Biochimica et biophysica acta最新文献_第9页

Effects of chronic renal failure on caveolin-1, guanylate cyclase and AKT protein expression. 慢性肾功能衰竭对小窝蛋白-1、鸟苷酸环化酶和AKT蛋白表达的影响。

Biochimica et biophysica acta Pub Date : 2004-11-05 DOI: 10.1016/j.bbadis.2004.06.013

Ram K Sindhu, Ashkan Ehdaie, Nosratola D Vaziri, Christian K Roberts

{"title":"Effects of chronic renal failure on caveolin-1, guanylate cyclase and AKT protein expression.","authors":"Ram K Sindhu, Ashkan Ehdaie, Nosratola D Vaziri, Christian K Roberts","doi":"10.1016/j.bbadis.2004.06.013","DOIUrl":"https://doi.org/10.1016/j.bbadis.2004.06.013","url":null,"abstract":"Chronic renal failure (CRF) has been documented to cause oxidative stress and alter nitric oxide (NO) metabolism. However, the effect of CRF on proteins related to NO bioactivity has not been investigated. The present study was designed to test the hypothesis that CRF would induce changes in caveolin-1 (Cav-1), soluble guanylate cyclase (sGC) and Akt, three proteins important in regulating NO synthase (NOS) functionality. Male Sprague-Dawley rats were randomized to CRF via 5/6 nephrectomy or sham-operated control groups. After 6 weeks, body weight, blood pressure, creatinine clearance, plasma creatinine, urinary cyclic guanosine monophosphate (cGMP) and immunodetectable levels of Cav-1, sGC and Akt were determined in the renal, aorta, heart and liver tissues from both groups. CRF resulted in marked decreases in body weight and creatinine clearance, and elevation of blood pressure and plasma creatinine. An apparent upregulation of sGC protein abundance in renal tissue was noted, with no change in aorta, heart and liver. This was accompanied by a reduction in urinary cGMP levels, indicative of sGC dysfunction. Cav-1 protein abundance was increased in aortic, liver and renal tissues. In contrast, CRF depressed Akt abundance in aorta, heart and liver tissues. These data document that CRF is characterized by alteration in the abundance of proteins regulating NO function in hepatic, vascular, cardiac and renal tissues, and a decrease in cGMP, which contributes to hypertension and changes in NO bioactivity previously noted in this model.","PeriodicalId":8811,"journal":{"name":"Biochimica et biophysica acta","volume":"1690 3","pages":"231-7"},"PeriodicalIF":0.0,"publicationDate":"2004-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.bbadis.2004.06.013","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24784660","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 32

Identification and characterisation of a novel KCNQ1 mutation in a family with Romano-Ward syndrome. 罗曼诺-沃德综合征家族中一个新的KCNQ1突变的鉴定和特征

Biochimica et biophysica acta Pub Date : 2004-11-05 DOI: 10.1016/j.bbadis.2004.06.024

J Zehelein, D Thomas, M Khalil, A-B Wimmer, M Koenen, M Licka, K Wu, J Kiehn, K Brockmeier, V A W Kreye, C A Karle, H A Katus, H E Ulmer, W Schoels

