Environmental toxicology and pharmacology最新文献

Isopropylate Triphenyl Phosphate (IPPP), a novel organophosphorus flame retardant, has become a widespread environmental pollutant. However, the toxic effects and mechanisms of IPPP remain unclear. In this study, we evaluated the neurodevelopmental toxicity effects of IPPP on zebrafish embryonic development, neurobehavior, and physiological and transcriptomic changes. The results showed that IPPP induced adverse developments such as low survival rates and hatching rates, decreased body length and eye distance, and also led to increased heart rates and embryonic malformation rates. The developmental defects mainly included typical pericardial edema, eye deformities, and a reduction in the number of newborn neurons. Mitochondrial energy metabolism disorders and apoptosis of cardiomyocytes may be responsible for heart malformation. Behavioral results showed that IPPP caused abnormal changes in swimming speed, total swimming distance and trajectory, and showed a low-dose effect. In addition, the decreased activity of neurotransmitters such as acetylcholinesterase (AchE) and dopamine (DA), and the changes in genes related to the central nervous system (CNS) and metabolism pathway may be the causes of neurodevelopmental toxicity of IPPP. Meanwhile, IPPP induced oxidative stress and apoptosis, and changed the ATPase activity of zebrafish larvae by altering nuclear factor erythroid2-related factor 2 (Nrf2) and mitochondrial signaling pathways, respectively. Transcriptome sequencing results indicated that Cytochrome P450 and drug metabolism, Energy metabolism-related pathways, Glutathione metabolism, Retinoid acid (RA) and REDOX signaling pathways were significantly enriched, and most of the genes in these pathways were up-regulated after IPPP treatment, which may be new targets for IPPP-induced neurodevelopment. In summary, the results of this study provide an important reference for a comprehensive assessment of the toxic effects and health risks of the new pollutant IPPP.

Lead toxicosis remains a concern in raptors, especially following feeding on carcasses sourced from hunting. Rapid diagnosis of lead exposure and easy field monitoring is desirable. The LeadCareII analytical system, validated for rapid diagnoses of lead toxicity in humans, has been described as a useful evaluation system in various species. For this study we attempt to validate the LeadCareII system in the Cape Vulture (CV) (Gyps coprotheres). Blood samples from CV housed under captive conditions and low background lead exposure, were pooled and spiked with known concentrations of a lead standard (0–60 µg/dL). Samples were analyzed by the LeadCareII system and by ICP-MS. The final results showed that despite good linearity the LeadCareII system underestimated lead concentrations by up to 50 %. While the results can be corrected by the derived equation, this is not supported due to the large underestimations evident. The reason for the underestimation is presently unknown.

Maternal offloading of polycyclic aromatic hydrocarbons (PAHs) poses a significant exposure route for developing embryos, with implications for subsequent generations. Despite known developmental effects regarding fish physiology and behavior, maternal PAH transfer assessments in elasmobranchii are still lacking. This study investigated PAH contamination and maternal transfer in one female Lesser Numbfish (Narcine brasiliensis) electric ray and seven embryos for the first time. Naphthalene was identified as the predominant low molecular weight PAH, and dibenzo[a,h]anthracene was the most abundant high molecular weight compound. Most embryos exhibited some level of PAH exposure, with varying accumulation patterns potentially influenced by size, developmental stage, and yolk absorption rates. Further investigation is warranted to understand the impacts of PAH maternal offloading on elasmobranchii uterine contents and embryos.

The current study aimed to explore the genotoxic impacts of the insecticide acetamiprid (ACP) on the myocardium and assess the ameliorative role of resveratrol (RSV). Male rats (10/group) were treated via oral route for 90 days: control; ACP (25 mg/kg); RSV (20 mg/kg); ACP+RSV. Peripheral blood micronucleus test, oxidative stress analysis, comet assay, 8-hydroxydeoxyguanosine and gene expression assessment were performed. The findings revealed that ACP has myocardial genotoxic effects, as demonstrated by increased micronucleus and 8-hydroxydeoxyguanosine formation and increased all comet parameters. Oxidative stress analysis demonstrated that ACP elevated H₂O₂ and NO levels while decreasing catalase and GST activities. Acetamiprid dysregulated the expression of genes related to oxidative stress and DNA damage response. However, RSV co-treatment resulted in significant protection against these genotoxic impacts. Resveratrol reduced DNA damage and restored the oxidative balance in the myocardium. Moreover, RSV modulated the Nrf2/HO-1 and Atm/P53 pathways, potentiating antioxidant defense and DNA repair.

Pests in agriculture cause significant economic damage by reducing production and product quality. While pesticides can be an alternative for pest control, their use has a significant impact on both the environment and human health. Chlorpyrifos, a widely used pesticide, affects both target and non-target organisms, including spiders. In this study, we investigated whether Misumenops maculissparsus spiders at three developmental stages (J0, J2, and adults) recognize the presence of the insecticide and how it affects their enzymatic activity. The results indicated that only J0 was able to recognize the insecticide and avoided surfaces treated with it. On the other hand, J0 and adults exhibited reduced acetylcholinesterase (AChE) activity and the activity of antioxidant enzymes was affected by the treatment. Superoxide dismutase (SOD) increased significantly in J0, catalase (CAT) in all stages, glutathione S-transferase (GST) in J2, and glutathione peroxidase (GPx) in J2 and adults. Chlorpyrifos exposure did not increase reactive oxygen species or alter cellular populations in any model.

