Decreased catalase activity is the underlying mechanism of oxidant susceptibility in glucose-6-phosphate dehydrogenase-deficient erythrocytes

Historically, it has been theorized that the oxidant sensitivity of glucose-6-phosphate dehydrogenase (G6PD)-deficient erythrocytes arises as a direct consequence of an inability to maintain cellular gluthione (GSH) levels. This study alternatively hypothesizes that decreased NADPH concentration leads to impaired to catalase activity which, in turn, underlies the observed oxidant susceptibility. To investigate this hypothesis, normal and G6PD-deficient erythrocytes and hemolysates were challenged with a H₂O₂-generating agent. The results of this study demonstrated that catalase activity was severely impaired upon H₂O₂ challenge in the G6PD-deficient cell whiel only decrease was observed in normal cells. Supplmentation of either normal or G6PD-deficient hemolysates with purified NADPH was found to significantly (P < 0.001) inhibit catalase inactivation upon oxidant challenge while addition of NADP⁺ had no effect. Analysis of these results demonstrated direct correlation between NADPH concentration and catalase activity (r = 0.881) and an inverse correlation between catalase activity and erythrocyte oxidant sensitivity (r = 0.906). In contrast, no correlation was found to exist between glutathione concentration (r = 0.170) and oxidant sensitivity. Analysis of NADPH/NADPt ration in acatalasemic mouse erythrocytes demonstrated that NADPH maintenance alone was not sufficient to explain oxidant resistance, and that catalase activity was required. This study supports the hypothesis that impaired catalase activity underlies the enhanced oxidant sensitivity of G6PD-deficient erythrocytes and elucidates the importance of NADPH in the maintenance of normal catalase activity.     

Molecular and chromosomal evolution in anoas (Bovidae: Bubalus spec.)

As a contribution to their taxonomy, population genetic data on zoo-living anoas are reported, and a review of the history of the captive stock is provided. Four different chromosome numbers of 44, 45, 47 and 48 chromosomes have been found, respectively, when karyotyping captive anoas descending from three breeding lines. The number of chromosome arms is 60 throughout, indicating that Robertsonian rearrangements are responsible for this cytogenetic variation. An electrophoretic comparison of isozymes and blood proteins representing 21 genetic loci revealed polymorphism in seven loci: haemoglobin, glyoxalase, superoxide dismutase, phosphoglucomutase, carbonic anhydrase, glucose phosphate isomerase, and an unidentified acid serum protein. Considering the small number of founder specimens and subsequent inbreeding, allozyme variability appears fairly high in anoas. Genetic distances between zoo populations amount to 0.0505 or less. Southern blot hybridizations of restricted DNA from anoas and African buffaloes with a probe from the DRB-like region of the chimpanzee's MHC class II genes also indicate a low degree of genetic differentiation between mountain and lowland anoas. The relevance of these genetic data for the taxonomic classification of mountain and lowland anoas, and for the conservation of anoas by captive breeding is discussed.     

八段锦联合抗阻运动对老年2型糖尿病患者糖脂代谢、氧化应激及生活质量的影响

摘要 目的：探讨八段锦联合抗阻运动对老年2型糖尿病（T2DM）患者糖脂代谢、氧化应激及生活质量的影响。方法：选取2021年4月~2022年5月期间在我院接受治疗的老年T2DM患者238例。按照随机数字表法分为对照组（在常规治疗的基础上,接受抗阻运动干预,119例）和联合组（在对照组的基础上,接受八段锦干预,119例）。观察两组糖脂代谢、氧化应激及生活质量的改善情况。结果：干预12周后,联合组体质量指数、腰臀比低于对照组（P<0.05）。干预12周后,联合组空腹血糖（FBG）、餐后2 h血糖（2hPG）、糖化血红蛋白（HbAlc）低于对照组（P<0.05）。干预12周后,联合组高密度脂蛋白胆固醇（HDL-C）高于对照组（P<0.05）,低密度脂蛋白胆固醇（LDL-C）、总胆固醇（TC）、甘油三酯（TG）低于对照组。干预12周后,联合组丙二醛（MDA）低于对照组,超氧化物歧化酶（SOD）、过氧化氢酶（CAT）高于对照组（P<0.05）。干预12周后,联合组的健康调查简表（SF-36）各维度评分均高于对照组（P<0.05）。结论：八段锦联合抗阻运动用于老年T2DM患者中,可有效改善患者的氧化应激、糖脂代谢,并提高患者的生活质量。     

人红细胞膜上阴离子交换蛋白和葡萄糖运输蛋白的相互影响

用细胞松弛素Ｂ抑制红细胞膜上葡萄糖运输蛋白（ＧｌｕＴ－１）对葡萄糖的运输,观察到对阴离子运输有促进作用。当ＧｌｕＴ－１结合其底物分子－葡萄糖后同样加快了阴离子运输速率．另一方面,实验办给出了葡萄糖跨膜运输特性和Ｃｌ－离子浓度的关系,表明随着Ｃｌ－离子浓度的加大能使葡萄糖运输过程中Ｋｍ减小、Ｖ（ｍａｘ）增大。这些结果表明了在完整红细胞膜上阴离子交换蛋白Ｂａｎｄ３和ＧｌｕＴ－１之间存在着双向联系,即一种膜蛋白的构象改变能影响另一种膜蛋白的功能。     

Invasion of tissue culture cells by diarrhoeagenic strains of Escherichia coli which lack the enteroinvasive inv gene