{"title":"Identification and characterisation of a novel KCNQ1 mutation in a family with Romano-Ward syndrome.","authors":"J Zehelein, D Thomas, M Khalil, A-B Wimmer, M Koenen, M Licka, K Wu, J Kiehn, K Brockmeier, V A W Kreye, C A Karle, H A Katus, H E Ulmer, W Schoels","doi":"10.1016/j.bbadis.2004.06.024","DOIUrl":"https://doi.org/10.1016/j.bbadis.2004.06.024","url":null,"abstract":"Romano-Ward syndrome (RWS), the autosomal dominant form of the congenital long QT syndrome, is characterised by prolongation of the cardiac repolarisation process associated with ventricular tachyarrhythmias of the torsades de pointes type. Genetic studies have identified mutations in six ion channel genes, KCNQ1, KCNH2, SCN5A, KCNE1 and KCNE2 and the accessory protein Ankyrin-B gene, to be responsible for this disorder. Single-strand conformation polymorphism (SSCP) analysis and subsequent DNA sequence analysis have identified a KCNQ1 mutation in a family that were clinically conspicuous due to several syncopes and prolonged QTc intervals in the ECG. The mutant subunit was expressed and functionally characterised in the Xenopus oocyte expression system. A novel heterozygous missense mutation with a C to T transition at the first position of codon 343 (CCA) of the KCNQ1 gene was identified in three concerned family members (QTc intervals: 500, 510 and 530 ms, respectively). As a result, proline 343 localised within the highly conserved transmembrane segment S6 of the KCNQ1 channel is replaced by a serine. Co-expression of mutant (KCNQ1-P343S) and wild-type (KCNQ1) cRNA in Xenopus oocytes produced potassium currents reduced by approximately 92%, while IKs reconstitution experiments with a combination of KCNQ1 mutant, wild-type and KCNE1 subunits yielded currents reduced by approximately 60%. A novel mutation (P343S) identified in the KCNQ1 subunit gene of three members of a RWS family showed a dominant-negative effect on native IKs currents leading to prolongation of the heart repolarisation and possibly increases the risk of malign arrhythmias with sudden cardiac death.","PeriodicalId":8811,"journal":{"name":"Biochimica et biophysica acta","volume":"1690 3","pages":"185-92"},"PeriodicalIF":0.0,"publicationDate":"2004-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.bbadis.2004.06.024","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24784742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 16

The oxidants hypochlorite and hydrogen peroxide induce distinct patterns of acute lung injury. 氧化剂次氯酸盐和过氧化氢诱导急性肺损伤的不同模式。

Biochimica et biophysica acta Pub Date : 2004-11-05 DOI: 10.1016/j.bbadis.2004.07.003

Stefan Hammerschmidt, Hans Wahn

{"title":"The oxidants hypochlorite and hydrogen peroxide induce distinct patterns of acute lung injury.","authors":"Stefan Hammerschmidt, Hans Wahn","doi":"10.1016/j.bbadis.2004.07.003","DOIUrl":"https://doi.org/10.1016/j.bbadis.2004.07.003","url":null,"abstract":"Oxidative stress due to activated neutrophils, macrophages and endothelial cells plays a crucial role in acute lung injury. This study compares the effects of the nonradical oxidants hypochlorite (HOCl) and hydrogen peroxide (H2O2) on pulmonary artery pressure [PAPtorr], capillary filtration coefficient (Kf,c), tissue lipid peroxidation (LPO) and reduced glutathione (GSH) depletion. HOCl, H2O2 (1000 nmol min(-1)) or buffer (control) is infused into isolated rabbit lungs. PAP, K(f,c) and lung weight were measured. Experiments were terminated after 105 min or when fluid retention exceeded 50 g. Lung tissue was analyzed for LPO products and GSH. The oxidants induced comparable maximum effects. However, the patterns of lung injury were distinct: H2O2 infusion evoked an early biphasic pressure response (DeltaPAPmax 2.8+/-0.22/4.2+/-0.37 after 5.7+/-1.4/39+/-4.0 min) and a sixfold increase in Kf,c after 90 min. HOCl application caused a late pressure response (DeltaPAPmax 7.6+/-1.7 after 50.6+/-3.7 min) and a sevenfold increase in Kf,c after 60 min. H2O2-induced effects were attenuated by desferal. This may suggest an involvement of transition metal catalysed hydroxyl radical formation. Different oxidants induced distinct patterns of changes in PAP and Kf,c , which are accompanied by a comparable accumulation of LPO products and by a distinct degree of GSH depletion.","PeriodicalId":8811,"journal":{"name":"Biochimica et biophysica acta","volume":"1690 3","pages":"258-64"},"PeriodicalIF":0.0,"publicationDate":"2004-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.bbadis.2004.07.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24784663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 30

Anti-amyloidogenic activity of tannic acid and its activity to destabilize Alzheimer's beta-amyloid fibrils in vitro. 单宁酸的抗淀粉样蛋白生成活性及其体外破坏阿尔茨海默β -淀粉样蛋白原纤维的活性。

