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排序方式: 共有62条查询结果,搜索用时 171 毫秒
1.
Timothy A. McCaffrey Constantine Tziros Jannet Lewis Richard Katz Robert Siegel William Weglicki Jay Kramer I. Tong Mak Ian Toma Liang Chen Elizabeth Benas Alexander Lowitt Shruti Rao Linda Witkin Yi Lian Yinglei Lai Zhaoqing Yang Sidney W. Fu 《International journal of biological sciences》2013,9(4):350-360
2.
Benjamin F. Dickens T. Russel Snow Vickie Green William B. Weglicki 《Molecular and cellular biochemistry》1988,79(1):91-94
Summary The apparent membrane fluorescence anisotropy of 1,6-diphenyl-1,3,5-hexatriene has been reported to be lower in intact erythrocytes than in isolated erythrocyte membranes. Although this difference was once suggested to be caused by the fluidizing effect associated with the loss of erythrocyte proteins during membrane isolation, it is currently thought to be an artifact resulting from intense light scattering properties of intact erythrocytes which overwhelm extrapolation methods of correcting for light scattering. This study confirmed that, at erythrocyte concentrations greater than 107 cells/ml, this difference was caused by intense light scattering; however, at erythrocyte concentrations less than 4.0 × 106 cells/ml, the anisotropy values for erythrocytes and isolated membranes are identical, demonstrating that intense light scattering can be overcome with dilute suspensions of cells. 相似文献
3.
4.
Scanlan BJ Tuft B Elfrey JE Smith A Zhao A Morimoto M Chmielinska JJ Tejero-Taldo MI Mak IuT Weglicki WB Shea-Donohue T 《Molecular and cellular biochemistry》2007,306(1-2):59-69
The aim of this study was to determine the effect of magnesium deficiency on small intestinal morphology and function. Rats
were assigned to 4 groups and placed on magnesium sufficient or deficient diet for 1 or 3 weeks. Infiltration of neutrophils
and mucosal injury were assessed in stained sections of small intestine. Magnesium deficiency alone induced a significant
increase in neutrophil infiltration and increased vascular ICAM-1 expression, in the absence of changes in mucosal injury
or expression of proinflammatory mediators. Magnesium deficiency was associated with hyposecretory epithelial cell responses
and vascular macromolecular leak in the small intestine and lung, which was attributed partly to reduced expression of NOS-3.
To determine the effect of hypomagnesmia on the intestinal responses to a known oxidative stress, groups of rats were randomized
to either sham operation or superior mesenteric artery occlusion for 10 (non-injurious) or 30 (injurious) minutes followed
by a 1- or 4-hour reperfusion period. In response to mesenteric ischemia/reperfusion, deficient rats showed exaggerated PMN
influx, but similar mucosal injury. Intestinal ischemia in sufficient animals induced vascular macromolecular leak in the
small intestine and lung at 4 hours of reperfusion, with levels similar to those observed in untreated deficient rats. Acute
magnesium repletion of deficient rats 24 h before surgery attenuated the exaggerated inflammation in deficient rats. These
data show that magnesium deficiency induced a subclinical inflammation in the small intestine in the absence of mucosal injury,
but with significant functional changes in local and remote organs and increased sensitivity to oxidative stress.
The opinions contained herein are those of the authors and are not to be construed as official policy or reflecting the views
of the Department of Defense 相似文献
5.
