Toxicology and Industrial Health最新文献

With the widespread use of manganese dioxide nanoparticles (nano MnO₂), health hazards have also emerged. The inflammatory damage of brain tissues could result from nano MnO₂, in which the underlying mechanism is still unclear. During this study, we aimed to investigate the role of ROS-mediated p38 MAPK pathway in nano MnO₂-induced inflammatory response in BV2 microglial cells. The inflammatory injury model was established by treating BV2 cells with 2.5, 5.0, and 10.0 μg/mL nano MnO₂ suspensions for 12 h. Then, the reactive oxygen species (ROS) scavenger (20 nM N-acetylcysteine, NAC) and the p38 MAPK pathway inhibitor (10 μM SB203580) were used to clarify the role of ROS and the p38 MAPK pathway in nano MnO₂-induced inflammatory lesions in BV2 cells. The results indicated that nano MnO₂ enhanced the expression of pro-inflammatory cytokines IL-1β and TNF-α, elevated intracellular ROS levels and activated the p38 MAPK pathway in BV2 cells. Controlling intracellular ROS levels with NAC inhibited p38 MAPK pathway activation and attenuated the inflammatory response induced by nano MnO₂. Furthermore, inhibition of the p38 MAPK pathway with SB203580 led to a decrease in the production of inflammatory factors (IL-1β and TNF-α) in BV2 cells. In summary, nano MnO₂ can induce inflammatory damage by increasing intracellular ROS levels and further activating the p38 MAPK pathway in BV2 microglial cells.

Nail technology, including the application of artificial nails and nail care, is a developing sector of the global beauty industry. Nail technicians are exposed to a variety of chemical substances through inhalation, as they spend extended periods of time in close proximity to these materials. This study aimed to evaluate the semi-quantitative health risk of dust-containing heavy metals among nail technicians. This analytical descriptive study employed the risk assessment method provided by the Singapore Occupational Health Department to evaluate the health hazards of lead, cadmium, nickel, chromium, and manganese. Dust samples from nail filing were collected from the respiratory zone of 20 nail technicians following the NIOSH 7300 method. The samples were analyzed using ICP-OES instrumentation. Monte Carlo simulation was utilized to characterize the risk and its uncertainties. Manganese and cadmium had the highest and lowest mean concentrations, respectively. The risk scores of the metals ranked from highest to lowest were as follows: $Ni>Cr>Cd>Mn>Pb$. All five metals had risk rankings below 2.8, signifying a minimal risk level. Sensitivity analysis using Spearman's correlation coefficient demonstrated a positive relationship between concentration, daily hours of exposure, and the number of workdays per week with the risk score (RR) and exposure level (ER). Conversely, the variable of weekly working hours (W) showed a negative correlation with these parameters. Despite the low-risk level of the examined metals, continuous exposure and potential long-term effects on nail technicians warrant preventive measures. Recommendations include implementing local exhaust ventilation systems, using table fans, establishing work-rest cycles, wearing N95 dust masks, and using reputable and high-quality nail polishes.

Exposure of zebrafish embryos to glucose is a suitable model for the fetal hyperglycemia seen in gestational diabetes. Diethylhexyl phthalate (DEHP), which is considered an endocrine-disrupting chemical, is one of the most common phthalate derivatives used in stretching plastic and is encountered in every area where plastic is used in daily life. In the present study, the effects of DEHP on pathways related to insulin resistance and obesity were examined in zebrafish embryos exposed to glucose as a fetal hyperglycemia model. Zebrafish embryos were exposed to DEHP, glucose, and glucose + DEHP for 72 h post-fertilization (hpf), and developmental parameters and locomotor activities were monitored. At 72 hpf ins, lepa, pparγ, atf4a, and il-6 expressions were determined by RT-PCR. Glucose, lipid peroxidation (LPO), nitric oxide (NO) levels, glutathione S-transferase (GST), superoxide dismutase (SOD), and acetylcholine esterase (AChE) activities were measured spectrophotometrically. Compared with the control group, glucose, LPO, GST activity, il6, and atf4a expressions increased in all exposure groups, while body length, locomotor, and SOD activities decreased. While AChE activity decreased in the DEHP and glucose groups, it increased in the glucose + DEHP group. Although glucose exposure increased pparγ and lepa expressions, DEHP significantly decreased the expressions of pparγ and lepa both in the DEHP and glucose + DEHP groups. Our findings showed that DEHP amplified oxidant and inflammatory responses in this fetal hyperglycemia model, predisposing insulin resistance in zebrafish embryos.

Triclosan (TCS), an antimicrobial drug, is known to occupy different compartments in aquatic ecosystems. The present study focused to evaluate the reproductive toxicity of triclosan, at environmentally relevant (0.009 and 9 μg L^-1) and sublethal (176.7 μg L^-1) concentrations for 90 days in the pre-spawning phase of the fish, Anabas testudineus. The reproductive biomarkers, namely, gonadal steroidogenic enzymes, expression of aromatic genes, levels of serum gonadotropins, sex hormones, and histology of gonads were analyzed. The weight of the animal, brain weights along with gonadosomatic index decreased while mucus deposition increased significantly at all concentrations of triclosan as the primary defensive mechanism to prevent the entry of toxicants. Triclosan disrupted gonadal steroidogenesis as evidenced by a reduction in the activities of gonadal steroidogenic enzymes. The expressions of cyp19a1a and cyp19a1b genes were up-regulated in the brain of both sexes and testis, while down-regulated in the ovary indicating estrogenic effects of the compound. The endocrine-disrupting effects of triclosan were confirmed. The current results suggest that chronic exposure to triclosan altered reproductive endpoints thereby impairing normal reproductive functions in fish.