Biochimica et biophysica acta Pub Date : 2004-11-05 DOI: 10.1016/j.bbadis.2004.06.008

Kenjiro Ono, Kazuhiro Hasegawa, Hironobu Naiki, Masahito Yamada

{"title":"Anti-amyloidogenic activity of tannic acid and its activity to destabilize Alzheimer's beta-amyloid fibrils in vitro.","authors":"Kenjiro Ono, Kazuhiro Hasegawa, Hironobu Naiki, Masahito Yamada","doi":"10.1016/j.bbadis.2004.06.008","DOIUrl":"https://doi.org/10.1016/j.bbadis.2004.06.008","url":null,"abstract":"Inhibition of the accumulation of amyloid beta-peptide (Abeta) and the formation of beta-amyloid fibrils (fAbeta) from Abeta, as well as the destabilization of preformed fAbeta in the CNS would be attractive therapeutic targets for the treatment of Alzheimer's disease (AD). We previously reported that nordihydroguaiaretic acid (NDGA) and wine-related polyphenols inhibit fAbeta formation from Abeta(1-40) and Abeta(1-42) as well as destabilizing preformed fAbeta(1-40) and fAbeta(1-42) dose-dependently in vitro. Using fluorescence spectroscopic analysis with thioflavin T and electron microscopic studies, we examined the effects of polymeric polyphenol, tannic acid (TA) on the formation, extension, and destabilization of fAbeta(1-40) and fAbeta(1-42) at pH 7.5 at 37 degrees C in vitro. We next compared the anti-amyloidogenic activities of TA with myricetin, rifampicin, tetracycline, and NDGA. TA dose-dependently inhibited fAbeta formation from Abeta(1-40) and Abeta(1-42), as well as their extension. Moreover, it dose-dependently destabilized preformed fAbetas. The effective concentrations (EC50) of TA for the formation, extension and destabilization of fAbetas were in the order of 0-0.1 microM. Although the mechanism by which TA inhibits fAbeta formation from Abeta as well as destabilizes preformed fAbeta in vitro is still unclear, it could be a key molecule for the development of therapeutics for AD.","PeriodicalId":8811,"journal":{"name":"Biochimica et biophysica acta","volume":"1690 3","pages":"193-202"},"PeriodicalIF":0.0,"publicationDate":"2004-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.bbadis.2004.06.008","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24784743","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 242

Deamidation and cross-linking of gliadin peptides by transglutaminases and the relation to celiac disease. 谷氨酰胺转胺酶对麦胶蛋白肽的脱酰胺和交联及其与乳糜泻的关系。

Biochimica et biophysica acta Pub Date : 2004-11-05 DOI: 10.1016/j.bbadis.2004.06.009

Hanne Skovbjerg, Claus Koch, Dorit Anthonsen, Hans Sjöström

{"title":"Deamidation and cross-linking of gliadin peptides by transglutaminases and the relation to celiac disease.","authors":"Hanne Skovbjerg, Claus Koch, Dorit Anthonsen, Hans Sjöström","doi":"10.1016/j.bbadis.2004.06.009","DOIUrl":"https://doi.org/10.1016/j.bbadis.2004.06.009","url":null,"abstract":"Activation of small intestinal gluten-reactive CD4+ T cells is a critical event in celiac disease. Such cells predominantly recognise gluten peptides in which specific glutamines are deamidated. Deamidation may be catalysed by intestinal tissue transglutaminase (TG2), a protein which is also the main autoantigen in celiac disease. Our aim was to study how the two main catalytic activities of transglutaminase--deamidation and transamidation (cross-linking) of an immunodominant gliadin epitope--are influenced by the presence of acceptor amines in the intestinal mucosa, and thereby contribute to further elucidation of the pathogenetic mechanisms in celiac disease. We prepared monoclonal antibodies, reacting specifically with the non-deamidated epitope QPFPQPQLPYPQPQ-amide and/or the deamidated epitope QPFPQPELPYPQPQ-amide. A solid phase immunoassay combined with gel filtration chromatography was used to analyse deamidation and cross-linking of these peptides to proteins. Our results show that QPFPQPQLPYPQPQ-amide was deamidated when incubated with purified TG2, with fresh mucosal sheets and with mucosal homogenates. Of other transglutaminases tested, only Streptoverticillium transglutaminase was able to generate the deamidated epitope. A fraction of the non-deamidated epitope was cross-linked to proteins, including TG2. The results suggest that intestinal TG2 is responsible for generation of the active deamidated epitope. As the epitope often occurs in a repeat structure, the result may be cross-linking of a deamidated, i.e., activated cell epitope. Alternatively, the deamidation may occur by reversal of the cross-linking reaction. The results provide a basis for the suggestion that binding of a peptide to a protein, in connection to its modification to a T cell epitope, might be a general explanation for the role of TG2 in celiac disease and a possible mechanism for the generation of autoantigens.","PeriodicalId":8811,"journal":{"name":"Biochimica et biophysica acta","volume":"1690 3","pages":"220-30"},"PeriodicalIF":0.0,"publicationDate":"2004-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.bbadis.2004.06.009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24784746","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 70

