Human & experimental toxicology
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Lipid emulsion attenuates extrinsic apoptosis induced by amlodipine toxicity in rat cardiomyoblasts.
Amlodipine-induced toxicity has detrimental effects on cardiac cells. The aim of this study was to examine the effect of lipid emulsion on decreased H9c2 rat cardiomyoblast viability induced by amlodipine toxicity. The effects of amlodipine, lipid emulsion, LY 294002, and glibenclamide, either alone or in combination, on cell viability and count, apoptosis, and expression of cleaved caspase-3 and -8, and Bax were examined. ⋯ LY 294002 and glibenclamide inhibited lipid emulsion-mediated inhibition of late apoptosis induced by amlodipine, but they did not significantly alter lipid emulsion-mediated inhibition of early apoptosis induced by amlodipine. Lipid emulsion decreased amlodipine-induced TUNEL-positive cells. These results suggest that lipid emulsion inhibits late apoptosis induced by amlodipine at toxic dose via the activation of phosphoinositide-3 kinase and ATP-sensitive potassium channels in the extrinsic apoptotic pathway.
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Spinal cord injury (SCI) is one of the most common destructive injuries, which may lead to permanent neurological dysfunction. Currently, transplantation of bone marrow mesenchymal stem cells (BMSCs) in experimental models of SCI shows promise as effective therapies. BMSCs secrete various factors that can regulate the microenvironment, which is called paracrine effect. ⋯ In in vivo studies, we found that hindlimb motor function was significantly improved in SCI rats with systemic administration of BMSCs-derived exosomes. We also observed that the expression of pro-apoptotic proteins and pro-inflammatory factors was significantly decreased, while the expression of anti-apoptotic proteins and anti-inflammatory factors were upregulated in SCI rats after exosome treatment. In conclusion, BMSCs-derived exosomes can inhibit apoptosis and inflammation response induced by injury and promote motor function recovery by inhibiting the TLR4/MyD88/NF-κB signaling pathway, which suggests that BMSCs-derived exosomes are expected to become a new therapeutic strategy for SCI.
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Observational Study
The relationship among plasma copeptin, carboxyhemoglobin, and lactate levels in carbon monoxide poisoning.
The aim of our study is to determine whether there is a change in the plasma levels of copeptin and there is a relationship among the plasma levels of carboxyhemoglobin (COHb), lactate, and copeptin levels in patients presenting to the emergency department with carbon monoxide (CO) poisoning. ⋯ Copeptin as a stress hormone can be used in the diagnosis and monitoring of patients with CO poisoning. However, the copeptin level was not superior to COHb and lactate levels.
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Welders' lung disease refers to mixed exposure to different kinds of metals and chemicals from welding fumes, which affect all parts of the respiratory tract including airways and parenchyma together. This study aimed to investigate the oxidative status in patients with welders' lung (PWL) by means of thiol-disulfide homeostasis and ischemia-modified albumin (IMA) levels. The male welder workers diagnosed with welders' lung disease and healthy individuals were recruited in the study. ⋯ IMA levels in PWL were significantly higher than the control group (1.37 (0.27) mg dL-1 vs. 0.49 (0.61) mg dL-1, p < 0.001), whereas CAT activities were significantly higher in the control group (106.6 (54.5) kU L-1 vs. 78.3 (67.8) kU L-1, p = 0.003). The findings of the present study revealed that oxidative stress plays a key role in the pathogenesis of welders' lung disease. Plasma thiol-disulfide homeostasis and IMA levels might be indicators of oxidative stress in PWL.
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Occupational exposure to the waste anaesthetic gases (WAGs) is a crucial problem for healthcare personnel. Cancer is among the potential long-term adverse effects of WAGs. The present occupational molecular epidemiology study was conducted in healthcare personnel (anaesthetists, nurses and technicians; n = 46), working in operating rooms (ORs; n = 34) and recovery units (RUs; n = 12) of the same hospital, to assess the genotoxicity risk of WAGs exposure. ⋯ Air sevoflurane levels in the breathing zone in three ORs and one RU did not exceed the established occupational exposure limits. Both in surrogate tissue (PBLs) and in target tissue (BECs) of the personnel of RUs and ORs of the same hospital, the genotoxicity risk was evident and similar. Originality of this study, in addition to the WAGs exposure confirmation of the healthcare personnel, was the involvement of the RU personnel for the genotoxicity assessment, which was the first time in the scientific literature.