Search Results (276)

Heavy metal pollution represents a pervasive environmental challenge that significantly exacerbates the ever-increasing crisis of antimicrobial resistance and the capacity of microorganisms to endure and proliferate despite antibiotic interventions. This review examines the intricate relationship between heavy metals and AMR, with an emphasis on the underlying molecular mechanisms and ecological ramifications. Common environmental metals, including arsenic, mercury, cadmium, and lead, exert substantial selective pressures on microbial communities. These induce oxidative stress and DNA damage, potentially leading to mutations that enhance antibiotic resistance. Key microbial responses include the overexpression of efflux pumps that expel both metals and antibiotics, production of detoxifying enzymes, and formation of protective biofilms, all of which contribute to the emergence of multidrug-resistant strains. In the soil environment, particularly the rhizosphere, heavy metals disrupt plant–microbe interactions by inhibiting beneficial organisms, such as rhizobacteria, mycorrhizal fungi, and actinomycetes, thereby impairing nutrient cycling and plant health. Nonetheless, certain microbial consortia can tolerate and detoxify heavy metals through sequestration and biotransformation, rendering them valuable for bioremediation. Advances in biotechnology, including gene editing and the development of engineered metal-resistant microbes, offer promising solutions for mitigating the spread of metal-driven AMR and restoring ecological balance. By understanding the interplay between metal pollution and microbial resistance, we can more effectively devise strategies for environmental protection and public health. Full article

Cadmium (Cd) is a highly toxic heavy metal that disrupts development and reproduction, primarily through oxidative stress. In this context, sulforaphane (SFN), an antioxidant compound, may serve as a promising agent to counteract Cd-induced oxidative damage and prevent developmental and reproductive abnormalities. This study aimed to evaluate the effect of SFN on reproductive toxicity induced by cadmium chloride (CdCl₂) in the nematode Caenorhabditis elegans (C. elegans). Five experimental groups were established: (I) Control: no treatment, (II) dimethyl sulfoxide (DMSO): 48 h with 0.01% DMSO, (III) CdCl₂: 24 h with 4600 µM CdCl₂, (IV) SFN + CdCl₂: 24 h with 100 µM SFN followed by 24 h with both SFN and CdCl₂, and (V) SFN: 48 h with 100 µM SFN. Co-exposure to SFN and CdCl₂ prevented the reduction in the percentage of adult nematodes and increased egg-laying. It also significantly improved hatching rates, allowing more embryos to reach the larval stage, and prevented reductions in body size. However, no effects were observed on glutathione S-transferase-4 (GST-4) levels in the transgenic CL2166 strain. In conclusion, SFN substantially prevents Cd-induced reproductive toxicity in C. elegans. Future studies should investigate the molecular mechanisms by which SFN enhances egg-laying and offspring viability in this model. Full article

Background/Objectives: The liver, the body’s primary detoxifying organ, is often affected by various inflammatory diseases, including hepatitis, cirrhosis, and non-alcoholic fatty liver disease (NAFLD), many of which can be exacerbated by secondary infections such as spontaneous bacterial peritonitis, bacteremia, and sepsis—particularly in patients with advanced liver dysfunction. The global rise in these conditions underscores the need for effective interventions. Natural products have attracted attention for their potential to support liver health, particularly through synergistic combinations of plant extracts. Epavin, a dietary supplement from Erbenobili S.r.l., formulated with plant extracts like Taraxacum officinale (L.), Silybum marianum (L.) Gaertn., and Cynara scolymus (L.), known for their liver-supporting properties, has been proposed as adjuvant for liver functions. The aim of this work was to evaluate of Epavin’s antioxidant, anti-inflammatory, and protective effects against heavy metal-induced toxicity. In addition, the antibacterial effect of Epavin against a panel of bacterial strains responsible for infections associated with liver injuries has been evaluated. Methods: The protection against oxidative stress induced by H₂O₂ was evaluated in HepG2 and BALB/3T3 cells using the dichlorofluorescein diacetate (DCFH-DA) assay. Its anti-inflammatory activity was investigated by measuring the reduction in nitric oxide (NO) production in LPS-stimulated RAW 264.7 macrophages using the Griess assay. Additionally, the cytoprotecting of Epavin against heavy metal-induced toxicity and oxidative stress were evaluated in HepG2 cells using the [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide] (MTT) and DCFH-DA assays. The antibacterial activity of Epavin was assessed by determining the minimum inhibitory concentration (MIC) and the minimum bactericidal concentration (MBC) against Gram-positive (Enterococcus faecalis ATCC 29212, and BS, Staphylococcus aureus 25923, 29213, 43300, and BS) and Gram-negative (Escherichia coli 25922, and BS, Klebsiella pneumoniae 13883, 70063, and BS) bacterial strains using the microdilution method in broth, following the Clinical and Laboratory Standards Institute’s (CLSI) guidelines. Results: Epavin effectively reduced oxidative stress in HepG2 and BALB/3T3 cells and decreased NO production in LPS-stimulated RAW 264.7 macrophages. Moreover, Epavin demonstrated a protective effect against heavy metal-induced toxicity and oxidative damage in HepG2 cells. Finally, it exhibited significant antibacterial activity against both Gram-positive and Gram-negative bacterial strains, with MIC values ranging from 1.5 to 6.0 mg/mL. Conclusions: The interesting results obtained suggest that Epavin may serve as a valuable natural adjuvant for liver health by enhancing detoxification processes, reducing inflammation, and exerting antibacterial effects that could be beneficial in the context of liver-associated infections. Full article

