Silica nanoparticles (SiNPs) can reduce both quality and quantity of sperm via inhibiting the progress of meiosis and mitosis and inducing apoptosis of spermatogenic cells, however, their specific mechanism and effects on the later stage of spermatogenesis are still unclear. To investigate the effects of SiNPs on the reproductive system, male mice were treated with SiNPs (0, 1.25, 5 and 20 mg/kg.bw) via intratracheal instillation once every 3 days and for a total of 15 days. Results revealed that exposure to SiNPs induced reduction in the rate of sperm activity, histological abnormalities in seminiferous epithelium as well as apoptosis of spermatogenic cells, which are associated with decreased level of Lethal (3) malignant brain tumor like 2 (L3MBTL2) and activation of DNA damage-p53-mitochondrial apoptosis pathways. Moreover, reduction in L3MBTL2 level caused by SiNPs also led to the lower expression of RNF8-ubH2A/ubH2B pathway, thus resulting in incomplete histone-to-protamine exchange. These results suggest that the inhibition of L3MBTL2 expression caused by SiNPs not only activates DNA damage-p53-mitochondrial apoptosis pathway leading to the apoptosis of spermatogenic cells, but also inhibits RNF8-ubH2A/ubH2B pathway resulting in incomplete histone-to-protamine exchange, thereby affected spermatogenesis. This indicates that L3MBTL2 plays an important role in reproductive toxicity of males caused by SiNPs.

Cyanobacterial blooms cause potential risk to submerged macrophytes and biofilms in eutrophic environments. This pilot-scale study investigated the growth, oxidative responses, and detoxification activity of aquatic plants in response to cyanobacterial blooms under different phosphorus concentrations. Variations of extracellular polymeric substances (EPSs) and microbial community composition were also assessed. Results showed that the biomass of Vallisneria natans increased with exposure to cyanobacterial blooms at higher phosphorous concentrations (P > 0.2 mg L⁻¹). The amount of microcystin compounds (MC-LR) released into the water and the accumulation of MC-LR into both plant tissue and biofilms changed according to the phosphorus concentration. Furthermore, a certain degree of oxidative stress was induced in the plants, as evidenced by increased activity of superoxide dismutase, catalase, and peroxidase, as well as increased malondialdehyde concentrations; significant differences were also seen in acid phosphatase and glutathione S-transferase activities, as well as in glutathione concentrations. Together, these responses indicate potential mechanisms of MC-LR detoxification. Broader α-D-glucopyranose polysaccharides (PS) increased with increasing phosphorous and aggregated into clusters in biofilm EPS in response to the cyanobacterial blooms. In addition, alterations were seen in the abundance and structure of the microbial communities present in exposed biofilms. These results demonstrate that cyanobacterial blooms under different concentrations of phosphorus can induce differential responses, which can have a significant impact on aquatic ecosystems.

Antibiotic resistance genes (ARGs) in the environment are an exposure risk to humans and animals and is emerging as a global public health concern. In this study, mercury (Hg) driven co-selection of ARGs was investigated under controlled conditions in two Australian non-agricultural soils with differing pH. Soils were spiked with increasing concentrations of inorganic Hg and left to age for 5 years. Both soils contained ARGs conferring resistance to tetracycline (tetA, tetB), sulphonamides (sul1), trimethoprim (dfrA1) and the ARG indicator class 1 integron-integrase gene, intI1, as measured by qPCR. The last resort antibiotic vancomycin resistance gene, vanB and quinolone resistance gene, qnrS were not detected. Hg driven co-selection of several ARGs namely intI1, tetA and tetB were observed in the alkaline soil within the tested Hg concentrations. No co-selection of the experimental ARGs was observed in the neutral pH soil. 16S rRNA sequencing revealed proliferation of Proteobacteria and Bacteriodetes in Hg contaminated neutral and alkaline soils respectively. Multivariate analyses revealed a strong effect of Hg, soil pH and organic carbon content on the co-selection of ARGs in the experimental soils. Additionally, although aging caused a significant reduction in Hg content, agriculturally important bacterial phyla such as Nitrospirae did not regrow in the contaminated soils. The results suggest that mercury can drive co-selection of ARGs in contaminated non-agricultural soils over five years of aging which is linked to soil microbiota shift and metal chemistry in the soil.

