Search Results (1,521)

(1) The growing interest in the use of natural and sustainable ingredients highlights the investigation of vegetable oils in dermato-cosmetic applications. In this context, the vegetable oil obtained from walnut (Juglans regia L.) is of actual interest due to its composition rich in unsaturated fatty acids. The aim of the present study was to investigate and characterize walnut oil from a physicochemical, structural, and rheological point of view. (2) The oil was obtained by a cold pressing process from walnut seeds, with a yield of about 51.03 ± 1.41%, and subsequently analyzed by complementary methods. (3) The results show an acceptable physicochemical profile, characterized by appropriate values of density, pH, and spreadability. The oxidative stability indicated a moderate resistance to degradation, specific to oils rich in polyunsaturated fatty acids. Fourier infrared transform spectrometry (FTIR) analysis confirmed the presence of functional groups characteristic of triglycerides, without indications of advanced oxidation, and atomic force microscopy (AFM) investigations revealed a heterogeneous morphology. The rheological properties indicated a pseudoplastic behavior, favorable for topical application. The determination of heavy metals confirmed the safety of the raw material for the intended dermato-cosmetic use. While arsenic levels were slightly above the strict Codex Alimentarius limits for foodstuffs, all values remained within the safety ranges established for cosmetic ingredients. A total of six fatty acids were found in cold-pressed walnut oil, determined using GC-MS methods. The number of compounds identified in the silylated sample was found to be 17. The antioxidant activity determined using DPPH and ABTS methods was generally considered good and relatively stable over time. The measured sun protection value (SPF) demonstrates a favorable capacity to act as a photoprotective ingredient against ultraviolet (UV) radiation. (4) Overall, the results demonstrate that walnut oil presents adequate physicochemical and structural properties, supporting its further use as a potential cosmetic raw material. Full article

Exposure to heavy metals remains a significant public health concern due to their environmental persistence, bioaccumulation, and ability to interfere with essential cellular processes. A large part of metal-induced toxicity converges on the establishment of a chronic oxinflammatory state, driven by the reciprocal interaction between oxidative stress and inflammation. In this review, we synthesize current mechanistic evidence describing how toxic metals, including aluminum, arsenic, cadmium, lead, mercury, and nickel, disrupt redox homeostasis, impair cellular integrity, and activate inflammatory signaling pathways. These metals promote the excessive generation of reactive oxygen and nitrogen species through multiple mechanisms, including mitochondrial dysfunction, displacement of essential metal cofactors, and inhibition of antioxidant systems. The resulting molecular damage leads to the formation of damage-associated molecular patterns (DAMPs), which activate redox-sensitive transcription factors and inflammatory cascades. Importantly, emerging metabolomic evidence indicates that these processes are accompanied by coordinated metabolic reprogramming involving amino acid, lipid, and energy metabolism, as well as microbiota-derived metabolites. These metabolic alterations not only reflect cellular adaptation to stress but also actively contribute to the propagation of a systemic inflammatory state. An integrated oxinflammatory and metabolic response underlies structural and functional alterations across multiple organ systems, including the liver, kidneys, cardiovascular system, nervous system, and reproductive organs. Persistent exposure, even at low doses, sustains this often subclinical and chronic process, reinforcing the need to understand metabolic changes as central components of metal-induced toxicity. Full article

