Environmental toxicology and pharmacology最新文献

Vanadium pentoxide (V₂O₅) is one of the compounds that have been reported to pose varying degrees of toxicity upon exposure; thus, making it a challenging environmental hazard that affects living organisms. This study investigated the cytotoxicity effects of daily sub-lethal oral doses of V₂O₅ on the bone marrow of male Oryctolagus cuniculus after 21 days. Male O. cuniculus (n = 60, ∼ 6 week old, 433.45 ± 5.00 g body weight) were simply randomized into four experimental groups and a control with three replicates of four animals each. Based on the estimated 96-h LD₅₀ value of 119.0 mg/kg, sub-lethal doses of V₂O₅ were prepared as 1 mg/kg, 5 mg/kg, 10 mg/kg and 20 mg/kg, and administered to the test animals daily by oral gavage for 21 days. Vanadium pentoxide induced cytotoxicity in the bone marrow cells (BMCs) of exposed groups, with significant changes in all evaluated haemopoietic bone marrow stem cells (erythrocytes, leukocytes, thrombocytes and plasma cells). There were mixed trends in the values of leucocyte differentials in the exposed animal. Oral exposure to V₂O₅ exerts cytopathologic effects in the forms of DNA damage on the bone marrow of O. cuniculus. These findings support previous reports on the environmental hazards vanadium pentoxide poses to living organisms.

The present study investigated the individual and mixture effects of Arsenic (As) and Chromium (Cr) at their environmental concentrations in zebrafish (Danio rerio). After 15, 30 and 60 days of exposure, increased frequencies of erythrocytic nuclear abnormalities (ENAs) were noticed. After 60 days of exposure, DNA damage was observed in liver and base excision DNA repair (BER) and mismatch DNA repair (MMR) pathways were studied to know the cellular responses. Altered expression of BER (ogg1, apex1, creb1, polb) and MMR (mlh1, msh2, msh6) genes indicated inhibition of DNA repair. Downregulation of tumor suppressor genes (p53 and brca2) occurred in mixture group. Downregulation of bax, caspase9 and decreased bax/bcl2 ratio indicated prevention of intrinsic apoptotic pathway in treated groups. Results indicated As and Cr-induced predisposition to genomic instability and carcinogenesis in zebrafish. Overall, this study confirmed the additive genotoxic effects of As and Cr in zebrafish erythrocytes and in liver after chronic exposure.

We evaluated both environmental (workplace) and biological (urine) exposure to the anesthetic isoflurane concerning the effects of such exposure on the hematological, hepatic, and renal parameters in veterinarians. Samples were collected from exposed and nonexposed (volunteers) groups to assess hematological and several biochemical markers, and isoflurane was measured in the workplace air and veterinarian's urine. Isoflurane was detected at high levels in the air and urine. No differences were observed in hematological parameters between the groups, although the number of monocytes increased among veterinarians, values were within the normal range. No significant differences were found in the hepatic enzymes or renal parameters between the groups, and all marker levels were within the normal range. In conclusion, urinary isoflurane is a suitable internal biomarker for monitoring occupational exposure and is associated with veterinary workplace measurements, and that occupational exposure is not associated with abnormal hematological or biochemical changes in veterinarians.

Biochemical blood parameters may serve as biomarkers of environmental pollution, with somatoform disorder (SD) being of interest. This study examined serum glycosylated hemoglobin (HbA1C), insulin, total protein, and SD prevalence in populations from polluted areas in Kazakhstan. It assessed the predictive value of these parameters for SD, along with other risk factors. A cross-sectional study of 1881 individuals (ages 18-52) in Kazakhstan used the PHQ-15 questionnaire to assess SD. HbA1C was measured via immunoturbidimetry, insulin via immunoassay, and total protein via colorimetry. HbA1C levels > 6.5 % identified undiagnosed diabetes in 2.4 % of control residents, with higher rates in Ust-Kamenogorsk (10.6 %), Berezovka/Aksay (4.8 %), and Borodulikha/Abay (3.7 %). Pollutant-exposed populations had higher rates of hyperinsulinemia. Moderate to severe SD was more common in Ust-Kamenogorsk (26.6 %) and Berezovka/Aksay (27.2 %) than in controls, with lower rates in Borodulikha/Abay (16.7 %). Age, HbA1c levels, and residence near the condensate gas extraction plant significantly increased the odds of having moderate to severe SD, while being male and of Kazakh ethnicity significantly decreased the odds. The study links environmental exposure to increased rates of SD, diabetes, and insulin resistance.

Diesel exhaust particles (DEPs) are atmospheric pollutants associated with adverse health effects. In response to their impact, natural gas (NG) has emerged as a promising alternative fuel due to its cleaner combustion. Although the cytotoxicity and genotoxicity of DEPs from diesel or NG engines have been extensively studied, the impact of dual natural gas-diesel systems remains unexplored. This study evaluated the toxicity of DEPs (PM2.5) emitted by an engine in diesel mode and dual natural gas-diesel mode on cellular parameters such as viability, apoptosis, oxidative stress, and DNA damage. The results showed that diesel DEPs reduced cell viability by up to 31 %, compared to a 19.2 % reduction with dual-mode DEPs. Apoptosis induction was also higher with diesel DEPs, with a 7 % increase compared to the dual mode. While dual-mode DEPs increased the production of reactive oxygen species (ROS) without causing DNA damage, diesel DEPs generated high ROS levels and measurable DNA damage. These differences could be attributed to the physicochemical characteristics of each mode, as diesel DEPs contained higher concentrations of polycyclic aromatic hydrocarbons (PAHs). This study addresses a research gap by quantifying the health effects of emissions from dual-fuel engines and highlights the potential of these systems to reduce DEP-induced toxicity.

