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https://www.selleckchem.com/EGFR(HER).html 5-exposed mice whereas molecules for lipid export were induced after long-term PM2.5 exposure. Therefore, ambient PM2.5 exposure disturbed hepatic lipid metabolism and the effects varied in different exposure duration. These findings in mice provide new insight into the biological basis of PM2.5-induced human metabolic dysfunction and specific strategies may be applied based on different exposure time periods.C60 fullerene (C60) is a nano-pollutant that can damage the respiratory system. Eugenol exhibits significant anti-inflammatory and antioxidant properties. We aimed to investigate the time course of C60 emulsion-induced pulmonary and spermatic harms, as well as the effect of eugenol on C60 emulsion toxicity. The first group of mice (protocol 1) received intratracheally C60 emulsion (1.0 mg/kg BW) or vehicle and were tested at 12, 24, 72 and 96 h (F groups) thereafter. The second group of mice (protocol 2) received intratracheally C60 emulsion or vehicle, 1 h later were gavaged with eugenol (150 mg/kg) or vehicle, and experiments were done 24 h after instillation. Lung mechanics, morphology, redox markers, cytokines and epididymal spermatozoa were analyzed. Protocol 1 Tissue damping (G) and elastance (H) were significantly higher in F24 than in others groups, except for H in F72. Morphological and inflammatory parameters were worst at 24 h and subsequently declined until 96 h, whereas redox and spermatic parameters worsened over the whole period. Eugenol eliminated the increase in G, H, cellularity, and cytokines, attenuated oxidative stress induced by C60 exposure, but had no effect on sperm. Hence, exposure to C60 emulsion deteriorated lung morphofunctional, redox and inflammatory characteristics and increased the risk of infertility. Furthermore, eugenol avoided those changes, but did not prevent sperm damage.In the current research work, a novel eco-friendly Fe3O4@SiO2 nanocomposite immobilized with Pseudomonas fluor

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