21 research outputs found

    DNA strand breaks (A), FPG- (B) and hOGG1-sensitive sites (C) in the liver of lean or obese Zucker rats.

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    <p>The results are presented as mean and SEM (n = 7–8 per group). *P<0.05 compared to same strain of rat. <sup>#</sup>P<0.05 compared to the lean counterpart at the same age.</p

    HMOX-1 protein the liver of lean and obese lean Zucker rats.

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    <p>The results are represented as mean ± SEM (n = 5 per group) relative band intensity in Western blot. *Statistical significantly increased compared to young Zucker rats.</p

    Nanomaterial-induced cell death in pulmonary and hepatic cells following exposure to three different metallic materials: The role of autophagy and apoptosis

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    <p>Autophagy is the catabolic process involving the sequestration of the cytoplasm within double-membrane vesicles, which fuse with lysosomes to form autolysosomes in which autophagic targets are degraded. Since most endocytic routes of nanomaterial uptake converge upon the lysosome and the possibility that autophagy induction by NMs may be an attempt by the cell to self-preserve following the external challenge, this study investigated the role of autophagy following exposure to a panel of widely used metal-based NMs with high toxicity (Ag and ZnO) or low toxicity (TiO<sub>2</sub>) in a pulmonary (A549) and hepatic (HepG2) cell line. The <i>in vitro</i> exposure to the Ag and ZnO NMs resulted in the induction of both apoptosis and autophagy pathways in both cell types. However, the progression of autophagy was blocked in the formation of the autolysosome, which coincided with morphologic changes in the actin cytoskeleton. This response was not observed following the exposure to low-toxicity TiO<sub>2</sub> NMs. Overall, the results show that high toxicity NMs can cause a dysfunction in the autophagy pathway which is associated with apoptotic cell death.</p

    Body weight, hepatic lipid load and serum concentrations of triglycerides, cholesterol, non-fasting glucose, insulin and ALT in lean and obese Zucker rats.

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    <p>The results have been reported previously [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0118773#pone.0118773.ref017" target="_blank">17</a>,<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0118773#pone.0118773.ref018" target="_blank">18</a>]. Lipid accumulation was assessed by Oil Red staining of liver tissue sections.</p><p>*P<0.05 compared to lean rats at the same age. The results is presented as the mean ± SEM (n = 6–8).</p><p>Body weight, hepatic lipid load and serum concentrations of triglycerides, cholesterol, non-fasting glucose, insulin and ALT in lean and obese Zucker rats.</p

    Glutathione status in lung tissue of <i>ApoE</i><sup><i>-/-</i></sup> mice after repeated i.t. instillations of carbon black (CB) or lipopolysaccharide (LPS).

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    <p>Total and reduced glutathione was measured at 24 h post-exposure in lung homogenate from <i>ApoE</i><sup><i>-/-</i></sup> mice of study 1 and 2. Data is presented as mean and SEM (n = 10 mice per group).</p
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