Cadmium (Cd) is a heavy metal pollutant to which most people are exposed daily through their diet because of its presence in nearly all food types, including potatoes, vegetables, cereals, grains, legumes, shellfish, and organ meat. Cd has no physiological role or nutritional value in the body and causes toxicity to multiple tissues and organs via oxidative stress and chronic inflammation; as such, at high prevalence, it is frequently associated with diseases, notably cancer, heart disease, diabetes, osteoporosis, and chronic kidney disease. Using kidneys and bones as critical toxicity targets, current dietary Cd exposure guidelines vary from 0.21 to 0.83 μg/kg b.w./d. There is a widespread concern about these guidelines because they were based on the excretion of β₂-microglobulin (β₂M) at a rate of 300 µg/g of creatinine as an endpoint. Concerningly, rice is a staple food for over 50% of the world’s population; however, the permissible Cd level in this commodity has not been adequately addressed. This narrative review focuses on critiquing existing food standards and exposure guidelines for Cd. It discusses the threshold-based risk assessment that was used to define the no-observed-adverse-effect level (NOAEL) for Cd, when β₂M excretion was used with Cd excretion at a rate of 5.24 µg/g of creatinine being a threshold. The estimated glomerular filtration rate (eGFR) is recommended as an appropriate kidney disease endpoint. The current view around how Cd uses various transport proteins to enter and induce toxicity to its target cells are summarized. The strategies to minimize Cd accumulation and mitigate its nephrotoxicity are highlighted. Full article

Ageing radically alters the physicochemical properties of microplastics, significantly increasing their affinity for environmental pollutants. However, the slow nature of natural degradation necessitates the development of efficient laboratory protocols. This study establishes an accelerated ageing methodology that reflects natural dynamics by comparing Polyethene terephthalate microplastics (PET MPs) exposed to sunlight (3 months) with those exposed to laboratory UV-C radiation (varying lamp numbers and 24–336 h). scanning electron microscopy (SEM) imaging confirmed progressive surface degradation, including increased roughness, micro-cavities, and erosion. Photo-oxidation was evidenced by an increase in the carbonyl index (CI) from 7.43 ± 0.30 to 8.97 ± 0.35 (UV-aged) and 11.45 ± 0.45 (sun-aged). Furthermore, crystallinity significantly decreased from 59.5% to 54.4% and 16.6%, respectively, while the point of zero charge (pH_PZC) shifted from near neutral (6.5–7.0) to below 2.0. Notably, high-intensity, short-term UV-C exposure accelerated surface functionalization, enhancing cadmium adsorption capacity (q_e = 1.9 mg/g). The laboratory protocol provides rapid reactivation on the surface, serving as a proxy for prolonged sunlight exposure. Consequently, these findings offer a framework for assessing heavy metal uptake and the broader environmental implications of microplastics in aquatic environments. This understanding supports pollutant evaluation and sustainable water management for aquatic ecosystem protection. Full article

Hyper-arid marine ecosystems, characterized by extreme environmental conditions, are experiencing intensified stress from the synergistic effects of climate change and pollution. This review synthesizes current knowledge on these interactions in Qatar’s coastal waters, serving as a model system for the Arabian Gulf. We document significant accumulations of heavy metals, petroleum hydrocarbons, microplastics, and emerging contaminants near urban and industrial zones. The region’s rapid warming, hypersalinity, and restricted circulation amplify pollutant toxicity through mechanisms such as increased bioavailability, oxidative stress, and impaired physiological responses. These synergies elevate mortality in sensitive species by 50–100% compared to single stressors, push organisms beyond their physiological limits, and trigger biodiversity loss. As an example, given a baseline of around USD 148 million, a 30% decrease in exploitable fish biomass might result in an annual loss of approximately USD 45 million in the value of Qatar’s fisheries and aquaculture industry. Despite growing evidence, critical gaps persist in understanding mixture toxicity under Gulf-specific extremes, endocrine and neurobehavioral endpoints, and quantitative ecosystem service valuations. We conclude by highlighting emerging solutions, including IoT-based monitoring, AI-driven forecasting, and nature-based remediation, as pathways to enhance resilience under accelerating environmental change. These findings have important implications for marine ecosystem sustainability, food security, and sustainable coastal management in Qatar and other hyper-arid regions. This synthesis establishes Qatar’s coastal ecosystem as a global model for understanding climate–pollution feedback in hyper-arid seas. Full article

