This study evaluated the toxic effects of water-accommodated fractions (WAFs) of very-low sulfur fuel oil (VLSFO) on freshwater and marine fish embryos. Embryos of Japanese medaka (Oryzias latipes), Java medaka (Oryzias javanicus), and grass puffer (Takifugu alboplumbeus) were exposed to various concentrations of VLSFO-WAF, and the effects on key parameters, such as hatching rate, hatching days, mortality, and malformations, were examined. Exposure of Japanese medaka to 50% WAF significantly reduced hatching rates and increased mortality and malformation rates. Similarly, Java medaka exhibited severe lethality, malformations, and shortened hatching days at 50% WAF. In grass puffer, exposure to 50% WAF caused a sharp increase in post-hatch mortality and malformation rates, although hatching rates remained largely unaffected. The median lethal and median effective concentrations (LC50 and EC50) were 34.8% and 15.6% WAFs for Japanese medaka; 21.3% and 8.8% for Java medaka; and 21.3% and 9.7% for grass puffer, respectively. These WAF-based toxicity endpoints were estimated from quantitatively measured chemical concentrations in the VLSFO and its WAFs: LC50 values of 41.9-68.6 μg/L for ΣPAHs and 213.2-348.3 μg/L for Σalkylated PAHs; and EC50 of 17.3-30.7 μg/L for ΣPAHs and 88.1-156.2 μg/L for Σalkylated PAHs, respectively. This study suggests that polycyclic aromatic hydrocarbons (PAHs) and alkylated PAHs present in VLSFO and its WAF strongly contribute to the observed toxicity. Additionally, VLSFO contains lower concentrations of PAHs than conventional heavy-fuel oils, although it is harmful to certain fish species.

Veterinary medicines, which reach the soil mostly through the application of contaminated manures, can affect beneficial soil microorganisms, such as nitrogen-fixing rhizobia bacteria, which engage in important symbiotic associations with plants. The anthelmintic compounds albendazole and fenbendazole were tested for toxicity against the nitrogen-fixing rhizobium Mesorhizobium loti and its symbiotic relationship with the model legume Lotus japonicus. The effects of anthelmintics on rhizobial growth were tested invitro in bacterial cultures, while their effects on the establishment of the symbiotic relationship were tested by phenotypic and molecular analyses of inoculated plants. None of the two compounds showed phytotoxicity. Albendazole and fenbendazole inhibited the growth of rhizobia at concentrations often (0.75 mg kg-1) or rarely (2.25 mg kg-1) found in agricultural soils. Albendazole reduced the number of infection threads formed in roots and downregulated key symbiosis-related genes, indicating inhibition of symbiosis at early stages, unlike fenbendazole, which showed no effects. However, nodulation and nitrogenase activity were not significantly affected by albendazole at advanced stages of the symbiosis, suggesting a recovery possibly associated with the progressive dissipation of albendazole. Our results suggest different toxicity of albendazole and fenbendazole to the symbiotic nitrogen fixation system that may have serious implications for soil health.

Diflubenzuron is used as an insect growth inhibitor, and its potential risk to human health was raised owing to the possibility of environmental residues and human exposure. This study aimed to investigate the toxic mechanism of diflubenzuron on trophoblastic cells such as HTR8/SVneo and JEG-3 cells. We investigated mitochondrial function, Ca2+ homeostasis, and expression of associated genes following diflubenzuron exposure (0, 1, 2, and 3 μg/mL). In addition, apoptosis induction, cell cycle arrest, and migration ability were evaluated. Diflubenzuron treatment induced a loss of mitochondrial membrane potential, disruption of Ca2+ homeostasis, and upregulation of endoplasmic reticulum stress markers such as IRE1α and GRP78. Furthermore, intrinsic apoptosis was triggered by BAX and BAK upregulation and BCL2 downregulation. Cell cycle arrest in the G0/G1 phase was induced, and the migration ability of trophoblastic cells was significantly reduced by diflubenzuron treatment. These alterations suggest that mitochondrial dysfunction with the downregulation of hormone receptors (progesterone receptor and estrogen receptor 1 and 2) may impair trophoblastic function. This study confirmed that diflubenzuron has a cytotoxic effect on trophoblastic cells and may impair trophoblastic functions related to implantation. Collectively, these results highlight the potential of diflubenzuron as a reproductive toxicant in disrupting early pregnancy processes. Further studies are needed to clarify exposure relevance and to evaluate potential risks to human reproductive health.

