Chemical hypoxia increases cytosolic Ca2+ and oxygen free radical formation

Borle, A. B.; Barsic, Mark

doi:10.1016/0143-4160(95)90077-2

Cited by 14 publications

(10 citation statements)

References 36 publications

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“…Several lines of evidence suggest that plasmalogens, by virtue of their vinyl ether, act as antioxidants. The generation of ROS during chemical hypoxia has been well established [11,30,31]. Our ability to partly rescue cells with the antioxidant Trolox demonstrated that reactive oxygen generation had a role in the chemical hypoxia-induced cytotoxicity.…”

Section: Discussionmentioning

confidence: 77%

Plasmalogens as endogenous antioxidants: somatic cell mutants reveal the importance of the vinyl ether

Zoeller

Lake

Nagan

et al. 1999

Biochemical Journal

178

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Exposure of plasmalogen-deficient variants of the murine cell line RAW 264.7 to short-term (0-100 min) treatment with electron transport inhibitors antimycin A or cyanide (chemical hypoxia) resulted in a more rapid loss of viability than in the parent strain. Results suggested that plasmalogen-deficient cells were more sensitive to reactive oxygen species (ROS) generated during chemical hypoxia ; the mutants could be rescued from chemical hypoxia by using the antioxidant Trolox, an α-tocopherol analogue, and they were more sensitive to ROS generation by plumbagin or by rose bengal treatment coupled with irradiation. In addition, the use of buffers containing #H # O greatly enhanced the cytotoxic effect of chemical hypoxia, suggesting the involvement of singlet oxygen. We used the unique enzymic deficiencies displayed by the mutants to differentially restore either plasmenylethanolamine (the major plasma-

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Section: Discussionmentioning

confidence: 77%

Plasmalogens as endogenous antioxidants: somatic cell mutants reveal the importance of the vinyl ether

Zoeller

Lake

Nagan

et al. 1999

Biochemical Journal

178

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“…This exposure did not disrupt integrity of the cell membrane, but in combination with reoxygenation not only damaged the capacity of the cell membrane to exclude trypan blue but also reduced cell proliferation. Changes in [Ca2+]i similar to those observed in hypoxic FRTL-5 cells have been observed in hypoxia-induced rat proximal tubule injury (7) and hepatocytes (8). This increase in [Ca2+]¡ may be mediated by the increase in the initial rate of iodide uptake caused by hypoxia (2).…”

Section: Discussionmentioning

confidence: 83%

“…These data are parallel to those obtained with [Ca2+]¡ and InsP3 in these cells. Using specific antibodies against PKC isoforms, we identified a, /3I, ySII, 8, e, and £ isoforms in FRTL-5 cells. The simultaneous expression of these five forms has been observed in PC 12 cells (41), human neuroblastoma SH-SY5Y (42), and human epidermoid A-431 cells (43).…”

Section: Discussionmentioning

confidence: 98%

“…Briefly, each cytosolic and membrane extract was incubated with [32P]-labeled acetylated myelin basic protein (4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14) for 10 sec in buffer containing 5 mM Tris-HCl, 0.5 mM EDTA, 2.5 mM EGTA, 12.5 mM 2-mercaptoethanol. Then 25 pL oí reaction mixture was spotted onto a phosphocellulose disc.…”

Section: Preparation Of Pkc Extractsmentioning

confidence: 99%

“…mediated increases in membrane permeability and activaHypoxia increased [Ca2+]¡ in rat proximal tubule injury tion of phospholipase (3). (7) and rat hepatocytes (8). It is known that an increase in Chronic hypoxia has been shown to inhibit thyroid func-[Ca2+]¡ leads to Ca2+-stimulated Ca2+ release from the intion in humans.…”

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confidence: 99%

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Heat Shock Inhibits the Hypoxia-Induced Effects on Iodide Uptake and Signal Transduction and Enhances Cell Survival in Rat Thyroid FRTL-5 Cells

