, 2011 and Qian et al., 2009) that can induce increased cell size and hypertrophy. These considerations prompted us to verify if the progression of the cell cycle in curcumin-treated HT-29 cells was deranged. Indeed, long-term exposure to 5.0–20 μM curcumin induced G1-phase arrest and S-phase depression (Fig. 10) in

HT-29 http://www.selleckchem.com/products/SP600125.html cells. While the cell cycle arrest may explain the increased volume observed in curcumin-treated HT-29 cells, the underlying mechanisms leading to the deranged progression of cell cycle in these cells need to be elucidated. It is worth to note however, that an arrest of cell growth in the G0/G1 phase is often associated with a significant decrease in IClswell (He et al., 2011, Klausen et al., 2007 and Shen

et al., 2000). Curcumin induces apoptosis through a wide variety of mechanisms (Reuter et al., 2008). These mechanisms include the activation of the mitochondrial pathway via activation of Bax/Bak (Shankar and Srivastava, 2007b) or BID (Anto et al., 2002). Moreover, evidence exists that curcumin activated caspase 3 and 8 with no activation of caspase 9, raising the hypothesis of an activation of a death receptor-dependent (non-mitochondrial) pathway via FasL-independent aggregation of Fas receptors (Bush et al., 2001). In addition, activation by curcumin of novel apoptosis-like pathways, independent of mitochondria and caspases, was described (Piwocka et al., 1999). Therefore, it is likely that curcumin could http://www.selleckchem.com/products/VX-765.html induce apoptosis also when the mitochondrial pathway is blocked. From the presented buy Fludarabine data we conclude that curcumin is able to affect cell survival and cell volume in a dose-dependent manner. At lower concentrations (<5.0 μM), curcumin indirectly activates IClswell, which is most likely the result of apoptosis induction. Higher curcumin concentrations (≥5.0 μM) indirectly lead to an inhibition of IClswell, an arrest of cell cycle in G1-phase and hence to cell swelling. Charity Nofziger is supported by the Lise Meitner stipend of the Fonds zur Förderung der Wissenschaftlichen Forschung (FWF) (M11108-B11).

The experimental work was further supported by the FWF and the FP-7 to M.P. (P18608; PIRSES-GA-2008-230661). None. We greatly appreciated the helpful discussion with M. Ritter. The authors acknowledge the expert secretarial assistance of Elisabeth Mooslechner. “
“Although the organophosphorus compounds (OPs), employed as insecticides exhibit preferential toxicity to insects, they are also toxic to humans and other animals due to the inhibition of AChE and the subsequent accumulation of acetylcholine at the neuron synapses (Johnson et al., 2000). In addition, some OPs can inhibit and age another esterase, known as the neuropathy target esterase (NTE) (Johnson, 1988), and cause a delayed effect that is known as organophosphorus-induced delayed neuropathy (OPIDN).