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Microplastics (MPs) have attracted significant attention due to their global distribution in living environments. Although some studies have reported MP-induced hepatotoxicity in mouse models, a systematic approach to MP-mediated liver toxicity was still lacking. Therefore, we used a mouse model to study the sub-chronic effects of MP exposure on the liver. Female C57BL/6 mice, aged 6 weeks, received an oral administration of 0.3 mg of Nile Red-labeled polystyrene (PS) microplastics, with particle sizes of 0.5 µm (submicron) and 5 µm (micron), via gavage, while control mice received vehicle only. Each mouse was exposed to MPs twice a week for 12 weeks. After sacrifice, the levels of MP accumulation, oxidative stress, inflammation, and pathological changes were measured in the mouse liver, and blood samples were collected for serum biochemistry analysis. Our results demonstrated that 0.5 µm PS-MPs were accumulated in mouse livers post-MP exposure, but not in the 5 µm MP exposure group. Simultaneously, increased levels of glucose, triglyceride, alanine transaminase (ALT), aspartate transaminase (AST), superoxide dismutase, 4-hydroxy-2-nonenal-mercapturic acid (HNE-MA), interleukin-6, and lipid droplets were found in the 0.5 µm MP exposure group, while the fewer responses, including elevated liver weight index, glucose, high-density lipoprotein, AST, and decreased HNE-MA were observed in 5 µm MP exposure group. These results indicate that sub-chronic exposure to submicron MPs causes MP deposition in mouse livers, which further induces oxidative stress, increases inflammatory cytokines and perturbs glucose and lipid homeostasis, which might trigger more severe metabolic dysfunction or non-alcoholic steatohepatitis-like hepatotoxicity.

The rapid growth of industrialization and urbanization results in deterioration of freshwater systems around the world, rescinding the ecological balance. Among many factors that lead to adverse effects in aquatic ecology, metals are frequently discharged into aquatic ecosystems from natural and anthropogenic sources. Metals are highly persistent and toxic substances in trace amounts and can potentially induce severe oxidative stress in aquatic organisms. In this study, adverse effects of the two metal elements zinc (maximum concentration of 167.25 mg/L) and mercury (104.2 mg/L) were examined using Chlorella vulgaris under acute and chronic exposure period (48 h and 7 days, respectively). The metal-induced adverse effects have been analyzed through photosynthetic pigment content, total protein content, reactive oxygen species (ROS) generation, antioxidant enzymatic activities, namely catalase and superoxide dismutase (SOD) along with morphological changes in C. vulgaris . Photosynthetic pigments were gradually reduced (~32–100% reduction) in a dose-dependent manner. Protein content was initially increased during acute (~8–12%) and chronic (~57–80%) exposure and decreased (~44–56%) at higher concentration of the two metals (80%). Under the two metal exposures, 5- to 7-fold increase in ROS generation indicated the induction of oxidative stress and subsequent modulations in antioxidant activities. SOD activity was varied with an initial increase (58–129%) followed by a gradual reduction (~3.7–79%), while ~1- to 12-fold difference in CAT activity was observed in all experimental condition (~83 to 1605%). A significant difference was observed in combined toxic exposure (Zn+Hg), while comparing the toxic endpoint data of individual metal exposure (Zn and Hg alone). Through this work, lethal effects caused by single and combined toxicity of zinc and mercury were assessed, representing the significance of appropriate monitoring system to trim down the release of metal contaminants into the aquatic ecosystems.

Secondary glaucoma is a typical normal tissue complication following radiation therapy involving ocular radiation exposure at high fractionated dose (several tens of Gy). In contrast, recent studies in acutely exposed Japanese atomic bomb survivors showed a significantly increased risk for normal-tension glaucoma (NTG, a subtype of primary open-angle glaucoma) at much lower dose, but such information is not available in any other cohorts. We therefore set out to evaluate the incidence of risk for primary glaucoma and its subtypes in a Russian cohort of Mayak Production Association nuclear workers who received chronic radiation exposure over many years. Of these, we found a significantly increased relative risk (RR) of NTG incidence (RR = 1.88 95% confidence intervals (CI): 1.01, 3.51; p = 0.047) in workers exposed to gamma rays at cumulative brain absorbed dose above >1 Gy. We observed the linear relationship between NTG incidence and brain absorbed gamma dose with an excess relative risk per unit brain absorbed dose of 0.53 (95% CI: 0.01, 1.68; p < 0.05), but not for any other subtypes nor for total primary glaucoma. Such elevated risk of radiogenic NTG incidence, if confirmed in other cohorts, has significant implications for normal tissue complications in radiotherapy patients receiving ocular radiation exposure, and for ocular radiation protection in radiation workers.