Kiang¹,

Wang²,

Ding³

et al. 1996

Thyroid

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Chronic hypoxia inhibits rat thyroid function in vivo. To determine possible mechanisms, we studied the effect of hypoxia on iodide uptake, the involvement of second messengers, and cell membrane permeability in rat thyroid FRTL-5 cells. Since sublethal heat stress protects tissues from ischemia, we also determined effects of heat stress. The initial rate of iodide uptake in untreated cells was between 12.98 and 15.28 pmol/micrograms DNA/min. Hypoxia (5% O2) increased the rate of uptake in a time-dependent manner. Heating cells at 45 degrees C for 15 min (heat shock) prior to exposure to hypoxia for 3 days inhibited the increase in the initial rate of I-uptake. Using fura-2, we found that the resting [Ca2+]i in suspended FRTL-5 cells was 65 +/- 7 nM (n = 16). [Ca2+]i was not increased in cells exposed to hypoxia for 1 day, while a 3-day exposure increased [Ca2+]i by 43 +/- 4% (p< 0.05); no additional increase occurred after 7 days of exposure. When cells were heated prior to hypoxia exposure for 3 days, the hypoxia-induced increase in [Ca2+]i did not occur. Similar observations were found with inositol trisphosphates (InsP3). Exposure of cells to hypoxia for 3 days increased InsP3 from 0.08 +/- 0.02 (n = 5) to 0.32 +/- 0.04% total cpm (n = 5, p < 0.05), but sublethal heating of cells prior to hypoxia exposure prevented the increase. Three-day hypoxia increased PKC activity in the membrane fraction (from 67 +/- 7 to 86 +/- 4% of total activity, p < 0.05), and heat shock inhibited these changes also. Immunoblots showed that hypoxia treatment alone and heat shock plus hypoxia resulted in the translocation of PKC-alpha, -delta, -epsilon, and -zeta isoforms, whereas heat shock alone translocated only PKC-beta I, -beta II, and -zeta. Cell membrane integrity was assayed by trypan blue exclusion. Hypoxia alone for 3 days did not affect membrane permeability, but only 49 +/- 3% of cells excluded trypan blue when a 3-day hypoxia exposure was followed by a 6 h reoxygenation. Heat shock prior to hypoxia and reoxygenation protected cell membrane function. Heat shock also induced heat shock protein 70 kDa (HSP-70) synthesis at the transcriptional level. Results suggest that heat shock protects FRTL-5 cells from hypoxic injury, perhaps by inhibiting the initial rate of iodide uptake and second messengers. It is likely that HSP-70 plays an essential role in the process of protection.

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The role of calcium and nitric oxide during liver enzyme release induced by increased physical forces as evidenced in partially hepatectomized rats

Díaz-Juárez¹,

Hernández‐Muñoz²

2011

Liver Transpl

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Although increased plasma enzyme activities could be diagnostic for tissue damage, the mechanisms controlling cellular enzyme release remain poorly understood. We found a selective and drastic elevation of serum enzyme activities accompanying rat liver regeneration after partial hepatectomy (PH), apparently controlled by a mechanism dependent on flow-bearing physical forces. In fact, this study assesses a putative role of calcium mobilization and nitric oxide (NO) production underlying rat liver enzyme release. The role of increased shear stress (by enhancing viscosity during perfusion) and the participation of cell calcium and NO were tested in isolated livers subjected to increasing flow rate. After PH, there was a drastic elevation of serum activities for liver enzyme markers, clearly predominating those of mitochondrial localization. Liver enzyme release largely depended on extracellular calcium entry, probably mediated by stretch-sensitive calcium channels, as well as by increasing NO production. However, these effects were differentially observed when comparing liver enzymes from cytoplasmic or mitochondrial compartments. Moreover, a possible role for cell-mediated mechanotransduction in liver enzyme release was suggested by increasing shear stress (high viscosity), which also selectively affected the release of the enzymes tested. Therefore, we show, for the first time, that flow-induced shear stress can control the amount of hepatic enzymes released into the bloodstream, which is largely regulated through modifications in cell calcium mobilization and production of liver NO, events markedly elevated in the proliferating rat liver. Liver Transpl 17:334-343, 2011. V C 2011 AASLD.Received May 13, 2010; accepted November 16, 2010.Above-normal plasma enzyme activities are considered as diagnostic features for several diseases, 1 and it seems that every organ can elicit a specific pattern of enzyme release. In fact, this phenomenon usually follows a respective gradient of concentration between an organ, such as the liver, and the blood compartments. [2][3][4] Moreover, values of released enzymes are much higher than the apparent disappearance rates constants and are consistent akin to decreasing concentration levels within the plasma, as reported for lactate dehydrogenase (LDH) and aspartate (AST) and alanine (ALT) aminotransferases after acute liver injury. 5 However, the mechanisms controlling cellular enzyme release remain poorly understood.A drastic increase of serum activities of ''liver enzyme markers'' does not necessarily have to reflect liver cell death, and indeed we demonstrated recently that an important fraction of the released hepatic enzymes depends largely on hemodynamic changes in the rat liver. 6 Taking advantage of the model of twoAbbreviations: ALT, alanine aminotransferase; AST, aspartate aminotransferase; ATP, adenosine triphosphate; [Ca 2þ ] i , intracellular calcium

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Chemical hypoxia increases cytosolic Ca2+ and oxygen free radical formation

Cited by 14 publications

References 36 publications

Plasmalogens as endogenous antioxidants: somatic cell mutants reveal the importance of the vinyl ether

Plasmalogens as endogenous antioxidants: somatic cell mutants reveal the importance of the vinyl ether

Heat Shock Inhibits the Hypoxia-Induced Effects on Iodide Uptake and Signal Transduction and Enhances Cell Survival in Rat Thyroid FRTL-5 Cells

The role of calcium and nitric oxide during liver enzyme release induced by increased physical forces as evidenced in partially hepatectomized rats

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