排序方式: 共有29条查询结果,搜索用时 31 毫秒
1.
Uric acid, despite being a major antioxidant in the human plasma, both correlates and predicts development of obesity, hypertension, and cardiovascular disease, conditions associated with oxidative stress. While one explanation for this paradox could be that a rise in uric acid represents an attempted protective response by the host, we review the evidence that uric acid may function either as an antioxidant (primarily in plasma) or pro-oxidant (primarily within the cell). We suggest that it is the pro-oxidative effects of uric acid that occur in cardiovascular disease and may have a contributory role in the pathogenesis of these conditions. 相似文献
2.
The phospholipids content in the cortex, hippocamp and stem tissues in rabbits with "late" posttraumatic epileptic focus (1 year after the light brain injury) was estimated. There was established an increase of the content of phosphatidylethanolamine, sphingomyeline, phosphatidylinosite, phosphatidic acid, non-identified phospholipids, decrease of the content of phosphatidylcholine and cardiolipine and appearance of lysophosphatidylcholine in the cortical epileptic focus tissues. The conclusion is made that the changes within the phospholipids pool may cause the epileptogenic disturbance in the neurons, i.e. the changes of functional properties of the excitable membranes and the activity of the mytochondrial phospholipid-dependent enzyme complex. 相似文献
3.
Miguel A. Lanaspa Laura G. Sanchez-Lozada Christina Cicerchi Nanxing Li Carlos A. Roncal-Jimenez Takuji Ishimoto Myphuong Le Gabriela E. Garcia Jeffrey B. Thomas Christopher J. Rivard Ana Andres-Hernando Brandi Hunter George Schreiner Bernardo Rodriguez-Iturbe Yuri Y. Sautin Richard J. Johnson 《PloS one》2012,7(10)
4.
Iu Iu Sautin 《Ukrainski? biokhimicheski? zhurnal》1987,59(4):69-75
The phospholipid composition, content of cholesterol and its esters in the carp (Cyprinus carpio L.) liver microsomes depend on the environmental temperature. The free cholesterol amount and cholesterol/phospholipids ratio in microsomes decrease after the lowering of temperature from 20 to 5 degrees C. The temperature elevation to 30 degrees C results in an increase of the cholesterol ester content. The relative proportions of phosphatidyl choline, phosphatidyl ethanolamine, sphingomyelin, phosphatidyl inositol, phosphatidyl serine, phosphatidic acid increase with a significant decrease of the unidentified phospholipids amount at 30 degrees C. Prolactin affects the cholesterol content and phospholipid composition of liver microsomes. The hormone has a more pronounced effect at subextremal temperatures (5 and 30 degrees C). The actions of prolactin and temperature on the cholesterol content are similar. The hormone influence on the membrane phospholipid composition is opposite to the effect of the temperature acclimation. The possible role of prolactin in the temperature adaptation of the membrane lipids metabolism in poikilotherms is discussed. 相似文献
5.
Miguel A. Lanaspa Laura G. Sanchez-Lozada Yea-Jin Choi Christina Cicerchi Mehmet Kanbay Carlos A. Roncal-Jimenez Takuji Ishimoto Nanxing Li George Marek Murat Duranay George Schreiner Bernardo Rodriguez-Iturbe Takahiko Nakagawa Duk-Hee Kang Yuri Y. Sautin Richard J. Johnson 《The Journal of biological chemistry》2012,287(48):40732-40744
Metabolic syndrome represents a collection of abnormalities that includes fatty liver, and it currently affects one-third of the United States population and has become a major health concern worldwide. Fructose intake, primarily from added sugars in soft drinks, can induce fatty liver in animals and is epidemiologically associated with nonalcoholic fatty liver disease in humans. Fructose is considered lipogenic due to its ability to generate triglycerides as a direct consequence of the metabolism of the fructose molecule. Here, we show that fructose also stimulates triglyceride synthesis via a purine-degrading pathway that is triggered from the rapid phosphorylation of fructose by fructokinase. Generated AMP enters into the purine degradation pathway through the activation of AMP deaminase resulting in uric acid production and the generation of mitochondrial oxidants. Mitochondrial oxidative stress results in the inhibition of aconitase in the Krebs cycle, resulting in the accumulation of citrate and the stimulation of ATP citrate lyase and fatty-acid synthase leading to de novo lipogeneis. These studies provide new insights into the pathogenesis of hepatic fat accumulation under normal and diseased states. 相似文献
6.
Johnson RJ Sautin YY Oliver WJ Roncal C Mu W Gabriela Sanchez-Lozada L Rodriguez-Iturbe B Nakagawa T Benner SA 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》2009,179(1):67-76
Uric acid has historically been viewed as a purine metabolic waste product excreted by the kidney and gut that is relatively
unimportant other than its penchant to crystallize in joints to cause the disease gout. In recent years, however, there has
been the realization that uric acid is not biologically inert but may have a wide range of actions, including being both a
pro- and anti-oxidant, a neurostimulant, and an inducer of inflammation and activator of the innate immune response. In this
paper, we present the hypothesis that uric acid has a key role in the foraging response associated with starvation and fasting.
We further suggest that there is a complex interplay between fructose, uric acid and vitamin C, with fructose and uric acid
stimulating the foraging response and vitamin C countering this response. Finally, we suggest that the mutations in ascorbate
synthesis and uricase that characterized early primate evolution were likely in response to the need to stimulate the foraging
“survival” response and might have inadvertently had a role in accelerating the development of bipedal locomotion and intellectual
development. Unfortunately, due to marked changes in the diet, resulting in dramatic increases in fructose- and purine-rich
foods, these identical genotypic changes may be largely responsible for the epidemic of obesity, diabetes and cardiovascular
disease in today’s society.