Cadmium (CAD) is a prevalent environmental contaminant that poses serious cardiotoxic risks. The heart, kidney, liver, and brain are just a few of the essential organs that can sustain serious harm from CAD, a very poisonous heavy metal. The cardiotoxic mechanism of CAD is linked to oxidative damage and inflammation. A trace element with anti-inflammatory, anti-apoptotic, and antioxidant qualities, selenium (SEL) can be taken as a dietary supplement. The biotoxicity of heavy metal CAD is significantly inhibited by SEL, a mineral that is vital to human and animal nutrition. Through ROS-induced PARP-1/ADPR/TRPM2 pathways, this study seeks to assess the preventive benefits of selenium against cardiovascular damage caused by CAD. The SEL showed encouraging results in reducing inflammatory and oxidative reactions. Rats were given 0.5 mg/kg SEL and 3 mg/kg 2-Aminoethyl diphenylborinate (2-APB) intraperitoneally for five days, in addition to 25 mg/kg CAD given via gavage. Histopathological examination findings revealed that the morphologic changes in the hearts of the CAD group rats were characterised by marked necrosis and the degeneration of myocytes and congestion of vessels. Compared to the rats in the CAD group, the hearts of the SEL, 2-APB and SEL+2-APB groups showed fewer morphological alterations. Moreover, in rats given CAD, there was an increase in cardiac malondialdehyde (MDA), total oxidant (TOS), reactive oxygen species (ROS), caspase (Casp-3-9), and TNF-α, whereas glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and total antioxidant (TAS) decreased. SEL improved antioxidants, avoided tissue damage, and reduced cardiac MDA, TOS, and ROS. In rats given CAD, SEL decreased cardiac PARP-1, TRPM2, TNF-α, and caspase. In summary, by reducing oxidative stress and cardiac damage and modifying the ROS/PARP-1/TRPM2 pathway, SEL protected against CAD cardiotoxicity. Full article

In high-pressure thermal power systems, corrosion-induced wall thinning in steam pipelines poses a significant threat to operational safety and efficiency. This study investigates the effects of gas–liquid two-phase flow on corrosion-induced wall thinning in pipe bends of high-pressure heaters in power plants, with particular emphasis on the mechanisms of void fraction and inner wall surface roughness. Research reveals that an increased void fraction significantly enhances flow turbulence and centrifugal effects, resulting in elevated pressure and Discrete Phase Model (DPM) concentration at the bend, thereby intensifying erosion phenomena. Simultaneously, the turbulence generated by bubble collapse at the bend promotes the accumulation and detachment of corrosion products, maintaining a cyclic process of erosion and corrosion that accelerates wall thinning. Furthermore, the increased surface roughness of the inner bend wall exacerbates the corrosion process. The rough surface alters local flow characteristics, leading to changes in pressure distribution and DPM concentration accumulation points, subsequently accelerating corrosion progression. Energy-Dispersive Spectroscopy (EDS) and Scanning Electron Microscopy (SEM) analyses reveal changes in the chemical composition and microstructural characteristics of corrosion products. The results indicate that the porous structure of oxide films fails to effectively protect against corrosive media, while bubble impact forces damage the oxide films, exposing fresh metal surfaces and further accelerating the corrosion process. Comprehensive analysis demonstrates that the interaction between void fraction and surface roughness significantly intensifies wall thinning, particularly under conditions of high void fraction and high roughness, where pressure and DPM concentration at the bend may reach extreme values, further increasing corrosion risk. Therefore, optimization of void fraction and surface roughness, along with the application of corrosion-resistant materials and surface treatment technologies, should be considered in pipeline design and operation to mitigate corrosion risks. Full article

