1,721,088 research outputs found
Exogenous factors in the immunotoxicity of oral PMN
No full textCurrent evidence indicates that periodontal disease is frequently due to inappropriate levels of gingival granulocyte functions. Reason of this failure may be the toxic effects of a number of local or systemic exogenous factors, capable of spreading through the gingival crevice environment, and strongly conditioning the granulocyte activities. The wide list includes bacteria and granulotoxic products, hedonistic drugs (mainly tobacco), and chemotherapeutic agents (especially antimicrobials used for preventing or reducing the accumulation of dental plaque). Almost always, their presence induces a time- and/or dose-dependent toxicity
A functional coupling between L- type calcium channel and P2 receptor in extracellular GTP-stimulated PC12 cells.
No full textChlorhexidine effects on polymorphonuclear leucocyte degranulation and LFA-1 expression.
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Cooperation in signal transduction of extracellular guanosine 5’ triphosphate and Nerve Growth Factor in neuronal differentiation of PC12 cells
No full textWe studied the transduction mechanisms activated by GTP in PC12 cells and found that addition of GTP (100 uM) increased intracellular calcium concentration ([Ca2+]i) in cells that were between 60 and 70% confluent. Addition of GTP also enhanced activation of NGF-induced extracellular regulated kinases (ERKs) and induced Ca2+ mobilization.
This mobilization, due to the activation of voltage-sensitive and ryanodine-sensitive calcium channels, as well as pertussis toxin-sensitive purinoceptors, modulates Ca2-activated K+ channels not involved in activation of ERKs. The results presented here indicate that GTP-triggered [Ca2+]i increase may be a key event in GTP signal transduction, which can modulate activity of ERKs. The physiological
importance of the GTP effect lies in its capacity to interact with the NGF-activated pathway to enhance neurite outgrowth from PC12 cells
Modulation of redox status and calcium handling by extremely low frequency electromagnetic fields in C2C12 muscle cells: A real-time, single-cell approach
No full textThe biological effects of electric and magnetic fields, which are ubiquitous in modern society, remain poorly understood. Here, we applied a single-cell approach to study the effects of short-term exposure to extremely low frequency electromagnetic fields (ELF-EMFs) on muscle cell differentiation and function using C2C12 cells as an in vitro model of the skeletal muscle phenotype. Our focus was on markers of oxidative stress and calcium (Ca2+) handling, two interrelated cellular processes previously shown to be affected by such radiation in other cell models. Collectively, our data reveal that ELF-EMFs (1) induced reactive oxygen species production in myoblasts and myotubes with a concomitant decrease in mitochondrial membrane potential; (2) activated the cellular detoxification system, increasing catalase and glutathione peroxidase activities; and (3) altered intracellular Ca2+ homeostasis, increasing the spontaneous activity of myotubes and enhancing cellular reactivity to a depolarizing agent (KCl) or an agonist (caffeine) of intracellular store Ca2+ channels. In conclusion, our data support a possible link between exposure to ELF-EMFs and modification of the cellular redox state, which could, in turn, increase the level of intracellular Ca2+ and thus modulate the metabolic activity of C2C12 cells
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