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71.
This brief review discusses recent advances in studies of mitochondrial Ca2+ signaling and considers how the relationships between mitochondria and Ca2+ responses are shaped in secretory epithelial cells. Perhaps the more precise title of this review could have been “How to win ATP and influence Ca2+ signaling in secretory epithelium with emphasis on exocrine secretory cells and specific focus on pancreatic acinar cells”. But “brevity is a virtue” and the authors hope that many of the mechanisms discussed are general and applicable to other tissues and cell types. Among these mechanisms are mitochondrial regulation of Ca2+ entry and the role of mitochondria in the formation of localized Ca2+ responses. The roles of Ca2+ signaling in the physiological adjustment of bioenergetics and in mitochondrial damage are also briefly discussed. 相似文献
72.
Criddle DN Gillies S Baumgartner-Wilson HK Jaffar M Chinje EC Passmore S Chvanov M Barrow S Gerasimenko OV Tepikin AV Sutton R Petersen OH 《The Journal of biological chemistry》2006,281(52):40485-40492
Oxidative stress may be an important determinant of the severity of acute pancreatitis. One-electron reduction of oxidants generates reactive oxygen species (ROS) via redox cycling, whereas two-electron detoxification, e.g. by NAD(P)H:quinone oxidoreductase, does not. The actions of menadione on ROS production and cell fate were compared with those of a non-cycling analogue (2,4-dimethoxy-2-methylnaphthalene (DMN)) using real-time confocal microscopy of isolated perfused murine pancreatic acinar cells. Menadione generated ROS with a concomitant decrease of NAD(P)H, consistent with redox cycling. The elevation of ROS was prevented by the antioxidant N-acetyl-l-cysteine but not by the NADPH oxidase inhibitor diphenyliodonium. DMN produced no change in reactive oxygen species per se but significantly potentiated menadione-induced effects, probably via enhancement of one-electron reduction, since DMN was found to inhibit NAD(P)H:quinone oxidoreductase detoxification. Menadione caused apoptosis of pancreatic acinar cells that was significantly potentiated by DMN, whereas DMN alone had no effect. Furthermore, bile acid (taurolithocholic acid 3-sulfate)-induced caspase activation was also greatly increased by DMN, whereas DMN had no effect per se. These results suggest that acute generation of ROS by menadione occurs via redox cycling, the net effect of which is induction of apoptotic pancreatic acinar cell death. Two-electron detoxifying enzymes such as NAD(P)H:quinone oxidoreductase, which are elevated in pancreatitis, may provide protection against excessive ROS and exert an important role in determining acinar cell fate. 相似文献
73.
P. G. Kostyuk S. L. Mironov A. V. Tepikin P. V. Belan 《The Journal of membrane biology》1989,110(1):11-18
Summary Using the fluorescent probe fura-2, we measured the cytoplasmic concentration of free Ca2+ ([Ca]
i
) and its changes in isolated, nonidentified neurons of the snailHelix pomatia. [Ca]
i
increased during membrane depolarization due to opening of Ca channels in the surface membrane. When the membrane potential returned to the resting level, [Ca]
i
recovered monoexponentially, with the time constant ranging from 10 to 30 sec. The rate of recovery remained unchanged after treatments that interferred with the normal functioning of both Ca/Na exchange and Ca-ATPase in the surface membrane or mitochondria. [Ca]
i
recovery slowed down upon cooling according to Q10=2.3 and after intracellular injection of vanadate. The data obtained suggest that the rate of [Ca]
i
recovery after membrane depolarization is mainly determined by Ca pump of intracellular stores (presumably by the endoplasmic reticulum). Ca release from these stores could be induced in the presence of millimolar caffeine or theophylline in the external medium when [Ca]
i
increased up to a certain threshold level. This depolarization-induced Ca load triggered further transient increase in [Ca]
i
, which was accompanied by membrane hyperpolarization due to the development of Ca-activated potassium conductance. 1mm procaine or tetracaine, but not lidocaine, inhibited this Ca-induced Ca release. In some cases stable oscillations of [Ca]
i
were observed. They could be induced by producing a steady Ca influx by membrane depolarization. 相似文献
74.
Miriam R Faria Mara S Hoshida Eloisa AV Ferro Francesca Ietta Luana Paulesu Estela Bevilacqua 《Reproductive biology and endocrinology : RB&E》2010,8(1):95
Background
Macrophage migration inhibitory factor (MIF) has special pro-inflammatory roles, affecting the functions of macrophages and lymphocytes and counter-regulating the effects of glucocorticoids on the immune response. The conspicuous expression of MIF during human implantation and early embryonic development also suggests this factor acts in reproductive functions. The overall goal of this study was to evaluate Mif expression by trophoblast and embryo placental cells during mouse pregnancy. 相似文献75.
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