Mg-Gluconate provides superior protection against postischemic dysfunction and oxidative injury compared to Mg-sulfate 总被引:1,自引:0,他引:1
Murthi SB Wise RM Weglicki WB Komarov AM Kramer JH 《Molecular and cellular biochemistry》2003,245(1-2):141-148
Cardioprotection by Mg Sulfate (MgSO4) during ischemia/reperfusion (I/R) is attributed largely to the Mg2+ cation. However, Mg-gluconate (MgGl2) may provide added benefit, possibly through its anion's antioxidant properties. Protective effects of both Mg-salts and their anions during 30 min global I and 50 min R were assessed in Langendorff-perfused (Krebs-Henseleit buffer) rat hearts. Recovery of function was compared between untreated hearts and those receiving supplement (2.4 mM MgGl2, MgSO4, or Na2SO4, or 4.8 mM NaGI) for 5 min prior to I and during the initial 30 min R. The final 20 min R was conducted without supplement. End diastolic pressure (EDP, mmHg) of the 50 min reperfused MgGl2 group (2.6) was lower than MgSO4 (16.2) and untreated (35.6) groups, and the NaGI group (25.2) was considerably lower than Na2SO4 (38.8). Recovery of developed pressure (% preischemic DP) at the onset of R for MgGl2 (74.9) was greater than MgSO4 (37.9) and untreated (33.2). After 50 min, MgGl2 (77.9) and MgSO4 (66.9) provided protection compared to untreated (51.8). In separate studies, ESR spin trapping with alpha-phenyl-N-tert-butylnitrone (3 mM PBN) showed that I/R alkoxyl radical production was reduced with MgGl2 (0.0 vs. 2.4 vs. 3.6 mM: 184 vs. 97 vs. 54.8 nM/g tissue x min) to a greater extent than seen with MgSO4 (3.6 mM: 108). Additional studies suggest that Gl(1-), unlike SO4(2-), may scavenge hydroxyl radicals, accounting for the added protection. MgGl2 treated hearts exhibited less postischemic dysfunction and oxidative injury compared to MgSO4, suggesting the contribution of Gl(1-) to cardioprotection. 相似文献
6.
J H Kramer F G Lightfoot W B Weglicki 《Cellular and molecular biology, including cyto-enzymology》2000,46(8):1313-1327
We determined whether prior treatment of rats (study 1) with subthreshold doses of iron (no evidence of cardiac tissue overload), or in vitro ischemic pre-conditioning (IP: 5 min. Ischemia (I)/5 min. Reperfusion (R) x 2 cycles) of hearts from untreated rats (study 2), can modulate redox-active cardiac tissue iron levels or distribution, leading to alterations in post-ischemic lipid peroxidation-derived free radical (FR) production and severity of reperfusion injury. In study 1, rats received biweekly i.p. injections of 0 (saline=S), 3, 6, or 12 mg FeCl3/ml for 3-wks prior to imposing 30 min. I/15 min. R in vitro. The highest dose caused no elevations in plasma or heart tissue Fe levels, but did further reduce post-ischemic recoveries of left ventricular developed pressure (17% lower), cardiac work (57%) and output (54%), and increased effluent lipid hydroperoxides (2.1-fold) compared to the S-group. Post-ischemic FR production was assessed in toluene-extracted effluent by ESR spectroscopy and alpha-phenyl-N-tert butylnitrone (PBN=2.5 mM perfusate) spin trapping. PBN/alkoxyl (alphaH=1.90 G, alphaN=13.63 G) was the dominant signal detected in all groups; however, Fe-treated groups displayed significant dose-dependent increases in total alkoxyl content (3, 6, 12 mg/ml: 1.8-, 2.3-, 2.7-fold higher) compared to the S-group. These data suggest that even mild, non-overloading doses of iron can be functionally and oxidatively detrimental to hearts when an I/R stress is imposed. In study 2, isolated hearts from untreated rats were exposed to two-IP cycles: during IP, total effluent iron content (atomic absorption) increased 11.4-fold compared to control and analysis of cardiovascular tissue iron distribution (X-ray microanalysis) suggested that iron loss from capillary endothelium was far greater than from tissue myocytes. Moreover, iron-catalyzed production of alkoxyl radicals following severe I/R stress (40 min. I/15 min. R) was substantially lower (73%) in IP hearts compared to the non-IP counterparts. These preliminary findings suggest that cardioprotection resulting from IP may, in part, be related to IP-induced release of cardiovascular endothelial iron (redox-active) prior to imposing severe I/R stress. 相似文献
7.