Abiotic stressors threaten honeybee health, jeopardizing pollination services critical to agriculture and biodiversity. Here, we identified the AmVgR gene, which encodes a member of the low-density lipoprotein receptor family, and examined its function in the response of Apis mellifera to adverse abiotic stress. AmVgR exhibited peak expression in adult workers and was significantly upregulated under heat, cold, heavy metal, and pesticide exposure. RNAi-mediated knockdown of AmVgR suppressed antioxidant enzyme activities, elevated the levels of oxidative damage markers, and downregulated antioxidant gene expression. Crucially, AmVgR silencing reduced survival under H₂O₂-induced oxidative stress, indicating its essential role in stress resilience. Our findings highlight AmVgR as a key regulator of antioxidant defense during development and environmental adaptation in Apis mellifera. This study provides mechanistic insights into bee stress physiology and proposes AmVgR as a novel target for enhancing pollinator protection strategies. Further research should elucidate its molecular pathways and translational applications in mitigating abiotic stress impacts. Full article

Heavy metals are naturally occurring elements that have numerous applications in industries, agriculture, and other sectors, leading to their widespread distribution in the environment. The constant emission of heavy metals into the environment raises concerns about their impact and harmful effects on living organisms, including human health. Key threats arise from exposure to heavy metals such as lead, cadmium, mercury, and arsenic, all of which are classified as carcinogens. Chronic exposure and bioaccumulation of these metals can result in toxic effects on various body systems, including the female reproductive system. Notably, heavy metals can induce oxidative stress, generate excessive reactive oxygen species, and impair antioxidant defense systems. These metals may also lead to DNA damage, enzyme inactivation, and epigenetic modifications, ultimately disrupting critical cellular processes such as growth, proliferation, differentiation, repair, and apoptosis. Furthermore, some heavy metals can mimic endogenous estrogens, interact with estrogen receptors, and cause hormonal disruptions, a mechanism particularly relevant to the pathogenesis of female-related cancers. Despite significant advances, many gaps remain in our understanding of the molecular mechanisms by which heavy metals contribute to cancer development. Addressing these gaps could facilitate the development of more effective strategies for the prevention and treatment of female cancers. This review highlights the potential effects of heavy metals on molecular pathways in female cancers, suggesting several mechanisms of cancer development. Full article

Dynamic random-access memory (DRAM) is a vital component in modern computing systems. Enhancing memory performance requires maximizing capacitor capacitance within DRAM cells, which is achieved using high-k dielectric materials deposited as thin, uniform films via atomic layer deposition (ALD). Precise film deposition that minimizes electronic defects caused by charged vacancies is essential for reducing leakage current and ensuring high dielectric strength. In this study, we fabricated metal–insulator–metal (MIM) capacitors in high-aspect-ratio trench structures using remote plasma ALD (RP-ALD) and direct plasma ALD (DP-ALD). The trenches, etched into silicon, featured a 7:1 aspect ratio, 76 nm pitch, and 38 nm critical dimension. We evaluated the electrical characteristics of HfO₂-based capacitors with TiN top and bottom electrodes, focusing on leakage current density and equivalent oxide thickness. Capacitance–voltage analysis and X-ray photoelectron spectroscopy (XPS) revealed that RP-ALD effectively suppressed plasma-induced damage, reducing defect density and leakage current. While DP-ALD offered excellent film properties, it suffered from degraded lateral uniformity due to direct plasma exposure. Given its superior lateral uniformity, lower leakage, and defect suppression, RP-ALD shows strong potential for improving DRAM capacitor performance and serves as a promising alternative to the currently adopted thermal ALD process. Full article