Abstract Invasive Escherichia coli strains of certain serotypes invade by the same mechanism as the Shigella sp. It has been proposed that invasion of epithelial cells by EPEC strains may also occur; this is a previously overlooked property. In the present study E. coli strains isolated from patients with diarrhoea or ulcerative colitis, lacking the inv plasmid mediating classical invasion, but hybridizing with probes for different adhesins, were analyzed for their ability to invade HeLa and Caco-2 cells. The majority of strains invaded Caco-2 cells to a higher extent than HeLa cells. Adhesion to Caco-2 cells was a prerequisite for subsequent invasion of the cells but EAF, eae , EAgg and other known virulence factors were not sufficient to mediate invasion. In 8/9 E. coli strains invasion was enhanced after growth under iron restriction. Growth during anaerobic conditions did not influence subsequent invasion by E. coli strains whereas 6/9 strains had their invasive ability significantly decreased after growth in the presence of 1% glucose. The invasive process was inhibited by mannose but not by lactose, fucose or galactose. Our data indicate that strains of E. coli may invade Caco-2 cells by novel mechanisms which require adhesion to the cells but which differ from those of Salmonella sp., Yersinia sp., Shigella sp. and classical enteroinvasive E. coli .     

Sodium channels in cultured neuroblastoma cells grown in high glucose or l-Fucose

Patch clamp techniques were used to record whole cell and single channel Na⁺ currents from NB41A3 neuroblastoma cells grown in culture. Cells were grown for two weeks in control medium or medium supplemented with 30 mm d-glucose of 30 mm l-fucose.Cells exposed to glucose or l-fucose had smaller whole cell Na⁺ currents than cells grown in unsupplemented medium, consistent with earlier studies (Yorek, Stefani & Wachtel, 1994). Whole cell macroscopic currents showed no change in activation or inactivation kinetics. Single channel current properties and opening probability were also unchanged.The number of [³H]saxitoxin binding sites, and therefore the total number of Na⁺ channels, was not reduced in cells grown in glucose or l-fucose (Yorek et al., 1994). Therefore, we conclude that some of the channels must have been rendered nonfunctional by the conditioning media. The finding that single channel properties are not altered suggests that channels become nonfunctional in an all-or-none manner.This work was supported by Merit Review Awards to M.A. Yorek and R.E. Wachtel from the Department of Veterans Affairs and by National Institutes of Health grant DK45453 to M.A. Yorek.     

Identification and characterization of regulatory elements in the phosphoenolpyruvate carboxykinase gene PCK1 of Saccharomyces cerevisiae

Phosphoenolpyruvate carboxykinase is a key enzyme in gluconeogenesis. The expression of the PCK1 gene in Saccharomyces cerevisiae is strictly regulated and dependent on the carbon source provided. Two upstream activation sites (UAS1_PCK1 and UAS2_PCK1) and one upstream repression site (URS_PCK1) were localized by detailed deletion analysis. The efficacy of these three promoter elements when separated from each other was confirmed by investigations using heterologous promoter test plasmids. Activation mediated by UAS1_PCK1 or UAS2_PCK1 did not occur in the presence of glucose, indicating that these elements are essential for glucose derepression. The repressing effect caused by URS_PCK1 was much stronger in glucose-grown cells than in ethanol-grown cells.     

陆地棉的核型模式

陆地棉的核型公式为2n=4x=52=30m+20sm(4SAT)+2st(2SAT); 染色体绝对长度平均3.40μm; 臂比值最大与最小的分别是4.02和1.14,平均1.77;随体3对,分别位于第12、19和26对同源染色体的短臂上;最长与最短染色体的比值为2.36;其核型属于Stebbin的2B类型。 Abstract:Karyotype formula of Gossypium hirsutum L.was 2n=4s=52=30m+20m (4SAT)+2st (2SAT); and its absolute lengths of chromosomes averaged 3.40μm; arm ratio differed from 1.24 to 4.02,with the mean value of 1.77; three pairs of satellite chromosomes; the ratio of the longest to the shortest chromosomes was 2.36; and the karyotype belonged to 2B in Stebbin’s classification.     

In Vitro Induction of Apoptosis or Differentiation by Dopamine in an Immortalized Olfactory Neuronal Cell Line

Abstract: Amyloid β-peptide (Aβ) is deposited as insoluble fibrils in the brain parenchyma and cerebral blood vessels in Alzheimer's disease (AD). In addition to neuronal degeneration, cerebral vascular alterations indicative of damage to vascular endothelial cells and disruption of the blood-brain barrier occur in AD. Here we report that Aβ25-35 can impair regulatory functions of endothelial cells (ECs) from porcine pulmonary artery and induce their death. Subtoxic exposures to Aβ25-35 induced albumin transfer across EC monolayers and impaired glucose transport into ECs. Cell death induced by Aβ25-35 was of an apoptotic form, characterized by DNA condensation and fragmentation, and prevented by inhibitors of macromolecular synthesis and endonucleases. The effects of Aβ25-35 were specific because Aβ1-40 also induced apoptosis in ECs with the apoptotic cells localized to the microenvironment of Aβ1-40 aggregates and because astrocytes did not undergo similar changes after exposure to Aβ25-35. Damage and death of ECs induced by Aβ25-35 were attenuated by antioxidants, a calcium channel blocker, and a chelator of intracellular calcium, indicating the involvement of free radicals and dysregulation of calcium homeostasis. The data show that Aβ induces increased permeability of EC monolayers to macromolecules, impairs glucose transport, and induces apoptosis. If similar mechanisms are operative in vivo, then Aβ and other amyloidogenic peptides may be directly involved in vascular EC damage documented in AD and other disorders that involve vascular amyloid accumulation.