Significantly increased fractions of transformed to total alpha2-macroglobulin concentrations in plasma from patients with multiple sclerosis. 多发性硬化症患者血浆中转化到总α - 2巨球蛋白浓度显著增加。

Biochimica et biophysica acta Pub Date : 2004-11-05 DOI: 10.1016/j.bbadis.2004.06.010

Poul Erik H Jensen, Signe Humle Jørgensen, Pameli Datta, Per Soelberg Sørensen

引用次数: 21

Methylthioadenosine phosphorylase gene expression is impaired in human liver cirrhosis and hepatocarcinoma. 甲基硫代腺苷磷酸化酶基因在肝硬化和肝癌中表达受损。

Biochimica et biophysica acta Pub Date : 2004-11-05 DOI: 10.1016/j.bbadis.2004.08.002

Carmen Berasain, Henar Hevia, Jokin Fernández-Irigoyen, Esther Larrea, Juan Caballería, José M Mato, Jesús Prieto, Fernando J Corrales, Elena R García-Trevijano, Matías A Avila

{"title":"Methylthioadenosine phosphorylase gene expression is impaired in human liver cirrhosis and hepatocarcinoma.","authors":"Carmen Berasain, Henar Hevia, Jokin Fernández-Irigoyen, Esther Larrea, Juan Caballería, José M Mato, Jesús Prieto, Fernando J Corrales, Elena R García-Trevijano, Matías A Avila","doi":"10.1016/j.bbadis.2004.08.002","DOIUrl":"https://doi.org/10.1016/j.bbadis.2004.08.002","url":null,"abstract":"Methylthioadenosine phosphorylase (MTAP) is a key enzyme in the methionine and adenine salvage pathways. In mammals, the liver plays a central role in methionine metabolism, and this essential function is lost in the progression from liver cirrhosis to hepatocarcinoma. Deficient MTAP gene expression has been recognized in many transformed cell lines and tissues. In the present work, we have studied the expression of MTAP in human and experimental liver cirrhosis and hepatocarcinoma. We observe that MTAP gene expression is significantly reduced in human hepatocarcinoma tissues and cell lines. Interestingly, MTAP gene expression was also impaired in the liver of CCl4-cirrhotic rats and cirrhotic patients. We provide evidence indicating that epigenetic mechanisms, involving DNA methylation and histone deacetylation, may play a role in the silencing of MTAP gene expression in hepatocarcinoma. Given the recently proposed tumor suppressor activity of MTAP, our observations can be relevant to the elucidation of the molecular mechanisms of multistep hepatocarcinogenesis.","PeriodicalId":8811,"journal":{"name":"Biochimica et biophysica acta","volume":"1690 3","pages":"276-84"},"PeriodicalIF":0.0,"publicationDate":"2004-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.bbadis.2004.08.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24784665","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 35

Transgenic mouse expressing human mutant alpha-galactosidase A in an endogenous enzyme deficient background: a biochemical animal model for studying active-site specific chaperone therapy for Fabry disease. 在内源性酶缺乏背景下表达人α -半乳糖苷酶A突变体的转基因小鼠:研究法布里病活性位点特异性伴侣治疗的生化动物模型