Cardiovascular diseases (CVDs) remain a leading global health concern, responsible for substantial morbidity and mortality. In recent years, as our understanding of the multifaceted nature of CVDs has increased, it has become increasingly evident that traditional risk factors alone do not account for the entirety of cardiovascular morbidity and mortality. Environmental toxins, a heterogeneous group of substances ubiquitous in our surroundings, have now entered the spotlight as offenders in the development and progression of CVDs. Environmental toxins include heavy metals, air pollutants, pesticides, and endocrine-disrupting chemicals, among others. Upon exposure, they can elicit oxidative stress, a condition characterized by an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to detoxify and repair the resulting damage. Oxidative stress triggers a cascade of events, including inflammation, endothelial dysfunction, lipid peroxidation, and vascular remodeling, which can contribute to the development of atherosclerosis, hypertension, and other cardiovascular pathologies. This article delves into the molecular mechanisms underpinning oxidative stress-mediated cardiovascular damage induced by environmental toxins, emphasizing the role of specific toxins in this process. Further research is necessary to understand how individual susceptibility and genotype influence the impact of environmental toxins on oxidative stress and the risk of CVD. Full article

Myo-inositol-1,2,3,4,5,6-hexakisphosphate (IP6) is commonly found in plant-derived foods and has important pharmacological properties against many pathologies. One of them appears to be neurodegeneration, which is notably stimulated by dysregulated metal metabolism. Consequently, we explore the role of IP6 in mitigating neurodegenerative events catalyzed by dysregulated free iron. More precisely, we performed spectrophotometric measurements in aqueous solutions to investigate the ability of IP6 to chelate Fe³⁺ and inhibit its role in catalyzing the oxidative degradation of dopamine and ascorbic acid, two key molecules in neuronal redox systems. Our results demonstrate that IP6 effectively prevents the formation of harmful intermediates, such as neuromelanin and reactive oxygen species, which are linked to neuronal damage. Additionally, we assessed the effect of IP6 on Fe³⁺-induced protein aggregation, focusing on α-synuclein, which is closely associated with Parkinson’s disease. Our data reveal that IP6 accelerates the conversion of toxic α-synuclein oligomers into less harmful amyloid fibrils, thereby reducing their neurotoxic potential. Our findings highlight the dual function of IP6 as a potent Fe³⁺ chelator and modulator of protein aggregation pathways, reinforcing its potential as a neuroprotective agent. Consequently, IP6 offers promising therapeutic potential for mitigating the progression of neurodegenerative disorders such as Parkinson’s and Alzheimer’s diseases. Full article

Nitric oxide (NO) and melatonin (MT) significantly influence photosynthetic processes by modulating redox homeostasis, chlorophyll content, stomatal conductance, and gene expression, particularly under abiotic stress conditions. This review summarizes the intricate crosstalk between NO and melatonin, focusing on their coordinated roles in regulating photosynthetic efficiency. Evidence from various plant species indicates that the application of exogenous NO and melatonin enhances chlorophyll content, photosystem efficiency (particularly PSII), and photosynthetic performance, mitigating stress-induced damage. Molecular analysis demonstrates that both molecules influence key photosynthetic gene modulating photosystems I and II, and Calvin cycle activities. Moreover, NO and melatonin collaboratively regulate stomatal movements through ABA, Ca²⁺, and H₂O₂ signaling pathways, involving genes such as PMRT1, CIPKs, and OST1. Experimental data from diverse plant species under stress conditions, including drought, salinity, heavy metals, and flooding, highlight their synergistic protective effects. Exploring these mechanisms further may enable practical agricultural strategies involving combined NO and melatonin treatments to improve crop resilience and productivity under increasingly challenging environmental conditions. Future research directions should emphasize unraveling detailed molecular interactions, enabling targeted biotechnological applications in crop improvement programs for enhanced global food security. Full article

Aquaculture has been rapidly growing during the past decade to accommodate the increasing need for seafood as a vital source of nutrients for human beings. The nutritional benefits of incorporating fish into one’s diet are paramount in promoting overall health, bolstering immunity and warding off diseases. Nonetheless, farm-raised aquatic species are frequently subjected to elevated contamination levels due to pesticides, antibiotics, and heavy metals in the marine environment. Pesticides affect fish differently based on species, class, dosage, and exposure duration. They can induce histological damage or neurobehavioral changes by inhibiting acetylcholinesterase production. This can promote liver dysfunction, metabolism deregulation, oxidative stress, and hematological imbalances, impair immune responses, and adversely affect fish reproduction. Furthermore, pesticides negatively affect the nutritional composition of fish by reducing the total protein levels in muscle, liver, gills, and kidney tissues. They disrupt lipid metabolism, resulting in lipid accumulation in the liver and a decrease in polyunsaturated fatty acids. Additionally, pesticides interfere with metabolism by altering carbohydrate levels in the gills, muscles, and kidneys while decreasing glycogen storage in the liver. Pesticide exposure has been linked to severe health impacts in humans, such as non-communicable diseases, reproductive issues, cognitive dysfunction, and cancer. The current review comprehensively emphasizes the harmful effects of pesticides on fish and human health, urging the establishment of environmental monitoring programs and biomonitoring studies. It accentuates the need for risk assessment models to evaluate pesticide impacts on marine ecosystems and advocates for stricter safety standards and lower pesticide residue limits in aquaculture products. Full article