Chmielinska JJ Tejero-Taldo MI Mak IT Weglicki WB 《Molecular and cellular biochemistry》2005,278(1-2):53-57
Substance P is elevated in plasma and in other tissues during Mg-deficiency, and was found localised to neuronal C-fibres
of cardiac and intestinal tissues, where it could promote neurogenic inflammation. Plasma prostaglandin E2 (PGE2), indicative of systemic inflammation, rose significantly (≥4 fold, p<0.01) after 1 week and remained elevated through week 2 and 3 in rat on the Mg-deficient (MgD) diet. Concomitantly, total
blood glutathione decreased by 50%. Immunohistochemical staining for endotoxin (lipopolysaccaride, LPS) receptor, CD14 was
prominent in macrophage-type cells in intestinal tissue; more importantly, cardiac tissue revealed both CD11b (monocyte/macrophage
surface protein) and CD14 positive cells after 3 weeks in rats on MgD diet. Western blot analysis indicated a significant
increase in the endotoxin receptor protein level in the 3 week MgD hearts. Since CD14 is known to be up-regulated in cells
exposed to LPS, these observations suggest that prolonged Mg-deficiency results in increased intestinal permeability to bacterial
products that induce the endotoxin receptor in cells localized to myocardial and intestinal tissues. These CD14 positive cells
may amplify the cardiomyopathic inflammatory process by stimulating TNF-α and other pro-inflammatory cytokines. (Mol Cell
Biochem 278: 53–57, 2005) 相似文献
8.
9.
Komarov Andrei M. Kramer Jay H. Mak I. Tong Weglicki William B. 《Molecular and cellular biochemistry》1997,175(1-2):91-97
Spin-trapping techniques combined with electron paramagnetic resonance (EPR) spectroscopy to measure nitric oxide (·NO) production were compared in the ischemic-reperfused myocardium for the first time, using both aqueous-soluble and lipophilic complexes of reduced iron (Fe) with dithiocarbamate derivatives. The aqueous-soluble complex of Fe and N-methyl-D-glucamine dithiocarbamate (MGD) formed MGD2-Fe-NO complex with a characteristic triplet EPR signal (aN12.5 G and giso = 2.04) at room temperature, in native isolated rat hearts following 40 min global ischemia and 15 min reperfusion. Diethyldithiocarbamate (DETC) and Fe formed in ischemic-reperfused myocardium the lipophilic DETC2-Fe-NO complex exhibiting an EPR signal (g = 2.04 and g = 2.02 at 77K) with a triplet hyperfine structure at g. Dithiocarbamate-Fe-NO complexes detected by both trapping agents were abolished by the ·NO synthase inhibitor, NG-nitro-L-arginine methyl ester. Quantitatively, both trapping procedures provi ded similar values for tissue ·NO production, which were observed primarily during ischemia. Postischemic hemodynamic recovery of the heart was not affected by the trapping procedure. (Mol Cell Biochem 175: 91–97, 1997) 相似文献
10.
Mak I. Tong Dickens Benjamin F. Komarov Andrei M. Wagner Tammy L. Phillips Terry M. Weglicki William B. 《Molecular and cellular biochemistry》1997,176(1-2):35-39
Sprague-Dawley rats (200 g) were fed either a Mg-deficient or Mg-sufficient diet for 3 weeks. An enriched neutrophil fraction (>85%) was isolated from the blood by sodium metrizoate/dextran gradient centrifugation. Using the superoxide dismutase (SOD)-inhibitable cytochrome c reduction assay, the basal activity of neutrophils isolated from the Mg-deficient rats were found elevated 5 fold after two weeks, and up to 7 fold after three weeks on the diet. Upon challenge by phorbol myristate acetate (PMA), unlike the Mg-sufficient cells, the Mg-deficient cells exhibited no significant activation. Treatment of the Mg-deficient rats with the nitric oxide (NO)-synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME) in the drinking water, significantly attenuated the basal superoxide producing activity of the neutrophils and partially restored its response to PMA challenge. In association with the neutrophil activation. Mg-deficiency resulted in 70% decrease in plasma glutathione and 220% increase in Fe-promoted, thiobarbituric acid reactive substance (TBARS) levels; both changes were significantly attenuated by L-NAME treatment. The results suggest that neutrophils from Mg-deficient rats are activated endogenously to generate oxy-radicals which might directly mediate the in vivo peroxidative indices during Mg-deficiency. Furthermore, the neutrophil activity was lowered by NO-synthase inhibition suggesting that NO overproduction during Mg-deficiency participates in the neutrophil activation process. 相似文献