Environmental Toxicology最新文献

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.

The effluents generated during the process of hair dyeing exhibit a complex composition, comprising chemical compounds with varying toxicity levels. While the adverse impact of hair dyes on human health is acknowledged, there is a notable absence of studies addressing the toxicity associated with effluents produced during these activities. The primary objective of this study was to assess two effluents emanating from beauty salons after brown hair dyeing: one resulting from hair washing with water, shampoo, and conditioner, referred to as the complete effluent (CE), and the other from washing the dyed hair solely with water, excluding surfactants, referred to as the dye effluent (DE). In vitro bioassays were conducted with the human hepatoma cell line (HepG2/C3A). Cytotoxicity was evaluated through 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and Trypan Blue tests, while genotoxicity and mutagenicity were assessed by comet assay and cytokinesis-block micronucleus test, respectively. The cells were exposed for 4 h to various dilutions of the two sampled effluents [100.0% (1); 50.0% (2); 25.0% (3); 12.5% (4); 6.25% (5); 3.125% (6)]. Cytotoxicity was induced by CE-1, DE-1, DE-2, and DE-3 dilutions as indicated by both assays, whereas CE-2 dilution exhibited cytotoxicity solely through the MTT assay. These findings suggest impaired cell membrane integrity, permeability, and mitochondrial activity. Nontoxic dilutions (4, 5, and 6) were viable for the comet assay and micronucleus test, revealing genotoxicity without mutagenic potential. Consequently, residual concentrations of effluents were found to induce nonlethal and reparable primary DNA damage. Moreover, the effluents decreased the cytokinesis-block proliferation index and the cell replication index, indicating interference and arrestment in the cell cycle. These outcomes highlight the potential threat posed by residual concentrations of hair DEs to environmental quality and human health, emphasizing the imperative need for pre-disposal treatments in salon settings.