Processing affects the oxidative and nutritional quality of yellow mealworm (Tenebrio molitor) before and after in vitro gastrointestinal digestion.

Lipid peroxidation marker malondialdehyde is an independent determinant of hepatitis B vaccine response in hemodialysis patients.

Disulfidptosis in neurodegenerative diseases: From redox imbalance to neuronal dysfunction.

Chronic exposure to copper ions, Cu(II), induces organ-specific oxidative damage and mitochondrial dysfunction, with distinct temporal and biochemical profiles across tissues. This study evaluated the protective effects of vitamin E (α-tocopherol) against Cu(II)-induced phospholipid and protein oxidation, redox imbalance, and bioenergetic disruption in rats. Cu(II) treatment led to early lipid peroxidation in the brain, heart and lung, followed by delayed oxidative damage in the liver and kidney. Vitamin E effectively prevented phospholipid oxidation in all organs, but its protection against protein oxidation and mitochondrial respiratory impairment was organ-specific and time-dependent. Mitochondrial respiration declined in brain and heart tissues, with partial recovery in the heart after prolonged vitamin E supplementation. Electron transport chain activity was altered by Cu(II), notably with increased complex I activity in the liver and decreased complex I and II activity in the lung and kidney. Vitamin E failed to prevent these changes in most tissues. Glutathione modulation revealed adaptive redox responses in the lung and oxidative depletion in kidney. These findings highlight the complexity of Cu(II)-induced oxidative damage and the limited but significant protective role of vitamin E, emphasizing the need for targeted antioxidant strategies to preserve mitochondrial integrity and cellular function under metal-induced stress.

The importance of sperm cryopreservation in cattle production is that it enables the flow of genetic variation and the speedy distribution of genetically superior bulls. Nevertheless, there are still considerable technological gaps because the quality of post-thaw sperm is always poor and differs significantly across breeding bulls. The aim of this review was to investigate the origin of reactive oxygen species (ROS) generation in the process of bovine sperm cryopreservation, discuss the effects of ROS-induced injury, and present the current knowledge of the measures the researcher can take to alleviate the impact of oxidative stress. A thorough literature review was made by searching the relevant scientific databases with the keywords: bull sperm cryopreservation, ROS, oxidative stress, antioxidants, non-antioxidants approaches and post-thaw sperm quality. Freeze-thaw stress causes extreme cellular and molecular stress and ROS overproduction, which is one of the major causes of sperm damage. The main causes of ROS production are changes in osmotic pressure, the presence of ice crystals, mitochondrial dysfunction and oxidative burst. In turn, excessive production of ROS causes lipid peroxidation of the plasma membrane, oxidation of proteins, fragmentation of the DNA and dysfunction of the mitochondria, which eventually decreases the sperm motility, viability and fertilization capacity. Enzymatic and non-enzymatic antioxidants, plant extract, nanoparticles, mitochondria-targeted antioxidants and non-antioxidants approaches have proven to be effective in curbing oxidative damage. Prevention of oxidative imbalance in cryopreservation is an important factor that can increase the quality of post-thaw sperm and increase the success of artificial insemination and in vitro fertilization programmes in cattle.

Predictable toxicity of antibiotics and disinfection by-products as well as their mixtures based on the mechanism-oriented analysis.

Gentisic acid confers multimodal neuroprotection in experimental Alzheimer's disease by targeting oxidative stress, neuroinflammation, and protein aggregation.

MIP-8, a Morchella importuna-derived peptide, protects against 6-OHDA-induced neurotoxicity via AKT signaling modulation.

Neurodegenerative disorders have recently emerged as one of the most difficult worldwide health challenges. Neuronal cell injury is a major factor in neurodegenerative diseases. There seems to be rising interest in developing effective neuroprotective drugs from natural sources. Nutraceuticals, or compounds produced from natural sources have shown neuroprotective effects in both in vitro and in vivo models of neuronal cell death and neurodegeneration. Carnosic acid (CA), a natural compound majorly obtained from rosemary and other herbs, has emerged as a promising neuroprotective agent in neurodegenerative diseases, particularly Alzheimer's and Parkinson's. This review covers the latest findings on the methods by which carnosic acid mitigates key pathological features such as oxidative stress, neuroinflammation, apoptosis, and protein aggregation as well as other pathways related to Parkinson's and Alzheimer's disease induction. Furthermore, we describe preclinical and clinical research that demonstrates the ability of carnosic acid to improve cognitive function and motor performance. This study will give a detailed overview of carnosic acid as a possible therapeutic agent, opening the path for future research into viable therapies for Alzheimer's and Parkinson's disorders.