Biochimica et biophysica acta Pub Date : 2004-11-05 DOI: 10.1016/j.bbadis.2004.07.001

Satoshi Ishii, Hidekatsu Yoshioka, Kazuaki Mannen, Ashok B Kulkarni, Jian-Qiang Fan

{"title":"Transgenic mouse expressing human mutant alpha-galactosidase A in an endogenous enzyme deficient background: a biochemical animal model for studying active-site specific chaperone therapy for Fabry disease.","authors":"Satoshi Ishii, Hidekatsu Yoshioka, Kazuaki Mannen, Ashok B Kulkarni, Jian-Qiang Fan","doi":"10.1016/j.bbadis.2004.07.001","DOIUrl":"https://doi.org/10.1016/j.bbadis.2004.07.001","url":null,"abstract":"Fabry disease is an inborn error of glycosphingolipid metabolism caused by the deficiency of lysosomal alpha-galactosidase A (alpha-Gal A). We have established transgenic mice that exclusively express human mutant alpha-Gal A (R301Q) in an alpha-Gal A knock-out background (TgM/KO mice). This serves as a biochemical model to study and evaluate active-site specific chaperone (ASSC) therapy for Fabry disease, which is specific for those missense mutations that cause misfolding of alpha-Gal A. The alpha-Gal A activities in the heart, kidney, spleen, and liver of homozygous TgM/KO mice were 52.6, 9.9, 29.6 and 44.4 unit/mg protein, respectively, corresponding to 16.4-, 0.8-, 0.6- and 1.4-fold of the endogenous enzyme activities in the same tissues of non-transgenic mice with a similar genetic background. Oral administration of 1-deoxygalactonojirimycin (DGJ), a competitive inhibitor of alpha-Gal A and an effective ASSC for Fabry disease, at 0.05 mM in the drinking water of the mice for 2 weeks resulted in 13.8-, 3.3-, 3.9-, and 2.6-fold increases in enzyme activities in the heart, kidney, spleen and liver, respectively. No accumulation of globotriaosylceramide, a natural substrate of alpha-Gal A, could be detected in the heart of TgM/KO mice after DGJ treatment, indicating that degradation of the glycolipid in the heart was not inhibited by DGJ at that dosage. The alpha-Gal A activity in homozygous or heterozygous fibroblasts established from TgM/KO mice (TMK cells) was approximately 39 and 20 unit/mg protein, respectively. These TgM/KO mice and TMK cells are useful tools for studying the mechanism of ASSC therapy, and for screening ASSCs for Fabry disease.","PeriodicalId":8811,"journal":{"name":"Biochimica et biophysica acta","volume":"1690 3","pages":"250-7"},"PeriodicalIF":0.0,"publicationDate":"2004-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.bbadis.2004.07.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24784662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 75

Respiratory terminal oxidases in the facultative chemoheterotrophic and dinitrogen fixing cyanobacterium Anabaena variabilis strain ATCC 29413: characterization of the cox2 locus. 兼性化养异养和固氮蓝藻变水藻ATCC 29413呼吸末端氧化酶:cox2位点的表征

Biochimica et biophysica acta Pub Date : 2004-11-04 DOI: 10.1016/j.bbabio.2004.06.009