Imidacloprid (IMI) is a widely used neonicotinoid insecticide that presents potential risks to non-target avian species. This study investigated the sublethal effects of IMI on the health of the eared dove (Zenaida auriculata), a common granivorous bird in South America. The objective was to characterize the impacts of subchronic oral exposure to IMI on behavioral, physiological, hematological, and biochemical parameters. Eighteen adult male doves (n = 18) were randomly assigned to three groups: a control group receiving water orally, and two treatment groups receiving IMI dissolved in water at doses equivalent to 1/15th (low dose, LD, 3.93 mg/kg b.m.) and 1/5th (high dose, HD, 11.8 mg/kg b.m.) of the oral LD50, administered daily by gavage for 21 days. Health biomarkers measured included water intake, body mass, somatic indices, hematological profiles, and plasma biochemical parameters. Results indicated a significant decrease in body mass in the HD group of doves exposed to IMI. In this group, only an increase in the heterophil/lymphocyte ratio was observed among the hematological parameters. Biochemical parameters showed decreased lactate dehydrogenase (LDH) and increased serum butyrylcholinesterase (BuChE) activities. These findings suggest that IMI, even at sublethal doses, can trigger physiological stress responses, generate metabolic alterations, and exert neurotoxic effects in eared doves. Exposure levels in this study were below those allowed for IMI-treated seeds in Argentina, underscoring the environmental risks to wild birds. Application of sensitive health biomarkers underscores the need for further ecotoxicological research and regulatory measures to mitigate the environmental impact of neonicotinoids on birds.

Cypermethrin (CYP) is a widely used insecticide. This study investigated the protective effects of sesame seed oil nanoemulsion (SEONE) against CYP-induced testicular toxicity in 60 rats. Parameters investigated included body and reproductive organ weights, semen quality, oxidative stress markers (catalase, superoxide dismutase, reduced glutathione, malondialdehyde, reactive oxygen species, reproductive hormones, and expression of apoptotic and antiapoptotic genes [p53, Bax, caspase-3, caspase-9, Bcl-2]), along with structural evaluation of testes. Compared to controls, CYP reduced body weight (-12%) and reproductive organ weights (-18% to -22%), decreased sperm count (5.62 ± 0.74 × 106) and motility (49.32% ± 2.89%), while increasing abnormal sperm (18.22% ± 1.24%). CYP administration induced oxidative damage, indicated by decreased activities of catalase (-46%) and superoxide dismutase (-55%), reduced levels of reduced glutathione (37.3% ± 2.1%), and elevated malondialdehyde (61.7% ± 23.6%), ROS (64.2% ± 3.2%), and hydrogen peroxide (145.3% ± 3.4%). Testosterone, luteinizing, and follicle-stimulating hormones levels were significantly decreased (-52% to -62%) in the CYP-treated group. These alterations were accompanied by significant upregulation of apoptotic genes p53, Bax, caspase-3, and caspase-9 and marked downregulation of the antiapoptotic gene Bcl-2. SEONE provided markedly better protection against CYP-induced testicular damage than unprocessed SEO (p < 0.05). Its administration resulted in higher body and reproductive organ weights, improved semen parameters, and restored testicular histology and ultrastructure, producing outcomes that closely resembled those of the control group. The superior performance of SEONE is likely linked to its improved physicochemical properties and multifaceted antioxidant and antiapoptotic protective actions. In conclusion, SEONE effectively mitigates CYP-induced testicular toxicity in rats, supporting its potential as a protective intervention against pesticide-induced reproductive damage.

