcumin effectively reduced the mRNA levels of IL6 and CCL2 in a dose-dependent manner, while treatment with 100 μM H2O2 together with curcumin upregulated the levels of pCHK2 and total CHK2 protein and reduced level of γH2AX, a biomarker of DNA damage. In addition, curcumin inhibits preadipocyte-to-adipocyte differentiation. In conclusion, our data demonstrated that curcumin reduced the pro-inflammatory response and DNA damage in adipocytes, controlling weight gain in mice with HFD-induced obesity.

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 (CAMs), oxidative stress and antioxidant parameters in TBI patients. This randomised, double-blind, placebo-controlled trial included forty-six TBI patients who were randomly assigned to receive either a probiotic supplement (n 23) or a placebo (n 23) for 14 d. 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, Zn, Cu and Se compared with the placebo group. This study provides evidence that probiotic supplementation for 14 d in TBI patients has beneficial effects on dietary intake. However, it did not affect serum levels of CAMs, oxidative stress or antioxidant parameters. These findings should be considered preliminary, and further research is needed to evaluate long-term and clinical outcomes.

The scientific literature indicates that chokeberry is widely used as a supplement to support the maintenance of the body’s homeostasis by reducing inflammation and oxidative stress. In recent years, positive effects of chokeberry on intestinal parameters have also been observed. Oxidative stress, inflammation and, according to recent reports, also the gut microbiome are closely related to the overall well-being and health of the population. This study, therefore, attempts to summarise all the health benefits of black chokeberry supplementation. This study was registered in PROSPERO (International Prospective Register of Systematic Reviews) under registration number CRD42023395969. Additionally, the systematic review was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) method. Electronic databases were searched in Web of Science, PubMed, Scopus and EBSCO using the following combination of the words ‘chokeberry or aronia’ and ‘inflammation or oxidative stress or microbiota or microbiome or permeability or gut’. Ultimately, fifty-seven studies were summarised in the review. Data analysis showed that black chokeberry has a positive effect on the reduction of inflammation, oxidative stress and intestinal microflora, but the size of the changes varies and depends on many variables. Therefore, the researchers concluded that the compounds found in black chokeberry play a pivotal role in maintaining the overall balance within the system. This is a crucial consideration given the tendency for disturbances in organismal homeostasis to accompany disease processes and various disorders. However, further research is necessary to elucidate the mechanisms and optimise its use fully.

The incidence of obesity-related glomerulopathy (ORG) is rising worldwide with very limited treatment methods. Paralleled with the gut–kidney axis theory, the beneficial effects of butyrate, one of the short-chain fatty acids (SCFA) produced by gut microbiota, on metabolism and certain kidney diseases have gained growing attention. However, the effects of butyrate on ORG and its underlying mechanism are largely unexplored. In this study, a mice model of ORG was established with a high-fat diet feeding for 16 weeks, and sodium butyrate treatment was initiated at the 8th week. Podocyte injury, oxidative stress and mitochondria function were evaluated in mice kidney and validated in vitro in palmitic acid-treated-mouse podocyte cell lines. Further, the molecular mechanisms of butyrate on podocytes were explored. Compared with controls, sodium butyrate treatment alleviated kidney injuries and renal oxidative stress in high-fat diet-fed mice. In mouse podocyte cell lines, butyrate ameliorated palmitic acid-induced podocyte damage and helped maintain the structure and function of the mitochondria. Moreover, the effects of butyrate on podocytes were mediated via the GPR43-Sirt3 signal pathway, as evidenced by the diminished effects of butyrate with the intervention of GPR43 or Sirt3 inhibitors. In summary, we conclude that butyrate has therapeutic potential for the treatment of ORG. It attenuates high-fat diet-induced ORG and podocyte injuries through the activation of the GPR43-Sirt3 signalling pathway.

Complex tumour ecosystem comprising tumour cells and its associated tumour microenvironment (TME) constantly influence the tumoural behaviour and ultimately impact therapy failure, disease progression, recurrence and poor overall survival of patients. Crosstalk between tumour cells and TME amplifies the complexity by creating metabolic changes such as hypoxic environment and nutrient fluctuations. These changes in TME initiate stem cell-like programmes in cancer cells, contribute to tumoural heterogeneity and increase tumour robustness. Recent studies demonstrate the multifaceted role of autophagy in promoting fibroblast production, stemness, cancer cell survival during longer periods of dormancy, eventual growth of metastatic disease and disease resistance. Recent ongoing studies examine autophagy/mitophagy as a powerful survival strategy in response to environmental stress including nutrient deprivation, hypoxia and environmental stress in TME. It prevents irreversible senescence, promotes dormant stem-like state, induces epithelial–mesenchymal transition and increases migratory and invasive potential of tumour cells. The present review discusses various theories and mechanisms behind the autophagy-dependent induction of cancer stem cell (CSC) phenotype. Given the role of autophagic functions in CSC aggressiveness and therapeutic resistance, various mechanisms and studies based on suppressing cellular plasticity by blocking autophagy as a powerful therapeutic strategy to kill tumour cells are discussed.