Cadmium (Cd) is a typical heavy metal pollutant in aquatic environments. It enters fish through the gills, digestive tract, and body surface, and accumulates mainly in the liver and kidneys, with species- and tissue-specific distribution. Cadmium triggers apoptosis by inducing oxidative stress, calcium imbalance, and DNA damage. These signals are integrated and amplified by the mitogen-activated protein kinase (MAPK), nuclear factor kappa B (NF-κB), phosphatidylinositol 3-kinase (PI3K)/AKT, and nuclear factor erythroid 2-related factor 2 (Nrf2) pathways, ultimately activating three downstream apoptotic execution pathways: the death receptor, mitochondrial, and endoplasmic reticulum stress pathways. These three pathways form an interactive network through molecular nodes such as BH3 interacting domain death agonist (Bid), Ca²⁺, c-Jun N-terminal kinase (JNK), and C/EBP homologous protein (CHOP), synergistically amplifying the apoptotic effect, with the mitochondrial pathway playing a central role. Cadmium-induced apoptosis is dose-dependent: low concentrations activate protective responses, whereas high concentrations strongly promote apoptosis. Current research gaps remain regarding dynamic pathway crosstalk, chronic low-dose effects, species differences, and fish-specific apoptotic molecules (e.g., caspase-12 homologs). Future studies should focus on constructing multidimensional response maps, clarifying pathway activation thresholds and interaction contributions, and developing composite protective strategies based on Nrf2 activators, metal chelators, and antioxidants, thereby promoting translation into ecological risk assessment and aquaculture pollution control. Full article

Nanoparticles (NPs) have great potential for stimulating plant growth and development, reducing the negative impact of various types of stress on plants, and increasing the yield of agriculturally important crops. Metal oxide NPs (MONPs) have been shown to have a significant effect on the physiological and biochemical processes in plants, enhancing plant resilience. Among them, CuO, Mn_xO_x, and ZnO NPs are of particular interest because they contain elements essential for plant function. However, widespread use in agrochemistry and plant protection requires a preliminary risk assessment due to their potential phytotoxic effects. Phytotoxicity manifests through the development of oxidative stress, genotoxicity, and transcriptional disruption. A decrease in plant growth and photosynthesis, increased lipid peroxidation (LPO), and the accumulation of toxic NPs in plant tissues were also observed. Among the studied MONPs, CuO and ZnO NPs exhibit the greatest phytotoxic effects. However, the effects of MONPs are dose-dependent. Numerous studies have shown that MONPs can stimulate plant biometric parameters and productivity, as well as influence biochemical processes. MONPs have been shown to influence the functioning of the plant antioxidant system, manifested by modulating the content of reactive oxygen species (ROS), the activity of antioxidant enzymes (AOEs), and the regulation of signaling pathways mediated by ROS and reactive nitrogen species. Furthermore, MONPs influence the accumulation of proline and phenols in plant tissues. MONPs have a pronounced effect on the functioning of the plant photosynthetic apparatus, manifested by changes in pigment content, the activity of photosynthetic enzymes, and the functioning of photosystems. MONPs can improve nutrient absorption, regulate osmotic balance, and activate plant defense mechanisms. ZnO NPs are effective in mitigating salt stress. CuO and Mn_xO_x NPs have shown promise in mitigating biotic stress. Furthermore, these NPs were found to reduce the toxicity of heavy metals to plants. Overall, when used wisely, MONPs hold promise for enhancing the physiological, biochemical, and agronomic performance of crop plants under conditions of global climate change, effectively addressing food security issues. Full article

