25 research outputs found
Exploring the Impact of Contaminants of Emerging Concern on Fish and Invertebrates Physiology in the Mediterranean Sea
In this historical context, the Mediterranean Sea faces an increasing threat from emerging pollutants such as pharmaceuticals, personal care products, heavy metals, pesticides and microplastics, which pose a serious risk to the environment and human health. In this regard, aquatic invertebrates and fish are particularly vulnerable to the toxic effects of these pollutants, and several species have been identified as bio-indicators for their detection. Among these, bivalve molluscs and elasmobranchs are now widely used as bio-indicators to accurately assess the effects of contaminants. The study focuses on the catshark Scyliorhinus canicular and on the Mediterranean mussel Mytilus galloprovincialis. The first one is a useful indicator of localised contamination levels due to its exposure to pollutants that accumulate on the seabed. Moreover, it has a high trophic position and plays an important role in the Mediterranean Sea ecosystem. The bivalve mollusc Mytilus galloprovincialis, on the other hand, being a filter-feeding organism, can acquire and bioaccumulate foreign particles present in its environment. Additionally, because it is also a species of commercial interest, it has a direct impact on human health. In conclusion, the increasing presence of emerging pollutants in the Mediterranean Sea is a serious issue that requires immediate attention. Bivalve molluscs and elasmobranchs are two examples of bio-indicators that must be used to precisely determine the effects of these pollutants on the marine ecosystem and human health
ACETYLSALIC ACID (ASA): PHYSIOLOGICAL CHANGES IN NON-TARGET ORGANISM MYTILUS GALLOPROVINCIALIS
From biocide to biohazard: influence of methylchloroisothiazolinone on physiological integrity of Mytilus galloprovincialis
Methylchloroisothiazolinone (CMIT), an isothiazolinone-based compound, is extensively used in several commercial products as a biocide and has recently been identified as an emerging contaminant in aquatic environments. This study investigates the impact of this substance on key cellular, physiological, and biochemical endpoints in the Mediterranean mussel (Mytilus galloprovincialis). Mussels were exposed for 14 days to two sublethal CMIT concentrations (0.01 and 0.1 mg L−1), and responses were assessed in haemocytes (H) and digestive gland (DG). Cytotoxic effects were determined in H and DG through cell viability assays. Phagocytic activity was quantified in H. The osmoregulatory performance of DG isolated cells was evaluated using the Regulatory Volume Decrease (RVD) assay. Furthermore, oxidative stress biomarkers catalase and glutathione (GHS/GSSG), cytochrome P450-related activity (EROD) and neurotoxicity were measured in DG. Results revealed significant impairments in physiological functionality and osmoregulatory capacity, accompanied by high susceptibility of biochemical responses. In the DG, a clear association was observed between EROD activation and oxidative stress manifestations indicating the toxicity of CMIT derivatives. Overall, these findings confirm CMIT's toxic potential toward vital physiological and biochemical processes in M. galloprovincialis and provide a basis for further research aimed at demonstrating the ecological consequences of isothiazolinone contamination, with potential implications for both marine ecosystem health and human well-being
Protective role of Pleurotus florida against streptozotocin-induced hyperglycemia in rats: A preclinical study
: Pleurotus florida (Mont.) Singer is a mushroom species known to be an antioxidant, immunomodulatory, and diuretic agent, reducing blood pressure and cholesterol. The aim of this study was to evaluate the in vivo potency of P. florida's anti-diabetic properties in rats affected by hyperglycemia induced by Streptozotocin (STZ) at 55 mg/kg (i.p.), characterized by oxidative stress impairment, and changes in insulin levels and lipid profile. After inducing hyperglycemia in the rats, they were treated with P. florida acetone and methanol extracts, orally administered for 28 days at doses of 200 mg/kg and 400 mg/kg body weight. The hyperglycemic control (DC) group showed significant increases (P < 0.05) in mean blood sugar, total cholesterol, triglycerides, low-density lipoprotein cholesterol, very low-density lipoprotein cholesterol, blood urea nitrogen, lipid hydroperoxides, and malondialdehyde, compared to the normal control (NC) group The high-density lipoprotein cholesterol, serum insulin, superoxide dismutase, catalase, glutathione disulfide, glutathione peroxidase, reduced glutathione, guaiacol peroxidase, and vitamin E and C levels showed a significant decrease (P < 0.05) in DC group, compared to the NC group. Blood glucose levels, lipid profiles, and insulin levels improved significantly after 28 days of treatment, in the group treated with glibenclamide (an oral hypoglycemic drug, used as positive control), and in the groups treated with P. florida extracts. In DC group, the treatment with P. florida was found to prevent diabetes, according to histopathological studies of the kidneys, pancreas, and liver of rats. In conclusion, this study has shown that the treatment with P. florida decreased oxidative stress and glucose levels in the blood, as well as restoring changes in lipid profiles
Molecular docking analysis and in vivo assessment of zinc oxide nanoparticle toxicity in zebrafish larvae