Osteoarthritis (OA), a disease with a multifactorial aetiology and an enigmatic root cause, affects the quality of life of many elderly patients. Even though there are certain medications utilised to reduce the symptomatic effects, a reliable treatment method to reverse the disease is yet to be discovered. Zinc is a cofactor of over 3000 proteins and is the only metal found in all six classes of enzymes. We explored zinc’s effect on the immune system and the bones as OA affects both. We also discussed zinc-dependent enzymes, highlighting their significant role in the disease’s pathogenesis. It is important to note that both excessive and deficient zinc levels can negatively affect bone health and immune function, thereby exacerbating OA. The purpose of this review is to offer a better understanding of zinc’s impact on OA pathogenesis and to provide clarity regarding its beneficial and detrimental outcomes. We searched thoroughly systematic reviews, meta-analysis, review articles, research articles and randomised controlled trials to ensure a comprehensive review. In brief, using zinc supplementation in the treatment of OA may act as a doubled-edged sword, offering potential benefits but also posing risks.

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.

Nuclear and chemical weapons of mass destruction share both a tragic and beneficial legacy in mankind’s history and health. The horrific health effects of ionizing radiation and mustard gas exposures unleashed during disasters, wars, and conflicts have been harnessed to treat human health maladies. Both agents of destruction have been transformed into therapies to treat a wide range of cancers. The discovery of therapeutic uses of radiation and sulfur mustard was largely due to observations by clinicians treating victims of radiation and sulfur mustard gas exposures. Clinicians identified vulnerability of leukocytes to these agents and repurposed their use in the treatment of leukemias and lymphomas. Given the overlap in therapeutic modalities, it goes to reason that there may be common mechanisms to target as protective strategies against their damaging effects. This commentary will highlight oxidative stress as a common mechanism shared by both radiation and sulfur mustard gas exposures and discuss potential therapies targeting oxidative stress as medical countermeasures against the devastating lung diseases wrought by these agents.

Neoadjuvant radiotherapy (RT) is commonly used as standard treatment for rectal cancer. However, response rates are variable and survival outcomes remain poor, highlighting the need to develop new therapeutic strategies. Research is focused on identifying novel methods for sensitising rectal tumours to RT to enhance responses and improve patient outcomes. This can be achieved through harnessing tumour promoting effects of radiation or preventing development of radio-resistance in cancer cells. Many of the approaches being investigated involve targeting the recently published new dimensions of cancer hallmarks. This review article will discuss key radiation and targeted therapy combination strategies being investigated in the rectal cancer setting, with a focus on exploitation of mechanisms which target the hallmarks of cancer.

Osteoarthritis (OA) commonly affects the knee and hip joints and accounts for 19.3% of disability-adjusted life years and years lived with disability worldwide (Refs 1, 2). Early management is important in order to avoid disability uphold quality of life (Ref. 3). However, a lack of awareness of subclinical and early symptomatic stages of OA often hampers early management (Ref. 4). Moreover, late diagnosis of OA among those with severe disease, at a stage when OA management becomes more complicated is common (Refs 5, 6, 7, 8). Established risk factors for the development and progression of OA include increasing age, female, history of trauma and obesity (Ref. 9). Recent studies have also drawn a link between OA and metabolic syndrome, which is characterized by insulin resistance, dyslipidaemia and hypertension (Refs 10, 11).

The primary goal of the investigation was to analyse the anti-inflammatory and antioxidant properties of Gamma-linolenic acid (GLA) on rats with indomethacin (IND)-induced gastric ulcers. Thirty rats were divided into five groups: Control, IND (50 mg/kg, p.o.), IND pretreated with GLA 100 mg/kg (p.o. for 14 d), IND pretreated with GLA 150 mg/kg (p.o. for 14 d) and IND pretreated with omeprazole (20 mg/kg, p.o. for 14 d). The stomach tissues were examined to calculate the ulcer index and pH and analyse biochemical markers (prostaglandin E2 (PGE2), cyclooxygenase 1 (COX1), TNF-1, IL-6 and intercellular adhesion molecule-1 (ICAM1)) and oxidative stress parameters (malondialdehyde: (MDA), superoxide dismutase (SOD), glutathione (GSH) and CAT (catalase)) as well as undergo histopathological assessment. GLA 100 and 150 mg/kg showed a protective effect against IND-induced gastric damage. It reduced levels of COX1, TNF-1, IL-6 and ICAM and increased PGE2 levels. GLA also normalised antioxidant function by modulating MDA, SOD, GSH and CAT. GLA intervention protects against IND-induced gastric ulcers by restoring oxidant/antioxidant balance and reducing inflammation.

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.