Due to their worldwide use and environmental persistence, antibiotics are frequently detected in various aquatic compartments. Their toxic properties raise environmental concerns to non-target organisms. Histopathology data is frequently applied in ecotoxicology studies to assess the effects of different classes of environmental stressors in fish, including antibiotics. Tissue alterations in gills and liver of gilthead seabream (Sparus aurata) individuals acutely (96 h) and chronically (28 days) exposed to environmentally relevant concentrations of the antibiotics erythromycin (ERY: 0.0002-200 μg/L) and oxytetracycline (OTC: 0.0004-400 μg/L), including a control non-exposed group, were evaluated. Several disorders (circulatory, regressive, progressive, and inflammatory) were observed in both organs of all exposed animals. The hereby obtained data showed a higher and significant increase in gill histopathological index of organisms acutely exposed to ERY and of those chronically exposed to OTC. In terms of categorical lesions, only a significant increase of regressive and progressive alterations occurred in gills after chronic exposure to OTC. For the liver, a significant increase in pathological index was also detected, as well as regressive changes, after chronic exposure to OTC. Furthermore, the present study indicates that most of the changes observed in gills and liver were of mild to moderate severity, which might be adaptive or protective, non-specific, and mostly reversible. Despite being observed, irreversible lesions were not significant in any of the fish organs analyzed. Although there were histological changes, gill apparatus was considered still functionally normal, as well as liver tissue, not supporting the occurrence of severe toxicity. In general, the observed histological changes were not stressor-specific, and toxicological mechanistic explanations for the alterations observed in gills and liver are presented. The obtained data showed that histopathological biomarkers can be successfully applied in ecotoxicological studies, evidencing their relevance, responsivity, and complementarity to other biochemical biomarker-based approaches.

Epidemiological and challenge studies in healthy subjects and in individuals with asthma highlight the health impact of environmental ozone even at levels considered safe. Acute ozone exposure in man results in sputum neutrophilia in 30% of subjects particularly young children, females, and those with ongoing cardiopulmonary disease. This may be associated with systemic inflammation although not in all cases. Chronic exposure amplifies these effects and can result in the formation of asthma-like symptoms and immunopathology. Asthmatic patients who respond to ozone (responders) induce a greater number of genes in bronchoalveolar (BAL) macrophages than healthy responders with up-regulation of inflammatory and immune pathways under the control of cytokines and chemokines and the enhanced expression of remodeling and repair programmes including those associated with protease imbalances and cell-cell adhesion. These pathways are under the control of several key transcription regulatory factors including nuclear factor (NF)-κB, anti-oxidant factors such as nuclear factor (erythroid-derived 2)-like 2 NRF2, the p38 mitogen activated protein kinase (MAPK), and priming of the immune system by up-regulating toll-like receptor (TLR) expression. Murine and cellular models of acute and chronic ozone exposure recapitulate the inflammatory effects seen in humans and enable the elucidation of key transcriptional pathways. These studies emphasize the importance of distinct transcriptional networks in driving the detrimental effects of ozone. Studies indicate the critical role of mediators including IL-1, IL-17, and IL-33 in driving ozone effects on airway inflammation, remodeling and hyperresponsiveness. Transcription analysis and proof of mechanisms studies will enable the development of drugs to ameliorate the effects of ozone exposure in susceptible individuals.

The increased mobilization of Rare Earth Elements (REEs), due to emerging technologies, could impact human health. The study assessed the effects of CeO2 nanopowder (100 μg/mL) in human intestinal cells (HT-29) following both acute (24 h) and, a novelty for in vitro study, sub-chronic exposure, treating subcultures of exposed cells to CeO2 NP up to 35 days. Recovery was also examined in exposed cells’ progeny. CeO2 NP internalization and acute cytotoxicity were dose and time dependent. A significant pro-oxidant effect was observed for up to 14 days. The highest mitochondrial impairment was detected after 7 days, but in post-exposure experiments the recovery was observed. Conversely, genotoxicity highlighted the saturation of the DNA repair mechanisms. The irreversible cell damage of sub-chronic exposure was highlighted by the percentage of death cells (p = 0.011) and by the weekly cell replication index (5.68 vs. 7.41). The homeostatic mitophagy pathway was able to counteract ROS-induced mitochondrial dysfunction, as shown by overexpression of ATG5, LC3, and BECN1 genes throughout the examined times. Instead, the overexpression of the pro-apoptotic gene Bax was very brief, highlighting that prolonged exposure might cause more widespread adverse effects, also involving cells that are not directly exposed to nanoceria.