Organophosphate flame retardants (OPFRs) are extensively used in the electronics industry, plastics, textiles, and other sectors to reduce flammability and enhance fire safety. However, excessive OPFR use has led to significant environmental accumulation, increasing ecological stress and potential human health risks. This study investigates the effects of 2-ethylhexyldiphenyl phosphate (EHDPP) on HepG2 cells, demonstrating that EHDPP exposure impairs normal cellular function through excessive autophagy, ultimately reducing cell viability. Our findings reveal a concentration-dependent decline in cell survival, with an LC50 of 120 μM. While lower concentrations (0, 1, 5, 10, and 50 μM) exerted minimal effects, 50 μM EHDPP significantly reduced cell viability. Further analysis confirmed that EHDPP exposure upregulates autophagy-related genes (ATG5, ATG12, VPS34, Beclin1, FIP200, ATG13, and ATG3), leading to an increased LC3-II/I ratio and a decrease in p62 levels, indicative of enhanced autophagic activity. Transmission electron microscopy (TEM) imaging confirmed a substantial increase in autophagosome formation at 50 μM EHDPP. These results provide new insights into the cytotoxic mechanisms of EHDPP, emphasizing its role in triggering excessive autophagy in hepatic cells.

Butylparaben (BuP) recurrently contaminates soils worldwide, mainly by incorporating sewage sludge into cultivated areas, using wastewater in irrigation, and leaching contaminated soils. However, there are few studies on the ecotoxicological effects of this paraben on edaphic organisms. The ecotoxicity of BuP was evaluated in seeds of Daucus carota , Allium cepa , and Cucumis sativus , in the roots of A. cepa bulbs, and in Eisenia fetida earthworms, at concentrations of 10, 50, 100, and 500 ng/L. In root meristems, the four concentrations of BuP induced lipid peroxidation and raised the levels of superoxide radicals, which triggered inhibition of cell division and mitotic spindle alteration, significantly reducing the growth of roots in seeds and bulbs. In animals, BuP at 10, 50, 100, and 500 ng/L caused 80%, 80%, 70%, and 90% evasion of earthworms from artificial soil, respectively. In addition, this paraben did not cause mortality in earthworms after 14 days of exposure. However, all concentrations increased the production of superoxide and hydroxyl radicals in cells and caused lipid peroxidation. Thus, increased exposure to this compound can affect the ecological functions negatively and/or cause the death of these animals. Therefore, recurrent contamination with BuP can negatively impact soil quality, posing a risk to agricultural productivity and the environment. This study is a pioneer in the ecotoxicological evaluation of BuP in plants at environmentally relevant concentrations and in the behavioral and oxidative stress study in earthworms.

In this study, we examined metal accumulation and biochemical responses of Azolla imbricata (Roxb.) Nakai exposed to water medium (WM) and nutrient medium (NM) under single and combined (co-exposure) treatments with five metals (As, Cd, Cu, Pb, and Zn) at 10% environmentally relevant concentrations. Marked differences between WM and NM highlighted the influence of nutrient availability on plant responses. An inverse relationship was observed, with higher biomass in NM (WM < NM) and greater metal accumulation in WM (WM > NM). Growth inhibition, reflected by reduced photosynthetic pigment contents, was accompanied by elevated stress indicators, including electrolyte leakage, proline, malondialdehyde, and anthocyanins, confirming metal-induced phytotoxicity. Metal interactions under co-exposure were predominantly antagonistic in WM and synergistic in NM. Metal accumulation patterns (mg/kg) varied across media and exposure types: under single exposure, values ranged from 83.8 (As) to 43 881 (Zn) in WM and from 11.7 (Cd) to 12 135 (Cu) in NM; under co-exposure, they ranged from 346 (Cd) to 12 688 (Cu) in WM and from 46 (Cd) to 2859 (Cu) in NM. Accumulation sequences did not correspond to exposure concentrations, indicating metal-specific and media-dependent uptake. Under co-exposure, concurrent accumulation of multiple metals was more frequent in WM than that in NM, suggesting nutrient availability constrained simultaneous uptake. Bioconcentration factor values exceeded common thresholds under certain treatments, indicating strong accumulation potential rather than definitive hyperaccumulation. Overall, these findings highlight the potential of A. imbricata for phytoremediation of metal-contaminated waters while emphasizing cautious application in agroecosystems due to potential soil-crop-food pathway transfer.