Exposure to polycyclic aromatic hydrocarbons (PAHs) during pregnancy is a risk factor for adverse neurobehavioral development outcomes. Mitochondrial DNA are sensitive to environmental toxicants due to the limited ability of repairing. The change of mitochondrial DNA copy number (mtDNAcn) might be a biologically mechanism linking PAH exposure and children’s neurobehavioral impairment. Our aims are to explore whether PAH metabolites in maternal urine were associated with children’s neurobehavioral development at 2 years old and umbilical cord blood mtDNAcn, and whether mtDNAcn was a mediator of PAH-related neurobehavioral development. We included 158 non-smoking pregnant women from Taiyuan City, Shanxi Province. Maternal urinary eleven PAH metabolites were detected by high performance liquid chromatography with tandem mass spectrometry (HPLC-MS/MS). MtDNAcn in cord blood was detected by real time quantitative polymerase chain reaction (RT-PCR). Children’s neurodevelopment was measured by Gesell Developmental Schedules (GDS) when children were two years age. Generalized linear models and restricted cubic spline models were applied to assess the relationships between PAH metabolites in maternal urine and GDS scores and mtDNAcn. A mediation analysis was also conducted. Generalized linear models showed the relationships of sum of PAH metabolites (Σ-OHPAHs) in maternal urine with decreased motor score, and Σ-OHPAHs with increased mtDNAcn (p for trend < 0.05). Urinary levels of Ln (Σ-OHPAHs) increased one unit was related to a 2.08 decreased in motor scores, and Ln (Σ-OHPAHs) increased one unit was related to 0.15 increased in mtDNAcn. Mediation analysis did not find mtDNAcn can be a mediator between PAH metabolites and neurobehavioral development. Our results suggest that prenatal exposure to PAH decreased children’s neurobehavioral development scores and increased mtDNAcn. And reducing exposure to PAH during pregnancy will benefit to improving neurobehavioral development in children.In our present cohort study, sum of PAH metabolites in urine of pregnant women were related with motor score and were positively associated with umbilical cord blood mtDNA copy number.

The adaptive fitness of insect species can be shaped by how males and females respond, both physiologically and behaviorally, to environmental challenges, such as pesticide exposure. In parasitoid wasps, most toxicological investigations focus only on female responses (e.g., survival and especially parasitism abilities), leaving the male contributions to adaptive fitness (survival, locomotion, mate search) poorly investigated. Here, we evaluated the toxicity of the spinosyn insecticide spinosad against the South American fruit fly, Anastrepha fraterculus, and we used the parasitoid wasp Diachasmimorpha longicaudata (Ashmead) to evaluate whether sex-linked locomotory and physiological responses would influence the susceptibility of these organisms to spinosad. Our results revealed that D. longicaudata males were significantly more susceptible (median lethal time (LT₅₀) = 24 h) to spinosad than D. longicaudata females (LT₅₀ = 120 h), which may reflect the differences in their locomotory and physiological (e.g., respiratory) responses to mitigate insecticide exposure. Compared to D. longicaudata females, male wasps were lighter (P < 0.001), walked for longer distances (P < 0.001) and periods (P < 0.001), and exhibited higher sensilla densities in their tarsi (P = 0.008), which may facilitate their intoxication with the insecticide. These findings indicate that male parasitoids should not be exempt from insecticide selectivity tests, as these organisms can be significantly more affected by such environmental challenges than their female conspecifics.