Dietmar Pils, Corinna Wilken, Ana Valladares, Enrique Flores, Georg Schmetterer

{"title":"Respiratory terminal oxidases in the facultative chemoheterotrophic and dinitrogen fixing cyanobacterium Anabaena variabilis strain ATCC 29413: characterization of the cox2 locus.","authors":"Dietmar Pils, Corinna Wilken, Ana Valladares, Enrique Flores, Georg Schmetterer","doi":"10.1016/j.bbabio.2004.06.009","DOIUrl":"https://doi.org/10.1016/j.bbabio.2004.06.009","url":null,"abstract":"Upon nitrogen step-down, some filamentous cyanobacteria differentiate heterocysts, cells specialized for dinitrogen fixation, a highly oxygen sensitive process. Aerobic respiration is one of the mechanisms responsible for a microaerobic environment in heterocysts and respiratory terminal oxidases are the key enzymes of the respiratory chains. We used Anabaena variabilis strain ATCC 29413, because it is one of the few heterocyst-forming facultatively chemoheterotrophic cyanobacteria amenable to genetic manipulation. Using PCR with degenerate primers, we found four gene loci for respiratory terminal oxidases, three of which code for putative cytochrome c oxidases and one whose genes are homologous to cytochrome bd-type quinol oxidases. One cytochrome c oxidase, Cox2, was the only enzyme whose expression, tested by RT-PCR, was evidently up-regulated in diazotrophy, and therefore cloned, sequenced, and characterized. Up-regulation of Cox2 was corroborated by Northern and primer extension analyses. Strains were constructed lacking Cox1 (a previously characterized cytochrome c oxidase), Cox2, or both, which all grew diazotrophically. In vitro cytochrome c oxidase and respiratory activities were determined in all strains, allowing for the first time to estimate the relative contributions to total respiration of the different respiratory electron transport branches under different external conditions. Especially adding fructose to the growth medium led to a dramatic enhancement of in vitro cytochrome c oxidation and in vivo respiratory activity without significantly influencing gene expression.","PeriodicalId":8811,"journal":{"name":"Biochimica et biophysica acta","volume":"1659 1","pages":"32-45"},"PeriodicalIF":0.0,"publicationDate":"2004-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.bbabio.2004.06.009","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24784870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 17

Molecular interference of Cd(2+) with Photosystem II. Cd(2+)与光系统II的分子干涉。

Biochimica et biophysica acta Pub Date : 2004-11-04 DOI: 10.1016/j.bbabio.2004.07.003

Kajsa G V Sigfridsson, Gábor Bernát, Fikret Mamedov, Stenbjörn Styring

{"title":"Molecular interference of Cd(2+) with Photosystem II.","authors":"Kajsa G V Sigfridsson, Gábor Bernát, Fikret Mamedov, Stenbjörn Styring","doi":"10.1016/j.bbabio.2004.07.003","DOIUrl":"https://doi.org/10.1016/j.bbabio.2004.07.003","url":null,"abstract":"Many heavy metals inhibit electron transfer reactions in Photosystem II (PSII). Cd(2+) is known to exchange, with high affinity in a slow reaction, for the Ca(2+) cofactor in the Ca/Mn cluster that constitutes the oxygen-evolving center. This results in inhibition of photosynthetic oxygen evolution. There are also indications that Cd(2+) binds to other sites in PSII, potentially to proton channels in analogy to heavy metal binding in photosynthetic reaction centers from purple bacteria. In search for the effects of Cd(2+)-binding to those sites, we have studied how Cd(2+) affects electron transfer reactions in PSII after short incubation times and in sites, which interact with Cd(2+) with low affinity. Overall electron transfer and partial electron transfer were studied by a combination of EPR spectroscopy of individual redox components, flash-induced variable fluorescence and steady state oxygen evolution measurements. Several effects of Cd(2+) were observed: (i) the amplitude of the flash-induced variable fluorescence was lost indicating that electron transfer from Y(Z) to P(680)(+) was inhibited; (ii) Q(A)(-) to Q(B) electron transfer was slowed down; (iii) the S(2) state multiline EPR signal was not observable; (iv) steady state oxygen evolution was inhibited in both a high-affinity and a low-affinity site; (v) the spectral shape of the EPR signal from Q(A)(-)Fe(2+) was modified but its amplitude was not sensitive to the presence of Cd(2+). In addition, the presence of both Ca(2+) and DCMU abolished Cd(2+)-induced effects partially and in different sites. The number of sites for Cd(2+) binding and the possible nature of these sites are discussed.","PeriodicalId":8811,"journal":{"name":"Biochimica et biophysica acta","volume":"1659 1","pages":"19-31"},"PeriodicalIF":0.0,"publicationDate":"2004-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.bbabio.2004.07.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24784869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 155