Abiotic stresses, including heavy metal contamination, can severely impair plant growth and antioxidative defense. However, their adverse effects may be mitigated through sustainable strategies such as biostimulant application. This study investigated the effects of humic substances (HSs), alone or combined with mycorrhizal inoculation (M), on oxidative stress and antioxidative responses in Cannabis sativa, Sorghum sudanense × bicolor, and Miscanthus × giganteus grown under field conditions on metal-contaminated agricultural soil exceeding regulatory thresholds for Zn, Pb, and Cd. Plant growth, lipid peroxidation, stress-related metabolites (proline, sugars), antioxidative enzyme activities (catalase, CAT; ascorbate peroxidase, APX; guaiacol peroxidase, GOPX; glutathione reductase, GR, and superoxide dismutase, SOD), and leaf metal concentrations were analyzed. Biostimulants increased proline and sugars in Sorghum (by up to 55% and 80%, respectively), accompanied by reduced oxidative stress indicators and improved biomass (by 26%). In Cannabis, higher Cd and Pb concentrations following biostimulant treatments were associated with increased SOD, APX, and GR activities (by 33–267%), without affecting growth. In Miscanthus, increased lipid peroxidation (by 37–60%) occurred alongside enhanced GR and APX activities. These results indicate strong species-specific responses and absence of consistent synergistic effects of HSs and M, highlighting distinct physiological strategies of stress adaptation and antioxidative defense on metal-contaminated soils. Future research should address physiological and molecular mechanisms underlying these responses. Full article

In situ coagulation is regarded as the most effective measure in response to the frequent metal spills in China. Excessive coagulant is often used in pursuit of extremely high removal rates of contaminants. Yet the secondary ecological impact of the iron-containing coagulation flocs left on the river sediments after emergency response is still unclear. In the current study, we investigated the impact of flocs derived from three different iron-based coagulants, polymeric ferric sulfate (PFS), polymeric ferric chloride (PFC), and ferric chloride (FeCl₃), on microbial communities in sediment based on microcosm experiments. Metagenomics, quantitative PCR, and determination of ammonia oxidation potential were adopted to elucidate community shifts. The results indicate that the community structure and function of microorganisms in sediments have been affected, especially processes and species related to nitrogen cycling, and the effect was coagulant-specific. Flocs retrieved from FeCl₃ caused a more pronounced decline in diversity, shifts in community composition, and decreased potential ammonia oxidation. Ammonia-oxidizing archaea (AOA) was more sensitive to iron-containing flocs than ammonia-oxidizing bacteria (AOB), while PFS-flocs tended to reduce multiple genes involved in nitrate reduction. This indicates that the pre-polymerization of inorganic coagulants may be the primary factor leading to different microbial ecological effects. Sulfate, on the other hand, may affect specific biogeochemical processes due to its competition for electron donors. Our results confirmed that even without heavy metals as contaminants, coagulant flocs alone could present an effect on nitrogen cycling in sediments. The results will provide a scientific basis for environmental emergency decision-making: in emergency response to metal pollution incidents, the use of coagulants should be limited to only the necessary level. Full article

Heavy metal contamination of foods remains a persistent global challenge for food safety and public health, driven by industrialization, mining activities, intensive agriculture, and ongoing environmental degradation. This scoping review synthesizes peer-reviewed literature on the occurrence of priority toxic metals—arsenic, cadmium, lead, mercury, and nickel—in food matrices, with emphasis on contamination pathways, analytical detection strategies, and documented human health effects. The reviewed studies reveal widespread accumulation of heavy metals in staple foods, including cereals, vegetables, seafood, and processed products, with concentrations frequently approaching or exceeding international regulatory limits, particularly in regions exposed to strong anthropogenic pressure. Conventional laboratory-based techniques, such as atomic absorption spectrometry and inductively coupled plasma methods, remain the reference standards for quantitative determination and regulatory compliance; however, their application to large-scale or continuous monitoring is often constrained by cost, infrastructure, and operational complexity. Consequently, increasing attention has been directed toward emerging detection approaches, including portable X-Ray fluorescence, Raman/SERS spectroscopy, electrochemical biosensors, electronic tongues, and in situ magnetic measurements, as complementary tools for rapid screening and field-based surveillance. Among these, environmental magnetism and in situ magnetic techniques stand out as non-destructive, low-cost proxies capable of identifying metal-associated particulate contamination linked to food production systems. Chronic dietary exposure to heavy metals is consistently associated with neurotoxicity, nephrotoxicity, carcinogenicity, and oxidative stress, underscoring the need for integrated, multi-tiered monitoring frameworks to support early detection, risk assessment, and prevention. Full article