At the present stage, heavy metal pollution, led by environmental exposure to cadmium (Cd), has caused incalculable losses in animal husbandry. The potential value of caprylic acid as a medium- and long-chain fatty acid with a unique role in regulating lipid metabolism has attracted much attention. Our previous study found that octanoic acid levels were significantly reduced under Cd-exposed conditions in Hu Sheep, on the basis of which we investigated the protective effect of sodium octanoate, a derivative of octanoic acid, against Cd exposure in Hu Sheep in the present study. In this study, an animal model of Cd exposure in Hu Sheep was established. Comprehensive assessment of Cd-induced intestinal injury using hematoxylin and eosin (H&E) staining, immunostaining and carried out in-depth analyses combined with lipid metabolomics and transcriptomics. The results showed that Cd exposure triggered intestinal inflammation, barrier function damage and oxidative stress imbalance. Lipid metabolomics analysis showed that Cd exposure severely disrupted lipid metabolic processes, especially the glycerophospholipid metabolic pathway, suggesting that lipid metabolic disorders are closely related to intestinal injury. Notably, sodium octanoate could partially reverse the lipid metabolism abnormality by regulating the Adenosine 5′-monophosphate (AMP)-activated protein kinase (AMPK) signaling pathway, effectively alleviating the Cd toxicity, which provides a brand-new prevention and control strategy for Cd-induced intestinal injury in the livestock industry pollution-mediated disease. Full article

Environmental pollution by heavy metals (HMs) has become a serious threat in recent years due to their potential consequences for human health and life. One such metal is vanadium (V). Despite its numerous benefits—including antibacterial, antifungal, and anticancer properties—V induces cellular damage through oxidative stress. Epigallocatechin gallate (EGCG), a potent antioxidant found in large quantities in green tea, is considered an effective protector against the damaging effects of HMs on cells. The aim of this study was to evaluate the possible effect of EGCG on CHO-K1 cells exposed to V. This is the first experiment of its kind on healthy cells. Cells were treated with V and EGCG for 24 h, either in combination or separately. The doses were selected in a preliminary stage of the experiment (V 50 and 100 µM; EGCG 0.5 and 1 µM). As part of the study, the cell viability, total ROS activity, and mitochondrial membrane potential were assessed. The results showed that at the tested concentrations, EGCG did not reduce the toxic effect of V on cells, but in fact exacerbated its adverse effects on cells. Further studies are needed to understand the exact mechanism of V–EGCG interaction in mammalian cells. Full article

Plants face various abiotic stresses in their natural environments that trigger the production of reactive oxygen species (ROS), leading to oxidative stress and potential cellular damage. This comprehensive review examines the interplay between plant antioxidant defense systems and ROS under abiotic stress conditions. We discuss the major enzymatic antioxidants, including superoxide dismutase, catalase, reductases, and peroxidases, as well as non-enzymatic antioxidants, such as ascorbic acid, glutathione, polyphenols, and flavonoids, which play crucial roles in ROS detoxification. This review elaborates on different types of ROS, their production sites within plant cells, and their dual role as both damaging oxidants and key signaling molecules. We discuss how various abiotic stresses—including heat, cold, drought, flooding, salinity, and heavy metal toxicity—induce oxidative stress and trigger specific antioxidant responses in plants. Additionally, the mechanisms of ROS generation under these abiotic stress conditions and the corresponding activation of enzymatic and non-enzymatic scavenging systems are discussed in detail. This review also discusses recent advances in understanding ROS signaling networks and their integration with other stress-response pathways. This knowledge provides valuable insights into plant stress-tolerance mechanisms and suggests potential strategies for developing stress-resistant crops by enhancing antioxidant defense systems. Moreover, the strategic ROS modulation through priming, exogenous antioxidants, nanoparticles, or genetic tools can enhance plant resilience. Integrating these methods with agronomic practices (e.g., irrigation management) offers a sustainable path to climate-smart agriculture. Our review reveals that ROS accumulation can be detrimental; however, the coordinated action of various antioxidant systems helps plants maintain redox homeostasis and adapt to environmental stress. Full article