Disclaimers Dr Johnson is listed as an inventor on several patent applications related to the role of uric acid in hypertension and metabolic
syndrome; Dr Johnson is also an author for a book on fructose and uric acid (The Sugar Fix) that was published by Rodale in
2008. 相似文献
7.
Phosphatidylinositol 3-kinase-mediated effects of glucose on vacuolar H+-ATPase assembly, translocation, and acidification of intracellular compartments in renal epithelial cells 总被引:1,自引:0,他引:1
下载免费PDF全文
![点击此处可从《Molecular and cellular biology》网站下载免费的PDF全文](/ch/ext_images/free.gif)
Vacuolar H+-ATPases (V-ATPases) are a family of ATP-driven proton pumps. They maintain pH gradients between intracellular compartments and are required for proton secretion out of the cytoplasm. Mechanisms of extrinsic control of V-ATPase are poorly understood. Previous studies showed that glucose is an important regulator of V-ATPase assembly in Saccharomyces cerevisiae. Human V-ATPase directly interacts with aldolase, providing a coupling mechanism for glucose metabolism and V-ATPase function. Here we show that glucose is a crucial regulator of V-ATPase in renal epithelial cells and that the effect of glucose is mediated by phosphatidylinositol 3-kinase (PI3K). Glucose stimulates V-ATPase-dependent acidification of the intracellular compartments in human proximal tubular cells HK-2 and porcine renal epithelial cells LLC-PK1. Glucose induces rapid ATP-independent assembly of the V1 and Vo domains of V-ATPase and extensive translocation of the V-ATPase V1 and Vo domains between different membrane pools and between membranes and the cytoplasm. In HK-2 cells, glucose stimulates polarized translocation of V-ATPase to the apical plasma membrane. The effects of glucose on V-ATPase trafficking and assembly can be abolished by pretreatment with the PI3K inhibitor LY294002 and can be reproduced in glucose-deprived cells by adenoviral expression of the constitutively active catalytic subunit p110alpha of PI3K. Taken together these data provide evidence that, in renal epithelial cells, glucose plays an important role in the control of V-ATPase-dependent acidification of intracellular compartments and V-ATPase assembly and trafficking and that the effects of glucose are mediated by PI3K-dependent signaling. 相似文献
8.
Proliferating cell nuclear antigen (PCNA) as a proliferative marker during embryonic and adult zebrafish hematopoiesis 总被引:4,自引:1,他引:3
Leung AY Leung JC Chan LY Ma ES Kwan TT Lai KN Meng A Liang R 《Histochemistry and cell biology》2005,124(2):105-111
We investigated the expression of proliferative cell nuclear antigen (PCNA) in zebrafish to delineate the proliferative hematopoietic
component during adult and embryonic hematopoiesis. Immunostaining for PCNA and enhanced green fluorescence protein (eGFP)
was performed in wild-type and fli1-eGFP (endothelial marker) and gata1-eGFP (erythroid cell marker) transgenic fish. Expression
of PCNA mRNA was examined in wild-type and chordin morphant embryos. In adult zebrafish kidney, the renal tubules are surrounded
by endothelial cells and it is separated into hematopoietic and excretory compartments. PCNA was expressed in hematopoietic
progenitor cells but not in mature neutrophils, eosinophils or erythroid cells. Some PCNA+ cells are scattered in the hematopoietic
compartment of the kidney while others are closely associated with renal tubular cells. PCNA was also expressed in spermatogonial
stem cells and intestine crypts, consistent with its role in cell proliferation and DNA synthesis. In embryos, PCNA is expressed
in the brain, spinal cord and intermediate cell mass (ICM) at 24 h-post fertilization. In chordin morphants, PCNA is significantly
upregulated in the expanded ICM. Therefore, PCNA can be used to mark cell proliferation in zebrafish hematopoietic tissues
and to identify a population of progenitor cells whose significance would have to be further investigated. 相似文献
9.
10.
Acclimation of carp both to the temperature fall (from 20 to 5 degrees C) and rise (from 20 to 30 degrees C) induces an increase in activity of cytoplasmic liver NADPH-generating enzymes--glucose-6-phosphate dehydrogenase (G6PDG) and malic-enzyme (ME) 6-phosphogluconate dehydrogenase (6PGDG) and NADP-isocitrate dehydrogenase (NADP-IDG) activities are unchanged. Actinomycin D does not prevent cold activation of G6PDG but blocks activation of ME. "Warm" G6PDG has minimal Km value for glucose-6-phosphate and "warm" ME has minimal Km value for glucose-6-phosphate and "warm" ME has minimal Km value for malate at 25 degrees C "Cold" G6PDG and ME have the warmest Km values at 5 degrees C. Isozyme composition of cytoplasmic G6PDG (2 bands with Rf 0.16 and 0.20) does not change within the limits of 5-30 degrees C. The prolactin action on G6PDG and ME is similar to the effect of cold acclimation (activity increases Km value decreases, isozyme pattern (for G6PDG) remains unchanged). It is supposed that activation of G6PDG and ME during cold adaptation may be a result of the prolactin action on substrate-binding ability without changes in the enzyme biosynthesis and isozyme pattern. 相似文献