The zinc oxide nanoparticles (ZnO-NPs) being widely employed in several industries and consumer products, are raising concerns about their safety on aquatic biota and human health. This study aims to investigate the possible toxicological effects of ZnO-NPs through a combined in vivo and in silico approach. Zebrafish embryos were exposed to several ZnO-NPs concentrations and morphological alterations and lipid peroxidation (MDA) were investigated. Furthermore, molecular docking simulations were applied to study the intermolecular interactions of ZnO-NPs against critical embryonic proteins namely zebrafish hatching enzyme1 (ZHE1) as well as the superoxide dismutase (SOD1). Treatment with ZnO-NPs resulted in an increase in MDA concentration and a decrease in antioxidant enzyme levels. Besides a significant decrease in mRNA expression of key enzymes of ROS detoxification genes, a modulation of inflammatory genes with a low downregulation of tnf-α, and an upregulation of il-1β were observed. Docking study suggests that the delayed hatching and increased cellular oxidative stress in zebrafish embryos may occur through a synergistic mechanism based on the ZnO-NP—dependent inhibition of ZHE1 and SOD1 enzymes. The integration of in vivo assessments with in silico computational modeling provided a more comprehensive evaluation of potential physiological risks in zebrafish embryos associated with nanomaterial exposure
When crayfish face painkillers: Tissue-specific cytotoxic and oxidative responses to indomethacin exposure in Procambarus clarkii
Non-steroidal anti-inflammatory drugs (NSAIDs) are increasingly recognized as emerging contaminants in freshwater ecosystems. However, their effects on aquatic invertebrates remain poorly investigated. This study evaluated for the first time both cellular and biochemical responses of the red swamp crayfish (Procambarus clarkii) following a long-term exposure to indomethacin, a widely used NSAID. Specimens were exposed for 28 days to 2.5, 5, and 10 mg/L, and biomarkers indicative of cytotoxicity and oxidative stress were evaluated. Viability of both hemolymph and hepatopancreas cells was assessed using Trypan Blue and Neutral Red assays, while oxidative stress biomarkers, including superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione S-transferase (GST), and malondialdehyde (MDA), were analyzed in hepatopancreas, gill, and muscle tissues. The results showed that indomethacin exposure induced significant, tissue-specific cytotoxic and oxidative responses. Notably, hepatopancreas cell viability decreased significantly at lower concentrations, with partial recovery at the highest dose, suggesting a possible hormetic effect of the contaminant. Oxidative stress biomarkers exhibited concentration-dependent changes: SOD and MDA levels were significantly altered in the hepatopancreas; GST activity was affected in the gills, and GPx activity increased in muscle at higher concentrations. Haemocyte viability remained unaffected, indicating resilience of circulating cells. The Integrative Biomarker Response-Threshold (IBR-T) index highlighted both hormetic and classical dose-response trends, depending on tissue type. From an ecological perspective, these findings suggest that P. clarkii may tolerate relatively high indomethacin concentrations without systemic oxidative collapse, potentially supporting its persistence and competitive advantage in contaminated habitats. However, the hepatopancreas sensitivity indicates possible sublethal metabolic impairment, which could affect long-term fitness and population dynamics. Overall, this study provides novel insights into the ecotoxicological effects of indomethacin in a keystone invasive species and underscore the importance of tissue-specific biomarker analysis for environmental risk assessment
Understanding and addressing microplastic pollution: Impacts, mitigation, and future perspectives
Improper disposal of household and industrial waste into water bodies has transformed them into de facto dumping grounds. Plastic debris, weathered on beaches degrades into micro-particles and releases chemical additives that enter the water. Microplastic contamination is documented globally in both marine and freshwater environments, posing a significant threat to aquatic ecosystems. The small size of these particles makes them susceptible to ingestion by low trophic fauna, a trend expected to escalate. Ingestion leads to adverse effects like intestinal blockages, alterations in lipid metabolism, histopathological changes in the intestine, contributing to the extinction of vulnerable species and disrupting ecosystem balance. Notably, microplastics (MPs) can act as carriers for pathogens, potentially causing impaired reproductive activity, decreased immunity, and cancer in various organisms. Studies have identified seven principal sources of MPs, including synthetic textiles (35%) and tire abrasion (28%), highlighting the significant human contribution to this pollution. This review covers various aspects of microplastic pollution, including sources, extraction methods, and its profound impact on ecosystems. Additionally, it explores preventive measures, aiming to guide researchers in selecting techniques and inspiring further investigation into the far-reaching impacts of microplastic pollution, fostering effective solutions for this environmental challenge
From Personal Care to Coastal Concerns: Investigating Polyethylene Glycol Impact on Mussel’s Antioxidant, Physiological, and Cellular Responses