Activation of sarco/endoplasmic reticulum Ca²⁺-ATPase 2 (SERCA2) reduces brain injury and improves cognitive function following ischemic stroke.

Curcumin-sensitized TiO2 composite photocatalyst: Synthesis, characterization and photocatalytic preservation performance on red shrimp (Solenocera crassicornis).

Effects of mitochondrial lipid molecules on release of ROS and beef muscle oxidation: a perspective on membrane system.

Effect and mechanism of protein oxidation on alkaline-induced egg white gel formation

Evaluation of oxidant stress markers in a population involved in a health care program.

Toxic effects of penconazole on the polychaete Nereis (Hediste) diversicolor: Oxidative stress, fatty acid alterations, and histopathology.

A majority of deaths associated with air pollution are attributed to cardiovascular and heart diseases. Carbon black that represents the carbon core of particulate matter, a major component of air pollution, has been shown to result in cardiac mitochondrial dysfunction. The goal of this study was to identify mechanisms that potentially regulate cardiac mitochondrial function in acute carbon black exposure. Specifically, we examined whether lysine acetylation, a post-translational modification, impacts cardiac mitochondrial function and contributes to mitochondrial dysfunction observed with carbon black exposure. C57BL/6J animals exposed to 10 mg/m3 CB for 3 h resulted in a significant increase in acetylation of fatty acid oxidation proteins-long and short chain acyl-CoA dehydrogenase and hydroxyacyl-CoA dehydrogenase-which correlated with decreased enzymatic activities. Further, a significant decrease in fatty acid import protein carnitine palmitoyl-transferase 1b was observed. An increase in acetylation of electron transport chain complexes I and V along with increased Complex V activity was observed in carbon black exposed animals. This decrease in import and utilization of fatty acid metabolism was counteracted by an increase in protein and activity level of glucose oxidation protein pyruvate dehydrogenase. These findings suggest that acute exposure to carbon black results in a switch in substrate utilization from fatty acids to glucose that in turn feeds the electron transport chain process in the exposed heart. Finally, these findings present the potential role of lysine acetylation mediated regulation of mitochondrial dysfunction in the acute carbon black exposed model.

This study investigated the effects of maternal nutrition on hepatic long non-coding RNA (lncRNA) expression in Nellore cattle offspring. To this end, a total of 126 pregnant cows were assigned to three dietary treatments: not programmed (mineral supplementation only), partial programming (late protein-energy supplementation), and full programming (protein-energy supplementation throughout pregnancy). At 676±28 days of age, liver samples were collected from the offspring to perform RNA-sequencing. Novel lncRNAs were identified with FEELnc and CPC2, and differentially expressed lncRNAs (DELs) with DESeq2. Partial correlation, information theory, and regulatory impact factor were used to identify key regulatory roles, while over-representation analysis was performed to detect enriched processes. Among the 3,257 lncRNAs identified, 17 were DELs (false discovery rate<0.1). The PPxNP comparison exhibited the highest transcriptional changes (10 DELs), including IncRNA TU7296, identified as a potential regulator of energy metabolism and immune function, as well as molecular functions associated with oxidative metabolism. The FPxNP comparison revealed distinct regulation of genes related to fatty acid transport and oxidative protein folding. The FPxPP comparison showed minimal differences, highlighting the similarity between these groups. This study provides insights into the role of maternal nutrition in modulating long-term epigenetic programming via lncRNA-mediated mechanisms in beef cattle offspring.

Given the central role of peroxisomes in lipid metabolism and redox homeostasis, we hypothesized that peroxisomal activity is critical for sustaining β cell function and identity. Pex5 deletion models were employed to investigate loss of peroxisomal function on glucose-stimulated insulin secretion (GSIS), oxidative stress, and β cell maturity markers. Peroxisome deficiency in male mice resulted in elevated GSIS. Glucose intolerance developed despite increased insulin secretion. Ion mobility mass spectrometry revealed oxidation of insulin proteins, and a truncated insulin 2-derived peptide, in islets from mice with a tissue-specific deficiency in peroxisomes. Peroxisome loss of function increased multiple markers of oxidative stress, including altered metabolite profiles, lipid peroxidation, and protein carbonylation. These findings reveal that increased secretion of oxidized insulin protein is insufficient to regulate whole-body glucose homeostasis. Peroxisome deficiency also reduced markers of β cell maturity. Based on these outcomes, we identified the peroxisome organelle as a key regulatory component of glucose homeostasis by protecting insulin from oxidative modification and degradation and by supporting maintenance of mature β cells.