Excessive exposure to cobalt (Co) is known to make adverse impact on the nervous system, but its detailed mechanisms of neurotoxicity have yet to be determined. In this study, C57BL/6 mice (0, 4, 8, 16 mg/kg CoCl₂, 30 days) and human neuroblastoma H4 cells (0, 100, 400, 600 μM CoCl₂) were used as in vivo and in vitro models. Our results revealed that CoCl₂ intraperitoneal injection caused significant impairments in learning and memory, as well as pathological damage in the nervous system. We further certificated the alteration of m⁶A methylation induced by CoCl₂ exposure. Our findings demonstrate for the first time, significant differences in the degree of m⁶A modification, the biological function of m⁶A-modified transcripts between cortex and H4 cell samples. Specifically, MeRIP-seq and RNA-seq elucidate that CoCl₂ exposure results in differentially m⁶A-modified and expressed genes, which were enriched in pathways involving synaptic transmission, and central nervous system (CNS) development. Mechanistic analyses revealed that CoCl₂ remarkably changed m⁶A modification level by affecting the expression of m⁶A methyltransferase and demethylase, and decreasing the activity of demethylase. We observed variation of m⁶A modification in neurodegenerative disease-associated genes upon CoCl₂ exposure and identified regulatory strategy between m⁶A and potential targets mRNA. Our novel findings provide novel insight into the functional roles of m⁶A modification in neurodegenerative damage caused by environmental neurotoxicants and identify Co-mediated specific RNA regulatory strategy for broadening the epigenetic regulatory mechanism of RNA induced by heavy metals.

Antibiotics are contaminants of emerging concern due to their potential effect on antibiotic resistance and human health. Antibiotics tend to sorb strongly to organic materials, and biochar, a high efficient agent for adsorbing and immobilizing pollutants, can thus be used for remediation of antibiotic-contaminated soil and water. The effect of ionizable antibiotics on surface characteristics and transport of biochar colloids (BC) in the environment is poorly studied. Column experiments of BC were conducted in 1 mM NaCl solution under three pH (5, 7, and 10) conditions in the presence of sulfamethazine (SMT). Additionally, the adsorption of SMT by BC and the zeta potential of BC were also studied. The experimental results showed that SMT sorption to BC was enhanced at pH 5 and 7, but reduced at pH 10. SMT sorption reduced the surface charge of BC at pH 5 and 7 due to charge shielding, but increased surface charge at pH 10 due to adsorption of the negatively charged SMT species. The mobility of BC was inhibited by SMT under acidic or neutral conditions, while enhanced by SMT under alkaline conditions, which can be well explained by the change of electrostatic repulsion between BC and sand grains. These findings imply that pH conditions played a crucial role in deciding whether the transport of BC would be promoted by SMT or not. Biochar for antibiotics remediation will be more effective under acidic and neutral soil conditions, and the mobility of BC will be less than in alkaline soils.

Antibiotics used in global aquaculture production cause various side effects, which impair fish health. However, the use of dietary composition such as carbohydrate, which is one of the dominant components in fish diets to attenuate the side effects induced by antibiotics, remains unclear. We determined the ability of high carbohydrate diet to protect Nile tilapia (Oreochromis niloticus) from oxytetracycline-induced side effects. Triplicate groups of thirty O. niloticus (9.50 ± 0.08 g) were fed on medium carbohydrate (MC; 335 g/kg) and high carbohydrate (HC; 455 g/kg) diets without and with 2.00 g/kg diet of oxytetracycline (80 mg/kg body weight/day) hereafter, MCO and HCO for 35 days. Thereafter, we assessed growth performance, hepatic nutrients composition and metabolism, microbiota abundance, immunity, oxidative and cellular stress, hepatotoxicity, lipid peroxidation and apoptosis. To understand the possible mechanism of carbohydrate protection on oxytetracycline, we assessed the binding effects and efficiencies of mixtures of medium and high starch with oxytetracycline as well as the MCO and HCO diets. The O. niloticus fed on the MCO and HCO diets had lower growth rate, nutrients utilization and survival rate than those fed on the MC and HC diets, respectively. Dietary HCO increased hepatosomatic index and hepatic protein content of O. niloticus than MCO diet. The O. niloticus fed on the HCO diet had lower mRNA expression of genes related to protein, glycogen and lipid metabolism compared to those fed on the MCO diet. Feeding O. niloticus on the HCO diet increased innate immunity and reduced pathogenic bacteria, pro-inflammation, hepatotoxicity, cellular stress and apoptosis than the MCO diet. The high starch with oxytetracycline and HCO diet had higher-oxytetracycline binding effects and efficiencies than the medium starch with oxytetracyline and MCO diet, respectively. Our study demonstrates that, high carbohydrate partially protects O. niloticus from oxytetracycline-induced side effects by binding the antibiotic. Incorporating high carbohydrate in diet formulation for omnivorous fish species alleviates some of the side effects caused by antibiotics.