Background: Cigarette smoking exposes the human body to a complex mixture of toxic and carcinogenic compounds that can exert widespread biological effects across different organ systems. From addictive responses and consequence maladaptive neuroendocrine responses, cigarette smoke delivers a variety of reactive oxygen species, polycyclic aromatic hydrocarbons, nitrosamines, and heavy metals that collectively contribute to oxidative stress, inflammation, endothelial dysfunction, and metabolic disruption. The liver, as the primary organ responsible for xenobiotic metabolism, plays a central role in processing these harmful substances and is therefore uniquely susceptible to their effects. This narrative review will aim to provide an overview of the current evidence of cigarette smoking effects on hepatic structure and function and discuss clinical implications. Methods: This narrative review synthesizes evidence from in vitro studies, animal models, and human clinical research examining the effects of cigarette smoking on liver biology. Mechanistic pathways of injury, metabolic and vascular alterations, and clinical consequences for liver disease were considered. Results: Smoking influences hepatic function both directly—through biotransformation pathways generating reactive intermediates—and indirectly via vascular impairment, immune modulation, hormonal alterations, and changes in lipid and glucose metabolism. Emerging evidence indicates that cigarette smoking contributes to hepatic steatosis, accelerates fibrosis progression, worsens outcomes in viral and alcohol-related liver disease, and increases the risk of hepatocellular carcinoma. Conclusions: Cigarette smoking exerts multifaceted deleterious effects on the liver. Recognition of smoking as a modifiable risk factor for liver-related morbidity underscores the importance of smoking cessation in patients with or at risk for liver disease and highlights implications for research and clinical practice. Full article

With the rapid progression of global industrialization and urbanization, heavy metal contamination has emerged as a major global threat, especially cadmium pollution. Consequently, optimizing remediation measures has become a pivotal means to solve cadmium contamination. Compared to traditional physical and chemical remediation methods, microbial remediation has great potential in addressing cadmium pollution. In this study, a novel bacterial strain, Chryseobacterium sp. HGX-24, exhibiting high cadmium resistance was successfully isolated and screened from cadmium-contaminated environments. A preliminary discussion of the response mechanisms of this strain under cadmium stress is provided. Additionally, preliminarily explored the synergistic remediation of microbial-plant in cadmium-contaminated soil. Under conditions of high cadmium concentration, cadmium ions were effectively adsorbed by strain HGX-24 through extracellular polymers and functional groups on the cell wall surface, including −COOH, −CONH−, −NH, −OH, and >C=O. Extracellular proteins and polysaccharides were secreted by strain HGX-24 to regulate the adverse effects of heavy-metal cadmium ions on bacterial growth. Furthermore, the expression of genes such as antioxidant defense and ROS scavenging (katG, fabG, ybjT), Fe-S cluster assembly (sufB, sufD), sulfur metabolism (cysAU), amino acid metabolism (hisA, cysD, aspC), phenylacetic acid catabolism (paaC), and ribosomal proteins (rplC, rpsC, rpsL, rplA, rplY, rpmC) was regulated, affecting the synthesis and metabolism of membrane transporters (ABC transporters and efflux RND transporters), antioxidant enzymes (SOD, COT, POD), Fe-S clusters, thioredoxin family proteins, and ribosomal proteins, thereby enhancing resistance to cadmium toxicity. Moreover, strain HGX-24 was found to regulate the activities of redox enzymes in Zea mays L., thereby alleviating oxidative stress and reducing the negative feedback effects of reactive oxygen species in Z. mays. Full article