Pharmaceutical and personal care products (PPCPs) containing persistent and potentially hazardous substances have garnered attention for their ubiquitous presence in natural environments. This study investigated the impact of polyethylene glycol (PEG), a common PPCP component, on Mytilus galloprovincialis. Mussels were subjected to two PEG concentrations (E1: 0.1 mg/L and E2: 10 mg/L) over 14 days. Oxidative stress markers in both gills and digestive glands were evaluated; cytotoxicity assays were performed on haemolymph and digestive gland cells. Additionally, cell volume regulation (RVD assay) was investigated to assess physiological PEG-induced alterations. In the gills, PEG reduced superoxide dismutase (SOD) activity and increased lipid peroxidation (LPO) at E1. In the digestive gland, only LPO was influenced, while SOD activity and oxidatively modified proteins (OMPs) were unaltered. A significant decrease in cell viability was observed, particularly at E2. Additionally, the RVD assay revealed disruptions in the cells subjected to E2. These findings underscore the effects of PEG exposure on M. galloprovincialis. They are open to further investigations to clarify the environmental implications of PPCPs and the possibility of exploring safer alternatives
LINKING NANOPARTICLES TO EMBRYONIC DEFORMITIES: EXPLORING THE TERATOGENICITY OF ZINC OXIDE NANOPARTICLES
The exponential growth of nanotechnology has led to significant advancements in engineered nanoparticles (ENPs) between 1 and 100 nm in size, with zinc oxide nanoparticles (ZnO-NPs) playing a prominent role across various industries and applications. Particularly in biomedicine, ZnO-NPs have emerged as versatile tools, serving as anti- bacterial agents, drug and gene delivery platforms for cancer treatment, cellular imaging enhancers, and high-performance biosensors. For these reasons the aim of this study is to explore their potential toxicity on zebrafish early life stage using a combined in vivo and in-silico approach. In the first phase by SEM-EDS analysis, the ZnO-NPs purity was confirmed. After the Fish Embryo Acute Toxicity Tests according to OECD test guideline No. 236 (OECD, 2013) were performed. The embryos were exposed to five con centrations of ZnO-NPs: 50, 100, 150, 200 and 250 mg/L. At 96 hours, LC20 of about 58.201 mg/L and NOED of <50 mg/L, were determined. The most common sub-lethal alterations were pericardial and yolk edema, blood stasis, reduced blood circulation, reduced heartbeat, skeletal alterations and delayed hatching. Later, to further assess the toxicity of ZnO nanoparticles, oxidative stress was evaluated by quantifying lipid peroxidation using the thiobarbituric Acid Reactive Substances assay. The results showed as the treatment with ZnO-NPs led to a significant increase in lipid peroxidation in zebrafish larvae, as evidenced by the elevated levels of MDA induced by the treatment, indicating a low detoxification capacity of reactive oxygen species. To further confirm these findings, the gene expression of key antioxidant enzymes such as catalase (cat), superoxide dismutase (sod), and glutathione S-transferase (gstm) was also evaluated via RT-PCR. The results demonstrated a decrease in the expression of all the enzymes, suggesting that nanoparticles may interfere with the redox state of zebrafish larvae. Furthermore, since the oxidative stress is often associated with inflammation also key genes related to inflammation tnfalpha and il1beta were assayed. Our results showed a modulation of inflammation’s genes, particularly treatment induced a low downregulation of tnfalpha and an opposite regulation of il1beta which expression increased at very high levels. Finally, molecular docking and dynamics approach were applied to further explore any potential molecular interactions between ZnO- NPs and critical embryonic proteins, such as hatching enzyme ZHE1, and superoxide dismutase, SOD 1, enzyme. Results shown that ZnO-NPs interfered with both enzymes inhibiting those activities, and causing a delayed hatching of zebrafish embryos most probably through a multi-modal mechanism. The integration of in silico and in vivo assessments provides a more comprehensive evaluation of the potential risks associated with exposure to nano- materials, contributing to the fields of nanotoxicology and developmental biology. However, we are discussing preliminary results that require further testing and examination to fully understand the molecular mechanisms and causes of ZnO-NP toxicity
Molecular docking analysis and in vivo assessment of zinc oxide nanoparticle toxicity in zebrafish larvae
: The zinc oxide nanoparticles (ZnO-NPs) being widely employed in several industries and consumer products, are raising concerns about their safety on aquatic biota and human health. This study aims to investigate the possible toxicological effects of ZnO-NPs through a combined in vivo and in silico approach. Zebrafish embryos were exposed to several ZnO-NPs concentrations and morphological alterations and lipid peroxidation (MDA) were investigated. Furthermore, molecular docking simulations were applied to study the intermolecular interactions of ZnO-NPs against critical embryonic proteins namely zebrafish hatching enzyme1 (ZHE1) as well as the superoxide dismutase (SOD1). Treatment with ZnO-NPs resulted in an increase in MDA concentration and a decrease in antioxidant enzyme levels. Besides a significant decrease in mRNA expression of key enzymes of ROS detoxification genes, a modulation of inflammatory genes with a low downregulation of tnf-α, and an upregulation of il-1β were observed. Docking study suggests that the delayed hatching and increased cellular oxidative stress in zebrafish embryos may occur through a synergistic mechanism based on the ZnO-NP-dependent inhibition of ZHE1 and SOD1 enzymes. The integration of in vivo assessments with in silico computational modeling provided a more comprehensive evaluation of potential physiological risks in zebrafish embryos associated with nanomaterial exposure