Water droplets containing the SARS-CoV-2 virus, responsible for coronavirus 2019 transmission, were introduced into a controlled-temperature and -humidity chamber. The SARS-CoV-2 virus with green fluorescent protein tag in droplets was used to infect Caco-2 cells, with viability assessed through flow cytometry and microscopic counting. Whereas temperature fluctuations within typical indoor ranges (20°C–30°C) had minimal impact, we observed a notable decrease in infection rate as the surrounding air’s relative humidity increased. By investigating humidity levels between 20% and 70%, we identified a threshold of ≥40% relative humidity as most effective in diminishing SARS-CoV-2 infectivity. We also found that damage of the viral proteins under high relative humidity may be responsible for the decrease in their activity. This outcome supports previous research demonstrating a rise in the concentration of reactive oxygen species within water droplets with elevated relative humidity.

Antibacterial clays in nature include a variety of clay mineral assemblages that are capable of killing certain human pathogens. Although clays have been used for medicinal applications historically, only in the last decade have analytical methods and instrumentation been developed that allow researchers to evaluate the antibacterial mechanisms of various clays applied medicinally. Comparisons of the mineralogical and chemical compositions of natural clays that kill bacteria have promoted a better understanding of the mineral properties that are toxic to a broad-spectrum of human pathogens, including bacteria that have developed resistance to antibiotics. Popular literature is filled with reports of ‘healing’ clays, that, when tested against pathogens in vitro and compared to controls, do not appear to have bactericidal properties. It is important, however, to differentiate what properties make a clay ‘healing,’ versus what makes a clay ‘antibacterial.’ Most antibacterial clays identified to date buffer pH conditions of a hydrated clay outside the range of conditions in which human pathogens thrive (circum-neutral pH) and require oxidation reactions to occur. It is the change in oxidation state and pH imposed by the hydrated clay, applied topically, that leads to a chemical attack of the bacteria. Healing clays, on the other hand, may not kill bacteria but have soothing effects that are palliative. This article reviews some of the historical uses of clays in medicine but focuses primarily on the common characteristics of natural antibacterial clays and early studies of their antibacterial mechanisms. In this era of bacterial resistance to antibiotics, mimicking the antibacterial mechanisms exhibited by natural clays could be advantageous in the development of new antimicrobial agents.

This experiment was conducted to investigate whether dietary chenodeoxycholic acid (CDCA) could attenuate high-fat (HF) diet-induced growth retardation, lipid accumulation and bile acid (BA) metabolism disorder in the liver of yellow catfish Pelteobagrus fulvidraco. Yellow catfish (initial weight: 4·40 (sem 0·08) g) were fed four diets: the control (105·8 g/kg lipid), HF diet (HF group, 159·6 g/kg lipid), the control supplemented with 0·9 g/kg CDCA (CDCA group) and HF diet supplemented with 0·9 g/kg CDCA (HF + CDCA group). CDCA supplemented in the HF diet significantly improved growth performance and feed utilisation of yellow catfish (P < 0·05). CDCA alleviated HF-induced increment of hepatic lipid and cholesterol contents by down-regulating the expressions of lipogenesis-related genes and proteins and up-regulating the expressions of lipololysis-related genes and proteins. Compared with the control group, CDCA group significantly reduced cholesterol level (P < 0·05). CDCA significantly inhibited BA biosynthesis and changed BA profile by activating farnesoid X receptor (P < 0·05). The contents of CDCA, taurochenodeoxycholic acid and glycochenodeoxycholic acid were significantly increased with the supplementation of CDCA (P < 0·05). HF-induced elevation of cholic acid content was significantly attenuated by the supplementation of CDCA (P < 0·05). Supplementation of CDCA in the control and HF groups could improve the liver antioxidant capacity. This study proved that CDCA could improve growth retardation, lipid accumulation and BA metabolism disorder induced by HF diet, which provided new insight into understanding the physiological functions of BA in fish.

This review discusses epigenetic mechanisms and the relationship of infertility in men and women in relation to parameters pertaining to nutrition. The prevalence of infertility worldwide is 8–12 %, and one out of every eight couples receives medical treatment. Epigenetic mechanisms, aging, environmental factors, dietary energy and nutrients and non-nutrient compounds; more or less energy intake, and methionine come into play in the occurrence of infertility. It also interacts with vitamins B12, D and B6, biotin, choline, selenium, zinc, folic acid, resveratrol, quercetin and similar factors. To understand the molecular mechanisms regulating the expression of genes that affect infertility, the environment, the role of genotype, age, health, nutrition and changes in the individual's epigenotype must first be considered. This will pave the way for the identification of the unknown causes of infertility. Insufficient or excessive intake of energy and certain macro and micronutrients may contribute to the occurrence of infertility as well. In addition, it is reported that 5–10 % of body weight loss, moderate physical activity and nutritional interventions for improvement in insulin sensitivity contribute to the development of fertility. Processes that pertain to epigenetics carry alterations which are inherited yet not encoded via the DNA sequence. Nutrition is believed to have an impact over the epigenetic mechanisms which are effective in the pathogenesis of several diseases like infertility. Epigenetic mechanisms of individuals with infertility are different from healthy individuals. Infertility is associated with epigenetic mechanisms, nutrients, bioactive components and numerous other factors.