Hexavalent chromium, a widespread heavy metal, induces apoptosis via the mitochondrial pathway through Bax (pro-apoptotic) and Bcl2 (anti-apoptotic) proteins. Hypericum perforatum, rich in antioxidants, can neutralise free radicals. This study investigated the effects of CrVI on the pancreas and the protective role of Hypericum perforatum. Five groups of animals were used: control, Cr (CrVI for 3 months), CrH (CrVI + 2.5% Hypericum perforatum extract made from flowers, for 3 months), Cr2 (CrVI for 3 months + distilled water for 1 month), and CrH2 (CrVI for 3 months + Hypericum perforatum extract for 1 month). Samples were collected for histological analysis, gene expression (qRT-PCR), and blood glucose level analysis. CrVI exposure (Cr, Cr2) caused pancreatic damage: oedema, reduced islet size, endocrine cell vacuolisation, and endothelial swelling. Lesions were milder in CrH, while CrH2 resembled the control group. The Bax/Bcl2 ratio increased under CrVI (highest in Cr2), indicating apoptosis, but decreased toward control values in CrH and CrH2. Blood glucose levels confirmed these findings. CrVI proved toxic to the endocrine pancreas, inducing structural and molecular alterations that impaired carbohydrate metabolism. Administration of Hypericum perforatum extract reduced these effects, confirming its antioxidant action and potential as a protective agent against CrVI-induced oxidative stress. Full article

Aquaculture sustainability in rapidly urbanizing regions is increasingly threatened by heavy metal contamination originating from complex anthropogenic land-use patterns. This study used an integrated model to evaluate the molecular-to-human health continuum in hybrid catfish (Clarias gariepinus × Clarias macrocephalus) sourced from Pathum Thani, Thailand’s primary aquaculture hub. We integrated geospatial land-use data with heavy-metal quantification, oxidative-stress biomarkers, and transcriptional profiling to assess how canal-specific water quality modulates fish health and consumer risk. The results revealed significant spatial heterogeneity in metal concentrations, corresponding to the province’s 27% urban–industrial land-use footprint. While water quality generally met regulatory limits, a pronounced aqueous–biotic discrepancy, “bioaccumulation paradox” was identified at certain sites, where muscle and hepatic tissues exhibited lead (Pb), chromium (Cr), and nickel (Ni) levels that substantially exceeded international safety standards. Biochemical and molecular analyses provided functional evidence of physiological distress, specifically significantly elevated malondialdehyde (MDA) levels, and the transcriptional modulation of cat, cyp1a, gpx, met, tnf, and star genes indicated that chronic metal exposure overwhelmed antioxidant defenses and induced potential endocrine disruption. Moreover, human health risk assessments revealed that the hazard index (HI) and target cancer risk (TR) exceeded unacceptable thresholds at multiple hotspots, indicating that Cr is a primary carcinogenic driver. These findings highlight a “GAP Paradox,” where farm-level certifications are insufficient to mitigate risks posed by the surrounding canal network. This study presents vital evidence-based risk profiles that necessitate a transition to a spatially based regulatory framework, incorporating geospatial land-use monitoring into national food safety policies to protect both aquaculture viability and public health. Full article

The MarR (multiple antibiotic resistance regulator) family regulators, which are widely conserved across various organisms, play pivotal roles in metabolism, stress response mechanisms, and virulence factor production. However, the regulatory functions of these factors in the degradation of aromatic compounds within Corynebacterium glutamicum remain largely uncharacterized. In this study, we identified a MarR-type regulator, designated AcsR (encoded by ncgl2425), which directly represses the expression of the catechol 2,3-dioxygenase gene ncgl2007 (c23o) and the heavy metal (nickel) transport system permease gene ncgl2351, while activating the expression of ncgl2258 encoding an ABC-type C4-dicarboxylate-binding periplasmic protein. AcsR binds specifically as a dimer to a 6 bp inverted repeat sequence, and this binding is disrupted by catechol in vitro. Correspondingly, catechol induces the expression of c23o in vivo. Phenotypic analysis revealed that the ΔacsR mutant exhibited enhanced resistance to multiple aromatic compounds but increased sensitivity to antibiotics, heavy metals, and oxidants. Collectively, these findings demonstrate that AcsR is an important regulator of stress adaptation in C. glutamicum and provide new insights into the regulatory mechanisms of aromatic compound degradation in this industrially important bacterium. Full article