Polybrominated diphenyl ethers (PBDEs) are flame retardants heavily utilized across plastic, textile and electronic industries. Although these PBDEs are effective in protecting property and human life from fire, their high production volumes have led PBDEs to become pervasive environmental contaminants and pose an ecological and health risk as high levels have been noted in environmental media including water and sediment, wildlife and human tissue. Here we investigate the developmental neurotoxicity of 2,2',4,4'-tetrabromodiphenyl ether (BDE-47), one of the more dominant PBDE congeners found in human tissue, on oligodendrocytes in the hindbrain and spinal cord. We utilized the zebrafish vertebrate model system and investigated low (5µM) and high concentrations (20µM) of BDE-47. We find that by 6 days post-fertilization, BDE-47 negatively affects oligodendrocyte development in the hindbrain and spinal cord in a concentration dependent manner.

Massylaea vermiculata snails are a significant gastropod pest in Egypt, threatening agriculture. Due to increasing concerns about conventional pesticides, it is imperative to find effective alternatives that are less harmful. We assessed the molluscicidal activity of abamectin, methoxyfenozide, and spinosad using the leaf-dipping method in vitro and the effect of LC₅₀ of these compounds on biochemical aspects and protein electrophoresis. Results showed that these compounds exhibited molluscicidal activity, with LC₅₀ values of 0.21, 0.63, and 0.65 mg/l for abamectin, methoxyfenozide and spinosad, respectively. Biochemical assays on treated snails showed increased aspartate and alanine aminotransferase and alkaline phosphatase activities and reduced total protein compared to controls. For the most effective compound (abamectin), these values were 195.36, 105.82, 276.76, and 2.49, compared to control values of 88.00, 47.67, 124.67, and 5.52, after 10 days post-treatment. Protein electrophoresis revealed variations in protein bands. Thus, these compounds can be effective within integrated control programs.

Carbendazim is widely applied in agriculture to control various fungal diseases during pre-harvest and post-harvest processes owing to its efficacy and cost-effectiveness. However, environmental and food contamination by carbendazim has become a global health issue. Indeed, the declining biodiversity of beneficial insects owing to agricultural intensification is currently of keen concern to the scientific community. The toxicological responses of Nauphoeta cinerea nymphs, a non-target insect, to ecologically realistic concentrations of carbendazim at 0, 0.25, 2.5, 5.0 and 25 μg/L for 50 uninterrupted days were assessed. Neurobehavioral data generated by video-tracking software revealed that chronic nymphal exposure to carbendazim significantly diminished the path efficiency, body rotation, maximum speed, turn angle and distance traveled but increased the immobility time, total time of freezing and episodes of freezing in insects. The deterioration in the locomotor and exploratory abilities of carbendazim-exposed insects was substantiated by high heat map intensity and reduced track plots. Further, chronic carbendazim exposure diminished acetylcholinesterase activity in head of the insects. Chronic carbendazim exposure significantly decreased antioxidant defense mechanisms but increased nitric oxide, hydrogen peroxide and lipid peroxidation levels in fat body, midgut and head of exposed insects. Activities of acid and alkaline phosphatases which play important roles in detoxification and metabolic processes were also markedly decreased in carbendazim-exposed insects when compared with control. Altogether, carbendazim represents an ecological threat to non-target insects through induction of oxido-inflammatory injury, providing valuable insights into the behavioral dysfunction and toxicological mechanisms of carbendazim in beneficial insects.

2,4-D dimethylammonium, a widely used herbicide, accumulates in aquatic animals, posing risks to both their populations and human consumers. This study evaluated the effects of 2,4-D on Riceland prawn (Macrobrachium lanchesteri) using Optical Coherence Tomography (OCT) to assess morphological changes. The activity of acetylcholinesterase (AChE), catalase (CAT), and glutathione S-transferase (GST) was also measured. Toxicity increased with both concentration and exposure duration. OCT revealed swelling in the gill region, tissue abnormalities, and muscle damage in the abdominal somite, telson, and uropod, along with tissue separation and degradation. Histological analysis confirmed muscle degeneration, hemocyte infiltration, and swelling. AChE expression was undetectable at 400 and 450 µL/L after 96 hours, with a molecular weight of 71 kDa. CAT and GST activities decreased at higher herbicide concentrations, further demonstrating the harmful effects of 2,4-D on prawn health.

DNA integrity is crucial for organismal health, and assessing DNA damage in aquatic organisms is essential for identifying environmental threats and informing conservation efforts. Pollutants such as metals, hydrocarbons, agrochemicals, pharmaceuticals, and climate change are linked to genetic damage, oxidative stress, and mutagenesis in several species, such as elasmobranchs (sharks and rays). Most studies focus on bivalves, crustaceans, and bony fish, with fewer assessments being carried out in cartilaginous fish. Concerning elasmobranchs, studies employing the micronucleus test and nuclear anomaly assays have aided in understanding how this group responds to contamination by organic and inorganic pollutants. Notably, each species deals differently with these contaminants, presenting varied DNA damage levels, including low levels of response, probably associated to feeding habits, trophic position, maturation stage, sex and metabolism. Further investigations should be conducted in elasmobranchs to elucidate these variations and better understand DNA damage in this important ecological group.