Environmental toxicology and pharmacology最新文献

The issue of toxic metal pollution is a considerable environmental concern owing to its complex nature, spatial and temporal variability, and susceptibility to environmental factors. Current water quality criteria and ecological risk assessments of metals are based on single-metal toxicity data from short-term, simplified indoor exposure conditions, ignoring the complexity of actual environmental conditions. This results in increased uncertainty in predicting toxic metal toxicity and risk assessment. Using appropriate bioavailability and effect modeling of metals is critical for establishing environmental quality standards and performing risk assessments for metals. Traditional dose-effect models are based on a static statistical relationship and fall short of revealing the bioavailability and effect processes of metals and do not effectively assess ecological impacts under complex exposure conditions. This paper summarizes the toxicokinetic–toxicodynamic (TK–TD) model, which is gaining interest in environmental and ecotoxicological research. The key concepts, and theories of its construction theories, are discussed and the application of the TK–TD model in toxicity prediction and risk assessment of different metals in the aquatic environment, and trends in the development of the TK–TD model are highlighted. The findings of our review prove that the TK–TD model can effectively predict toxic metal toxicity in real time and under complex exposure conditions in the future.

Partamona helleri is an important pollinator in the Neotropics. However, this bee faces an increased risk of pesticide exposure, potentially affecting both individual bees and entire colonies. Thus, this study aimed to evaluate the effects of the herbicide tebuthiuron on behavior, antioxidant activity, midgut morphology, and signaling pathways related to cell death, cell proliferation and differentiation in P. helleri workers. tebuthiuron significantly reduced locomotor activity and induced morphological changes in the midgut. The activity of the detoxification enzymes superoxide dismutase and glutathione S-transferase increased after exposure, indicating a detoxification mechanism. Furthermore, the herbicide led to alterations in the number of positive cells for signaling-pathway proteins in the midgut of bees, suggesting induction of apoptotic cell death and disruption of midgut epithelial regeneration. Therefore, tebuthiuron may negatively impact the behavior, antioxidant activity, morphology, and physiology of P. helleri workers, potentially posing a threat to the survival of this non-target organism.

Equine atypical myopathy (AM) is a severe rhabdomyolysis syndrome primarily caused by hypoglycin A (HGA) and methylenecyclopropylglycine protoxins. This study aimed to refine diagnostic and prognostic criteria for AM while exploring apparently healthy cograzers. Blood samples from 263 horses, including AM cases (n= 95), cograzers (n= 73), colic horses (n= 19), and controls (n= 76), were analyzed for HGA, its toxic metabolite, and acylcarnitines profile. Diseased horses exhibited alterations in acylcarnitines that strongly distinguished them from controls and colic horses. Regression analyses identified distinct acylcarnitines profiles among groups, with cograzers showing intermediate alterations. Age and gelding status emerged as protective factors against AM. Furthermore, serum acylcarnitines profiling was valuable in predicting AM survival, with isovaleryl-/2-methylbutyrylcarnitine (i.e., C5 acylcarnitine) showing promise as both a diagnostic and prognostic marker. Subclinical alterations in cograzers underscore a novel aspect: the presence of subclinical cases of AM.

DNA damage in embryos shapes the development of an organism. Understanding life stage-specific differences between fish species is essential for ecological risk assessment measures. We explored DNA damage sensitivity in two nonmodel fish species, sterlet (Acipenser ruthenus) and common carp (Cyprinus carpio). Embryos of these species were exposed to a model genotoxicant, camptothecin (CPT), during cleavage (2-cell) stage and gastrulation. Results revealed a species-specific DNA damage sensitivity only at cleavage stage. 3 nM CPT caused lethality in sterlet embryos while carp embryos hatched normally. Multiple nuclear abnormalities were observed in sterlet embryos by early gastrula stage. However, carp embryos exhibited nuclear abnormalities and DNA fragmentation at neurula stage only when exposed to 7 nM CPT. Moreover, increased expression of tp53 in carp embryos at gastrula stage suggests activation of apoptosis mechanism. These findings suggest that carp embryos activate DNA damage response more efficiently than sterlet embryos at same developmental stage.

This study aimed to evaluate the environmental impact of dental materials: commercial composite Tetric EvoCeram®, glass ionomer Equia Forte® HT Fil, laboratory-prepared composite, alkasite Cention® Forte, amalgam Amalcap® Plus, and samples from dental chair drainage systems (DCDS). Methacrylate monomers were detected in the eluates of experimental and commercials composites, and alkasite. In DCDS samples solely mercury was found at concentrations of 0.08–1.86 μg/L. The experimental composite (48 h incubation) exhibited the highest toxicity on zebrafish Danio rerio (LC₅₀=0.70 g/L), followed by amalgam (LC₅₀=8.27 g/L) < Tetric EvoCeram® (LC₅₀=10.94 g/L) < Equia Forte® HT Fil (LC₅₀=24.84 g/L) < Cention® Forte (LC₅₀=32.22 g/L). Exposure of zebrafish to DCDS samples resulted in decreased larval body length and increased occurrences of edema and blood accumulation. The results obtained highlight the need for additional monitoring and further research on the release of unreacted monomers and mercury from dental materials and their environmental impact.

