Anemia, characterized by decreased hemoglobin levels and impaired oxygen-carrying capacity, remains a major global public health concern. Conventional therapies, such as blood transfusions and oral iron supplementation, are often associated with adverse effects and limited absorption, highlighting the need for safer and more effective alternatives. Natural products rich in polyphenols and essential minerals have attracted increasing attention due to their multifunctional therapeutic potential. In this context, the present study is the first to investigate the anti-anemic potential of Pinus pinaster Aiton and Pinus halepensis Mill. bark extracts through an integrated phytochemical, nutritional, in vivo, in vitro, and in silico approach. Phytochemical profiling by HPLC-MS/MS revealed several major phenolic compounds, including quercetin, catechin, protocatechuic acid, and taxifolin-3-O-glucoside. The extracts exhibited high total polyphenol and flavonoid contents and strong antioxidant activity, as demonstrated by DPPH, ABTS, PR, and TAC assays. Mineral analysis revealed significant levels of essential elements, including iron, magnesium, potassium, sodium, and zinc. In phenylhydrazine-induced anemic Wistar rats, 21-day treatment with the extracts significantly restored hematological parameters (RBC, Hb, and HCT), serum iron and ferritin levels, and improved renal and hepatic biomarkers compared with untreated anemic controls. In vitro assays further demonstrated anti-hemolytic activity and enhanced erythrocyte membrane stability. Molecular docking analysis supported these findings by revealing favorable interactions between the major phenolic compounds and key targets involved in erythropoiesis, iron metabolism, and oxidative stress, including the erythropoietin receptor, superoxide dismutase, and ferrochelatase. Collectively, these findings highlight the potent anti-anemic and protective effects of Pinus bark extracts and suggest their potential as promising natural therapeutic agents.
Salmonella remains a major foodborne pathogen associated with poultry production, posing significant public health and economic challenges worldwide. Increasing restrictions on antibiotic use have intensified the search for alternative control strategies in poultry systems. Zinc, an essential trace mineral, has emerged as a promising nutritional intervention due to its multifunctional roles in host defense and microbial regulation. This narrative review synthesizes current evidence on the effectiveness of zinc in reducing Salmonella in poultry, with emphasis on underlying mechanisms, comparative efficacy of different zinc sources, and practical applications in production systems. Available evidence indicates that zinc enhances innate and adaptive immune responses, preserves intestinal barrier integrity, modulates gut microbiota toward beneficial populations, and exerts direct antibacterial effects. These combined actions position zinc as a key regulator of host–pathogen interactions, linking trace element homeostasis with immune function and microbial dynamics. Consequently, zinc supplementation is associated with reduced cecal colonization, decreased fecal shedding, and limited systemic dissemination. Compared with conventional inorganic zinc sources, many organic zinc complexes have demonstrated improved bioavailability and enhanced functional responses under comparable experimental conditions. However, the magnitude of these benefits varies according to ligand chemistry, dietary composition, bird age, physiological status, and study design. Zinc is most effective when integrated with complementary strategies, including probiotics, organic acids, and vaccination programs. Overall, zinc represents a practical component of sustainable, antibiotic-free approaches to improving poultry health and food safety, although further field validation and optimization are required to ensure consistent performance under commercial conditions.
Chronic obstructive pulmonary disease (COPD) and chronic kidney disease (CKD) are common non-communicable diseases associated with disturbances in metal and metalloid homeostasis and an increased risk of cardiovascular disorders. However, the mechanisms underlying these associations remain incompletely understood. Therefore, this study investigated whether COPD or CKD is associated with altered accumulation of selected metals and metalloids in the left ventricular myocardium. We analyzed 57 autopsy-derived left ventricular myocardial specimens, including 12 individuals with COPD, 11 with CKD, and 34 controls (mean age 70 ± 14 years). Concentrations of arsenic, lead, calcium, cadmium, mercury, manganese, magnesium, iron, copper, nickel, and zinc were determined using inductively coupled plasma mass spectrometry (ICP-MS). Individuals with COPD had significantly higher myocardial cadmium concentrations, whereas individuals with CKD exhibited lower myocardial iron concentrations in unadjusted analyses. Zn levels and Zn/Cu and Zn/Fe ratios were inversely correlated with Pb, As, and Hg. After adjustment for the presence of cardiomyopathy, myocardial cadmium concentrations remained significantly higher, while magnesium concentrations were significantly lower in individuals with COPD compared with controls. No significant differences remained between individuals with CKD and controls. Higher myocardial cadmium and lower magnesium concentrations in individuals with COPD suggest altered myocardial metal homeostasis that may be relevant to COPD-associated cardiac alterations. Further studies are needed to clarify the mechanisms and clinical significance of these findings.
Cadmium (Cd) is a toxic heavy metal that causes multi-organ damage, including neurotoxicity. Carvacrol (CAR), a natural phenolic compound obtained from aromatic plants, is known for its protective properties. This study investigated the effects of CAR against Cd-induced toxicity through comprehensive behavioral assessments including the Open Field Test (OFT), Elevated Plus Maze (EPM), Barnes Maze, and Rotarod test, while plasma biochemical parameters, liver and kidney histopathology, and untargeted metabolomic profiles (plasma and brain) were also evaluated. Male Wistar albino rats were randomly divided into six groups and orally administered Cd (50 mg/kg) and/or CAR (20 or 40 mg/kg body weight) for 12 days. CAR alone increased locomotor activity, altered neuroprotective related metabolic pathways and did not cause weight loss. Cd exposure significantly increased body weight loss and anxiety-like behaviors while elevating cortisol, urea, AST, ALT levels and inducing significant histopathological damage in liver and kidney tissues (p < 0.05). Integrated plasma–brain metabolomic analyses revealed that Cd exposure disrupts multiple interconnected biological systems, including the antioxidant defence system, mitochondrial energy pathways, and cell membrane integrity. Although Cd-CAR co-administration partially reversed worsening of the anxiolytic-like behavior, locomotor activity, and renal tissue integrity, it failed to fully prevent Cd-induced toxicity and further aggravated weight loss, biochemical alterations (creatinine, AST, ALT), and metabolic disturbances (p < 0.05). In conclusion, co-administration of CAR with Cd provided only limited and heterogeneous protection that was insufficient to counteract Cd-induced multisystem toxicity. This current study presents a wide assessment to the systemic use of CAR against Cd according to results of behavioral, histopathological, biochemical, and metabolomic parameters.
Cinnabar (ZS) is a commonly used in traditional Chinese medicine (TCM), but its clinical application is limited owing to mercury (Hg) related toxicity. This study aimed to explore the kidney toxic and related mechanisms of ZS combined with sodium selenite (Na2SeO3). Eighty specific-pathogen-free (SPF) male Kunming (KM) mice were randomly divided into ten groups: control (0.5