Arsenic contamination in aquatic ecosystems is a major environmental concern. Selenium (Se) helps mitigate oxidative stress and hence could reduce the toxic effects of arsenic. However, Se can also be toxic at high concentrations. Given that these metalloids commonly co-occur in the environment, there is a pressing need for further research into their combined effects on aquatic life. To investigate this interplay, zebrafish embryos were exposed to As alone (as arsenite) or in combination with two different chemical forms of Se including As 120 μg/L alone (as arsenite), As 120 μg/L + Se 25 μg/L (as selenite), As 120 μg/L + Se 120 μg/L (as selenite), and As 120 μg/L + Se 2.5 μg/L (as selenomethionine, SeMet) until 4 days postfertilization. There was no significant difference in the survival, hatching, and deformity rate when fish were exposed to both As and Se. Co-exposure to As and Se significantly affected thigmotaxis and reflexive movement (for all p < 0.05), with 2.5 μg/L Se mitigating As-induced impairments. While reactive oxygen species (ROS) levels were elevated in larvae exposed to As alone and As + Se 25 μg/L, there were markedly reduced ROS levels in the As + Se 120 μg/L and As + Se 2.5 μg/L treatments, highlighting Se's antioxidant efficacy. A marked suppression of genes related to antioxidant, neurogenesis, dopaminergic, serotonergic, and motor neurons was observed following arsenic exposure. At the same time, co-treatment with As + Se 25 μg/L partially restored nrf2a expression (p < 0.05). These findings highlight the potential for naturally co-occurring Se to modulate As toxicity in aquatic environments, underscoring the importance of considering chemical interactions when assessing ecological risks.

Acrylamide (AA) exerts neurotoxicity and genotoxicity in wildlife and humans. This study measured the ability of curcumin, an antioxidant, and curcumin Nano lipid carriers (Cur-NLCs) to alleviate biochemical biomarkers of AA-induced neurotoxicity in the cortex and hippocampus of exposed rats. Thirty adult female albino rats were assigned into one of five experimental groups: (1) negative control, (2) vehicle control, (3) acrylamide (50 mg/kg b.wt), (4) acrylamide (50 mg/kg b.wt) with curcumin (100 mg/kg b.wt), and (5) acrylamide (50 mg/kg b.wt) with Cur-NLCs (10 mg/kg b.wt). Treatments were orally administered to rats for 5 days/week for 2 weeks. Acrylamide administration caused body weight loss, abnormal gait, and histopathological damage to both the cortex and hippocampus. Curcumin and Cur-NLCs treatment reduced the occurrence of abnormal behavior and mitigated histopathological changes observed in rats treated with AA. The level of norepinephrine (NE), dopamine (DA), gamma-aminobutyric acid (GABA), serotonin (5-HT), reduced glutathione (GSH), and adenosine triphosphate (ATP) were all decreased with AA treatment. Following treatment with curcumin, AA-induced reductions in glutathione (GSH), dopamine (DA), 5-hydroxy indole acetic acid (5-HIAA), norepinephrine (NE), adenosine monophosphate (AMP), aspartate (ASP), and gamma-aminobutyric acid were restored to the control level in the cortex. In the hippocampus, GSH, 8-hydroxydeoxyguanosine (8-OHdG), DA, 5-hydroxy tryptamine (5-HT), 5-HIAA, NE, ATP, ASP, GABA and glutamate (Glu) improved to that observed in control rats. Co-treatment with Cur-NLCs also had protective effects on malondialdehyde (MDA) and NE in the cortex, and 5-HIAA and ASP in the hippocampus. Upon comparison, Cur-NLCs at 10 mg/kg/day showed less benefit than curcumin alone (100 mg/kg/day) based on several endpoints of oxidative stress, DNA damage, and histopathology. We conclude there are tissue specific responses to these formulations in the CNS and suggest that a more effective means of treating AA-induced neurotoxicity with these antioxidants may be a mixture of both unmodified curcumin and its Nano-formulation.