The frequent exposure of bees to a wide variety of fungicides, on crops where they forage, can be considered a stressor factor for these pollinators. The organisms are exposed both to the fungicide active ingredients and to the adjuvants of commercial formulations. All these ingredients are brought to the hive by bee foragers through contaminated pollen and nectar, thus exposing also immature individuals during larval phase. This work aimed to compare the effects of larval exposure to the fungicide pyraclostrobin (active ingredient and commercial formulation) and its influence on the cytotoxicity to midguts in adults, which were inoculated with the Nosema ceranae spores in the post-emergence stage. Under laboratory conditions, Apis mellifera larvae received an artificial diet containing fungicide solution from the third to the sixth day of the feeding phase. One-day-old adult workers ingested 100,000 infectious N. ceranae spores mixed in sucrose solution. Effects on midgut were evaluated through cellular biomarkers of stress and cell death. The exposure to the fungicide (active ingredient and commercial formulation) did not affect the larval post-embryonic development and survival of adult bees. However, this exposure induced cytotoxicity in the cells of the midgut, showed by the increase in DNA fragmentation and alteration in the HSP70 immunolabeling pattern. Without the pathogen, the midgut cytotoxic effects and HSP70 immunolabeling of the organisms exposed to the commercial formulation were lower when compared to the exposure to its active ingredient. However, in the presence of the pathogen, the cytotoxic effects of the commercial formulation to the adult bees’ midgut were potentialized. The pathogen N. ceranae increased the damage to the intestinal epithelium of adult bees. Thus, realistic doses of pyraclostrobin present in beebread consumed by larvae can affect the health and induce physiological implications to the midgut functions of the adult bees.

Lindane, a lipophilic pollutant, may be toxic to organisms. To explore the toxic effects of lindane and the underlying mechanisms of this toxicity, the animal model Caenorhabditis elegans (C. elegans) was exposed to lindane for 3 d at environmentally relevant concentrations (0.01–100 ng/L) and the physiological, biochemical, and molecular indices were evaluated. Subacute exposure to 10–100 ng/L of lindane caused adverse physiological effects on the development, reproduction, and locomotion behaviors in C. elegans. Exposure to 1–100 ng/L of lindane increased the accumulation of Nile red and blue food dye, which suggested high permeability of the intestine in nematodes. Lindane exposure also significantly influenced the expression of genes related to intestinal development (e.g., mtm-6 and opt-2). Moreover, reactive oxygen species production, lipofuscin accumulation, and expression of oxidation resistance genes (e.g., sod-5 and isp-1) were significantly increased in C. elegans exposed to 10–100 ng/L of lindane, which indicated that lindane exposure induced oxidative stress. According to Pearson correlation analyses, oxidative stress and intestinal damage were significantly correlated with the adverse physiological effects of lindane. Therefore, the adverse effects of lindane may have been induced by intestinal damage and oxidative stress, and mtm-6, opt-2, sod-5, isp-1, and mev-1 might play important roles in the toxicity of lindane.