The chemotherapeutic agent cisplatin for solid tumors frequently induces cancer-associated cachexia characterized by weight loss and decreased skeletal muscle mass. These adverse cisplatin-related symptoms are dose‑limiting, and the ability to counteract drug-initiated muscle atrophy in cancer-associated cachexia remains a pharmacological challenge. The aim of this study was to determine the protective efficacy of lobetyolin, a natural compound derived from Codonopsis pilosula, known to exert antioxidant, anti‑inflammatory, and anti‑apoptotic activities, against cisplatin-induced skeletal muscle wasting and subsequently elucidate a potential underlying molecular mechanism of action using a mouse model. Mice were injected with cisplatin (4 mg/kg, i.p. every other day, 4 doses in total) with concurrent oral lobetyolin (20 or 40 mg/kg daily) for 8 days. Lobetyolin inhibited cisplatin-induced reductions in body weight and grip strength, ameliorated gastrocnemius muscle atrophy, and preserved myofiber cross‑sectional area. Mechanistically, lobetyolin restored superoxide dismutase (SOD) activity and glutathione (GSH) levels while diminishing malondialdehyde (MDA) content in gastrocnemius muscle. Lobetyolin was found to activate the AKT signaling axis as evidenced by enhanced phosphorylation of AKT (Ser473) and FoxO3α (Thr32), which suppressed FoxO3α nuclear translocation and downregulated the E3 ubiquitin ligase Fbx32, thereby diminishing proteasomal protein degradation. Concurrently, lobetyolin normalized the Bax/Bcl‑2 ratio to inhibit myocyte apoptosis. These findings demonstrated that lobetyolin may be considered as a multi‑targeted therapeutic candidate to counteract oxidative injury, protein catabolism, and myocyte apoptosis initiated by cisplatin. Data suggest that lobetyolin's potential as a safe adjunctive agent against chemotherapy‑induced muscle wasting might involve AKT/FoxO3α pathway.

Rheumatoid arthritis (RA) is a chronic autoimmune disease that causes joint inflammation, disability, and reduced quality of life. Current mesenchymal stem cell (MSC) therapies face limitations due to cell variability and lack of standardization, highlighting the need for effective, cell-free alternatives that replicate MSCs' immunomodulatory functions. This study aimed to enhance MSC secretion of regulatory factors to modulate inflammation in an RA model. In this experimental study, MSCs were isolated from mouse bone marrow and characterized by CD73 expression and lack of CD45/CD80. MSCs were treated with Muramyl dipeptide (MDP; 0 and 10 μg/mL) for 24 hours, followed by washing and further culture for 48 hours to obtain conditioned medium (CM). The resulting CM from untreated MSCs and MDP-primed MSCs (MDP-CM) was collected for subsequent in vivo administration. RA was induced in male Wistar rats (160-180 g) via intradermal injection of Freund's complete adjuvant. Treatments with CM derived from either untreated MSCs or MDP-pulsed MSCs (MDP-CM) were initiated on day 7 post-induction and repeated after 5 days via intraperitoneal injection (n=10 per group). MDP did not affect MSC viability but significantly altered the CM's immunological profile: MDP-CM had lower levels of IFN-γ, IL-6, and IL-1β, and higher levels of indoleamine 2,3-dioxygenase, TGF-β, and IL-10 compared to control CM. in vivo administration of MDP-CM significantly attenuated RA severity and promoted body weight recovery more effectively than CM alone. In addition, MDP-CM significantly reduced systemic inflammatory markers , such as TNF-α, IL-1β, myeloperoxidase, nitric oxide, and C-reactive protein (CRP), and more strongly modulated T-cell- associated gene expression in joint tissue, evidenced by upregulation of FOXP3 and downregulation of T-bet, Gata3, and Rorc compared with RA rats receiving CM. The CM derived from appropriately primed MSCs may represent a more potent and standardized "off-theshelf" alternative to direct stem cell transplantation.