Pesticides pivotal in controlling pests, can represent a threat for human health. Regulatory agencies constantly monitor their harmful effects, regulating their use. Several studies support a positive association between long-term exposure to pesticides and chronic pathologies, such as cancer. Geno-toxicological biomonitoring has proven to be valuable to assess genetic risks associated with exposure to pesticides, representing a promising tool to improve preventive measures and identify workers at higher risk. In this study, a differential gene expression analysis of 70 candidate genes deregulated upon pesticide exposure, was performed in 10 GEO human gene expression DataSets. It was found that six genes (PMAIP1, GCLM, CD36, SQSTM1, ABCC3, NR4A2) had significant AUC predictive values. Also, CD36 was upregulated in non-transformed cell samples and healthy workers, but downregulated in cancer cells. Further validation in larger groups of workers will corroborate the importance of the identified candidates as biomarkers of exposure/effect.

This study assessed the ability of α₁ and α₂-adrenergic drugs to decrease fentanyl-induced locomotor and ventilatory depression. Rats were given saline or fentanyl, followed by: (1) naltrexone, (2) naloxone, (3) nalmefene, (4) α₁ agonist phenylephrine, (5) α₁ antagonist prazosin, (6) α_1D antagonist BMY-7378, (7) α₂ agonist clonidine, (8) α₂ antagonist yohimbine or (9) vehicle. All µ-opioid antagonists dose-dependently reversed fentanyl-induced locomotor and ventilatory depression. While the α₁ drugs did not alter the effects of fentanyl, clonidine dose-dependently decreased locomotion and respiration with and without fentanyl. Conversely, yohimbine given at a low dose (0.3–1 mg/kg) stimulated ventilation when given alone and higher doses (>1 mg/kg) partially reversed (∼50 %) fentanyl-induced ventilatory depression, but not locomotor depression. High doses of yohimbine in combination with a suboptimal dose of naltrexone reversed fentanyl-induced ventilatory depression, suggestive of additivity. Yohimbine may serve as an effective adjunctive countermeasure agent combined with naltrexone to rescue fentanyl-induced ventilatory depression.

Atrazine (ATRA) and ciprofloxacin (CPRO) are widely detected, persistent and co-existing aquatic pollutants. This study investigated effects of 14-day single and joint ATRA and CPRO exposure on juvenile Clarias gariepinus. Standard bioassay methods were used to determine responses of oxidative stress, hepatic condition, and immunological biomarkers on days 7 and 14. Seven groups were used: Control, CPRO_EC, CPRO_Subl, ATRA_EC, ATRA_Subl, CPRO_EC+ATRA_EC, and CPRO_Subl+ATRA_Subl. The test substances caused decreased activity of superoxide dismutase, catalase, and glutathione peroxidase. Lipid peroxidation was elevated, especially in CPRO-ATRA mixtures. Serum aminotransferases (ALT, and AST), and alkaline phosphatase activity increased significantly. Total protein, albumin, total immunoglobulin, and respiratory burst decreased significantly. Therefore, single and joint exposure to CPRO and ATRA poses adverse consequences on aquatic life.

Chemical compounds in the environment, which exhibit toxic and genotoxic activity, increase the mutational pressure on biota. This study aimed to investigate the genotoxic, mutagenic, and toxic effects of water from the Ile River and the Kapshagai Reservoir, both sites of active economic activities. Cytogenetic analysis of bone marrow from mice exposed to water samples from the Ile River and the Kapshagai Reservoir revealed a statistically significant increase in aberrant (p<0.05) and polyploid cells (p<0.01), as well as a decrease in the mitotic index (p<0.001), compared to the negative control. The water samples caused statistically significant increases in single- and double-strand DNA breaks in cells across various organs in the experimental mice compared to unexposed animals (p<0.001). These observations suggest the existence of chemical compounds within the water samples from the Kapshagai Reservoir and the Ile River, which exhibit genotoxic, mutagenic, and toxic properties.

The ability of organophosphate pesticides to disturb immune function has been demonstrated by in vivo and in vitro studies, but evidence of such effects on humans remains scarce. To assess the association between organophosphate pesticides exposure and cytokine levels in Mexican flower workers, a cross-sectional study was carried out. A questionnaire was provided to 121 male flower workers, and urine and blood samples were collected. Using gas chromatography, urinary concentrations of dialkylphosphate metabolites were determined. The serum cytokine levels, IL-4, IL-5, IL-6, IL-8, and IL-10, were measured using multiplex analysis, and levels of INF-γ and TNF-α by ELISA. We found that a higher dialkylphosphate concentration decreased the pro-inflammatory cytokines INF-γ (β = −0.63; 95 % CI: −1.22, −0.05), TNF-α (β= −1.18; 95 % CI: −2.38, 0.02), and IL-6 (β= −0.59; 95 % CI: −1.29, 0.12), and increased IL-10 (β=0.56; 95 % CI: 0.02, 1.09), the main anti-inflammatory cytokine, suggesting an imbalance of the immune response in flower workers.