Zinc oxide nanoparticles (ZnO NPs) are increasingly used in several personal care products, with high potential to be released directly into marine environment with consequent adverse impact on marine biota. This paper aimed to compare the ecotoxicological effect of ZnO NPs (< 100 nm) towards three marine organisms widely used in toxicity assessment: an algal species ( Dunaliella tertiolecta ), a bioluminescent bacterium ( Vibrio fischeri ), and a crustacean ( Artemia salina ). Bulk ZnO (ZnO bulk, 200 nm) and ionic zinc were also investigated for understanding the role of size and of ionic release in the ZnO toxic action. To this aim, different ecotoxicological tests were used: the inhibition of bioluminescence with V. fischeri at three exposure times (5, 15, and 30 min); the D. tertiolecta growth inhibition at 24, 48, and 72 h; the A. salina mortality at 24–96 h, and A. salina mortality and body growth each 3 days along chronic exposure (14 days). For all selected species, ZnO NPs toxicity was strictly dependent on the exposure time and different sensitivities were recorded: ZnO NPs were more toxic towards algae (EC 50 2.2 mg Zn/L) but relatively less toxic towards bacteria (EC 50 17 mg Zn/L) and crustaceans (EC 50 96 h 58 mg Zn/L). During the 14-day chronic exposure of A. salina , ZnO NPs had a significant inhibition of vitality and body length (EC 50 14d 0.02 mg Zn/L), while the effect of ZnSO 4 was not statistically different from the control. ZnO NP toxicity was related to zinc ions and to interactions of particle/aggregates with target organisms and therefore to NP behavior in the testing matrix and to the different testing time exposures.

This study was aimed to evaluate the effect of sublethal concentrations of lead chloride on physiological and histopathological studies in Gambusia affinis . A total of 500 fish were collected from the bank of the river east of Mosul city. The fish in the aquarium were divided into five groups (control, acute exposure(20,25mg/l) and chronic exposure(5,10mg/l)). The bioaccumulation of lead in acute and chronic periods of exposure showed a significant difference in values between control and treatment. The greatest level was seen in the kidney of fish treated with lead dichloride at 10 mg/l for 30 days. The level of antioxidant Glutathione has a significant decrease in different kidneys of fish treated with pbcl2 exposed to acute and chronic concentrations. The lowest decrease was seen in kidneys of fish treated with Pbcl2 at 10 mg/l for a month. At the same time, a significant increase in lipid peroxidation (malondialdehyde) level was seen in all kidney treated with PbCl2. Histological study of the kidney showed varying degrees of pathological lesions. The glomeruli in the kidney shrank, and  degeneration of Bowman's capsule. The Pb accumulation increases with increasing concentration and period of exposure. Both acute and chronic effects caused a change in the level of antioxidants and histopathological changes in kidney of the fish. Histopathological study may be a useful indicator for determining the extent of aquatic contamination. It could be concluded that the kidney changes caused by lead exposures in fish may serve as a biomarker for the contamination of sub-lethal levels of heavy metals and other anthropogenic contaminants.

Background Bisphenol S (BPS) is a common bisphenol A (BPA) substitute, since BPA is virtually banned worldwide. However, BPS and BPA have both endocrine disrupting properties. Their effects appear mostly in adulthood following perinatal exposures. The objective of the present study was to investigate the impact of perinatal and chronic exposure to BPS at the low dose of 1.5 μg/kg body weight/day on the transcriptome and methylome of the liver in 23 weeks-old C57BL6/J male mice. Results This multi-omic study highlights a major impact of BPS on gene expression (374 significant deregulated genes) and Gene Set Enrichment Analysis show an enrichment focused on several biological pathways related to metabolic liver regulation. BPS exposure also induces a hypomethylation in 58.5% of the differentially methylated regions (DMR). Systematic connections were not found between gene expression and methylation profile excepted for 18 genes, including 4 genes involved in lipid metabolism pathways (Fasn, Hmgcr, Elovl6, Lpin1), which were downregulated and featured differentially methylated CpGs in their exons or introns. Conclusions This descriptive study shows an impact of BPS on biological pathways mainly related to an integrative disruption of metabolism (energy metabolism, detoxification, protein and steroid metabolism) and, like most high-throughput studies, contributes to the identification of potential exposure biomarkers. Graphical abstract

Knowledge regarding complex radiation responses in biological systems can be enhanced using genetically amenable model organisms. In this manuscript, we reviewed the use of the nematode, Caenorhabditis elegans (C. elegans), as a model organism to investigate radiation’s biological effects. Diverse types of experiments were conducted on C. elegans, using acute and chronic exposure to different ionizing radiation types, and to assess various biological responses. These responses differed based on the type and dose of radiation and the chemical substances in which the worms were grown or maintained. A few studies compared responses to various radiation types and doses as well as other environmental exposures. Therefore, this paper focused on the effect of irradiation on C. elegans, based on the intensity of the radiation dose and the length of exposure and ways to decrease the effects of ionizing radiation. Moreover, we discussed several studies showing that dietary components such as vitamin A, polyunsaturated fatty acids, and polyphenol-rich food source may promote the resistance of C. elegans to ionizing radiation and increase their life span after irradiation.