Pharmaceutical active compounds (PhACs) are detected pollutants in aquatic environments worldwide at concentrations ranging from ng L⁻¹ to µg L⁻¹. Currently, PhAC monitoring is poorly realized in Mexico. This study proposes a priority list of PhACs in Mexican aquatic environments, considering their occurrence and environmental and human health risks. Ecological risks were assessed as Risk Quotients (RQ) values using the PhAC concentrations detected in surface water, obtaining high risks (RQ > 1) against aquatic organisms, especially of naproxen, ibuprofen, diclofenac, acetaminophen, 17β-estradiol, carbamazepine, ketoprofen, caffeine. In contrast, potential human health risks (RQ_H) were assessed on the Mexican population using the concentrations quantified in groundwater, demonstrating potential risks (RQ_H > 0.2) on the population, particularly of DCF and CBZ. Thus, a priority list of PhACs can be used as a reference for environmental monitoring in Mexican water supplies as well as PhACs monitoring in countries of the Caribbean region and Central America.

The anticonvulsant sodium valproate (SV) is frequently administered as a medicament but bears several negative effects in case of exposure during development. We analyzed extensively these early development effects of using the zebrafish model. Zebrafish embryos were exposed as eggs to two sublethal concentrations of SV, 10 and 25 mg/L. A general embryo toxicity analysis revealed extended anomalies in the cardiovascular system, and in the craniofacial and the spinal skeleton, as well as high mortality, in the embryos exposed to SV. The teratogenic potential of SV was confirmed in hacthed larvae by morphometric and cartilage profile analysis. Last, neurobehavioral impairments due to SV were highlighted in subjects’ activity, anxiety, response to stimulations, habituation learning, and daily synchronization of locomotor activity, overall mirroring typical phenotypes associated with autistic spectrum disorders. In conclusion, our results confirmed the presence of extended and multifaced impacts of exposure to SV during development.

Perfluorobutane sulfonate is a short-chain PFAS that is a less toxic replacement for the rather more toxic long-chain perfluorooctane sulfonate. PFBS is widespread in the environment and has raised environmental and health concerns. The study goal was to investigate whether dietary ingestion of PFBS would induce hepatic damage. Sprague-Dawley rats were assigned to three PFBS treatment groups for 11 weeks followed by clinical markers analyses in the serum and liver. There was a significant increase in liver and body weights of PFBS rats. Total antioxidant capacity was significantly reduced in the PFBS-treated group. ALT levels increased based on concentration ingested. Close to 1000 gene transcripts were differentially expressed. Further, transmembrane transport and oxidation-reduction processes were the most up-regulated biological processes. Inflammatory genes were up-regulated in the exposed group and those associated with oxidative damage were down-regulated. In conclusion, PFBS ingestion produced mild effects in the liver of Sprague Dawley rats.

Endocrine disruptors (EDs) pose significant risks to human and environmental health, with potential implications for neurotoxicity. This study investigates the synergistic neurotoxic effects of perfluorooctane sulfonate (PFOS) and glyphosate (GLY), two ubiquitous EDs, using SHSY5Y neuronal and C6 astrocytic cell lines. While individual exposures to PFOS and glyphosate at non-toxic concentrations did not induce significant changes, their combination resulted in a marked increase in oxidative stress and neuroinflammatory responses. Specifically, the co-exposure led to elevated levels of interleukin-6, tumor necrosis factor alpha, and interferon gamma, along with reduced interleukin-10 expression, indicative of heightened neuroinflammatory processes. These findings underscore the importance of considering the synergistic interactions of EDs in assessing neurotoxic risks and highlight the urgent need for further research to mitigate the adverse effects of these compounds on neurological health.

This study aimed to explore whether there is an association between environmental exposure to POPs and kidney tumor induction, and whether blood POP concentrations reflect kidney tissue concentrations. POP derivatives were determined in blood, tumor tissue, tumor surrounding tissue, and perirenal fat tissue samples taken from patients who underwent surgery for renal tumors. A voluntary control group was recruited for blood and urine samples as well. Urinary excretions of o,o′-dityrosine, chlorotyrosine, nitrotyrosine, and 8-OHdG were measured in the same patients. The possible role of genetic polymorphisms in CYP1A1, GST isozymes P, M, and T, and hOGG1 genes on the predisposition to renal cancer was investigated. Some POPs have been found to be associated with kidney cancer, as evidenced by their significantly high ORs. 8-OHdG levels were significantly higher compared to the control group. The GSTT1 null polymorphism can be a risk factor for malignant but not for benign kidney tumors.