Environmental Toxicology最新文献

The present study was conducted to evaluate the impact of α-Cypermethrin (αCYP), the second most commonly used pesticide in India, on the ovine ovarian granulosa cells (GCs) viability, growth, apoptosis, and steroidogenesis. GCs collected from abattoir-derived ovine ovaries were cultured for 3/6 days in the presence of various concentrations of αCYP (0, 1, 10, 25, 50, and 100 μM). The results revealed a binary effect on GCs, where metabolic activity and viability rates were significantly (p < 0.05) lower from 25 μM onwards. Estrogen concentration was significantly low from the 1 μM dose, whereas progesterone concentration showed a significant increase (10 μM) in the spent media of cultured GCs. The cytotoxicity in the GCs exposed to αCYP revealed significant changes in LDH, ROS, CUPRAC, and GST activity (all at 25 μM) and MDA (at 10 μM) compared to those observed in the control group. The gene expression profiles of cultured GCs showed a significant up-regulation of CYP11A1, FSHR (all at 1 μM), StAR, BAX, and CASP3 (all at 10 μM), 3βHSD1 (at 25 μM), and significant down-regulation of CYP17A1 and ERS2 (all at 25 μM), CYP19A1 and 17βHSD (all at 1 μM), ESR1 and BCL2 (all at 10 μM) in comparison to those observed in control groups. The results of the present experiment demonstrated that αCYP affected the growth and functional parameters of GCs, the expression of steroid hormone-associated genes, and hormone secretion.

Fine particulate matter (PM_2.5) can exacerbate the instability of atherosclerotic plaques although the exact chemical process driving atherosclerosis remains unknown. In order to create atherosclerotic models, a high-fat diet and vitamin D3 injections were given to 56 Wistar rats in this investigation. The atherosclerotic rats were split into four groups at random and given different doses of PM_2.5 (0, 1.5, 7.5, and 37.5 mg/kg) for 4 weeks. To investigate the mechanism, foam cells were exposed to PM_2.5 (0, 25, 50, and 100 μg/mL) for 24 h. The results showed that PM_2.5 exposure caused collagen fibers thinner and muscle fibers were disorganized. PM_2.5 exposure significantly affected the expression of MMP2, MMP9, TIMP2, and vimentin in aortas of atherosclerotic rats. Moreover, PM_2.5 exposure increased the expression of the Notch signaling pathways which was correlated with the expression of atherosclerotic plaque stability-related genes. PM_2.5 exposure also increased the apoptosis rate of foam cells. The expression of MMP2, MMP9, and vimentin was increased and TIMP2 was decreased with the increasing PM_2.5 dose in foam cells. The inhibition of the Notch signaling pathway can alleviate the alteration of atherosclerotic plaque stability-related genes. The findings demonstrated that PM_2.5 exposure can cause atherosclerotic plaques to become unstable, aggravating the progression of atherosclerosis, a process in which the Notch signaling pathway is crucial.

Flurochloridone (FLC) is a selective herbicide that can cause reproductive toxicity in male rats. However, limited information is available regarding the toxicity of FLC in the developmental stages of aquatic organisms. This study aimed to investigate the effects of FLC exposure during embryonic development and elucidate its potential mechanism of action. Zebrafish embryos were exposed to 6.25, 12.5, 25, and 50 μg/mL FLC for 4-144 hpf. The developmental status of embryos was recorded; the indicators of oxidative stress and embryonic apoptosis were determined. We found that FLC exposure caused severe embryonic malformations, such as pericardial edema, spinal curvature, and growth retardation, accompanied by a decreased hatching and survival rate. After exposure until 144 h postfertilization, the median lethal concentration (LC₅₀) of FLC in zebrafish embryos was 36.9 μg/mL. Subsequently, FLC induced the accumulation of reactive oxygen species and malondialdehyde, enhanced the activity of superoxide dismutase, and activated the Keap1-Nrf2 signaling pathway. Further studies confirmed that FLC can induce apoptosis in zebrafish embryos through the activation of caspase. These results suggest that FLC induced developmental toxicity in zebrafish embryos, which provides new evidence regarding FLC toxicity in aquatic organisms and to assess human health risks.

Numerous contemporary diseases are linked to food contamination. Pathogenic agents might stem from certain food ingredients or result from pollution stemming from food processing or packaging. One such contaminant is 3-Chloro-1,2-propanediol (3-MCPD), it has been previously reported to be produced during the preparation of chemical sauces, as well as during the heating of baked goods. Yet, uncertainty surrounds its potential to induce embryonic developmental toxicity. In this study, zebrafish were employed as the focal point to assess the impact of 3-MCPD on initial embryonic development, heart functionality, and behavior. The research unveiled that exposure of zebrafish embryos to 18, 36, and 54 mM 3-MCPD led to cardiac anomalies, including pericardial edema, reduced heart rate, and elongated SV-BA distance. Additionally, 3-MCPD exposure triggered aberrations in cardiac-related gene expression and an elevation in oxidative stress. Notably, behavioral changes were observed in 3-MCPD-exposed zebrafish embryos, while vascular development appeared unaffected. This study introduces a novel basis for comprehensive exploration of 3-MCPD toxicity.

Fluoride (F^-) is a major groundwater contaminant spread across the world. In excess concentrations, F^- can be detrimental to living beings. F^- exposure is linked to cellular redox dyshomeostasis, leading to oxidative stress-mediated pathologies including heart dysfunction. Due to its potent antioxidant properties, various phytochemicals are found to alleviate the symptoms of F^- toxicity. Hence, we explore the protective effect of esculin (Esc), a coumarin glucoside on F^--induced oxidative stress and cardiotoxicity in zebrafish larvae. The experimental groups consisted of NaF (50 ppm) and Esc (100 μM) groups treated alone and in combination with a control group for 6 h. The groups were maintained till 78 hpf after which the level of oxidants (ROS, LPO, and PCC) and antioxidants (GST, GSH, GPx, SOD, and CAT) were assessed. The results revealed that Esc pretreatment restored the depleted antioxidant markers and reduced the levels of oxidant in the Esc+NaF group, exhibiting its antioxidant potential. In addition, analyses of the heartbeat rate and hemoglobin integrity using o-Dianisidine staining were conducted in the control and experimental groups. Esc treatment prevents F^- induced cardiac changes including tachycardia and altered blood flow. Further, the mRNA expression level of antioxidant genes (nrf2, gstp1, hmox1a, prdx1, and nqo1) and cardiac developmental genes (bmp2b, nkx2.5, myh6, and myl7) confirmed that Esc acts as a potent free radical scavenger and antioxidant defense enhancer, protecting zebrafish larvae from NaF-induced oxidative stress and heart dysfunction.