Free radical biology & medicine最新文献_第4页

The Gdac1 locus modifies spontaneous and Salmonella-induced colitis in mice deficient in either Gpx2 or Gpx1 gene. gda1基因座修饰Gpx2或Gpx1基因缺失小鼠的自发性和沙门氏菌诱导的结肠炎。

IF 7.4

Free radical biology & medicine Pub Date : 2013-12-01 Epub Date: 2013-10-01 DOI: 10.1016/j.freeradbiomed.2013.09.013

R Steven Esworthy, Byung-Wook Kim, Yufeng Wang, Qiang Gao, James H Doroshow, Thomas L Leto, Fong-Fong Chu

{"title":"The Gdac1 locus modifies spontaneous and Salmonella-induced colitis in mice deficient in either Gpx2 or Gpx1 gene.","authors":"R Steven Esworthy, Byung-Wook Kim, Yufeng Wang, Qiang Gao, James H Doroshow, Thomas L Leto, Fong-Fong Chu","doi":"10.1016/j.freeradbiomed.2013.09.013","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2013.09.013","url":null,"abstract":"We previously identified the Gdac1 (Gpx-deficiency-associated colitis 1) locus, which influences the severity of spontaneous colitis in Gpx1- and Gpx2-double-knockout (Gpx1/2-DKO) mice. Congenic Gpx1/2-DKO mice in the 129S1/SvImJ (129) background but carrying the Gdac1(B6) allele have milder spontaneous colitis than 129 Gpx1/2-DKO mice carrying the Gdac1(129) allele. Here, we evaluated the effect of the Gdac1(B6) allele on 129 strain non-DKO mice that had a wild-type (WT) Gpx1 or Gpx2 allele and WT mice. We found that the congenic Gdac1(B6) Gpx2-KO, Gpx1-KO, and WT mice also had better health than the corresponding 129 mice measured by at least one of the parameters including disease signs, colon length, or weight gain. The Gdac1(B6) allele prevented loss of goblet cells and crypt epithelium exfoliation in the Gpx1/2-DKO mice, but did not affect epithelial cell apoptosis or proliferation. Because Gdac1(B6) affects gut dysbiosis in the DKO mice, we then tested its impact on bacteria-induced colitis in non-DKO mice. First, we found both Gpx1-KO and Gpx2-KO mice were susceptible to Salmonella enterica serotype typhimurium (S. Tm)-induced colitis under conditions where WT B6 and 129 mice were resistant. Second, the S. Tm-infected Gdac1(B6) Gpx1-KO mice had stronger inflammatory responses than 129 Gpx1-KO or 129 Gpx2-KO with both Gdac1 alleles and WT mice by having higher mRNA levels of Nod2, Nox2, Tnf, and Cox2. We conclude that the Gdac1 locus affects both spontaneous and S. Tm-induced colitis in 129 non-DKO mice, although in opposite directions. ","PeriodicalId":505743,"journal":{"name":"Free radical biology & medicine","volume":" ","pages":"1273-1283"},"PeriodicalIF":7.4,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.freeradbiomed.2013.09.013","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31779131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 9

Investigation of spin-trapping artifacts formed by the Forrester-Hepburn mechanism. 由forrest - hepburn机制形成的自旋捕获伪影的研究。

Free radical biology & medicine Pub Date : 2013-12-01 Epub Date: 2013-07-10 DOI: 10.1016/j.freeradbiomed.2013.07.006

Fabian Leinisch, Jinjie Jiang, Eugene F DeRose, Valery V Khramtsov, Ronald P Mason

{"title":"Investigation of spin-trapping artifacts formed by the Forrester-Hepburn mechanism.","authors":"Fabian Leinisch, Jinjie Jiang, Eugene F DeRose, Valery V Khramtsov, Ronald P Mason","doi":"10.1016/j.freeradbiomed.2013.07.006","DOIUrl":"10.1016/j.freeradbiomed.2013.07.006","url":null,"abstract":"Free radical detection with ESR spin trapping relies on the specific addition of the radical to nitrone/nitroso compounds. It also has been proposed that spin traps can react in biological systems to give false-positive results. For nitrone spin traps, the reaction with nucleophiles, first described by Forrester and Hepburn, has been discussed as the most critical source of artifacts. For artifact identification, the ESR preincubation method may be used, which employs isotopically marked spin traps. Here we investigated the influence of fast sulfite-hydroxylamine equilibrium chemistry on the validity of this assay. Using the (faster) aspiration technique, we found that the Forrester-Hepburn mechanism also contributes to DMPO/(•)SO3(-) adduct formation during ferricyanide-mediated sulfite oxidation, but no evidence for artifactual DMPO/(•)SO3(-) formation was found if the more potent horseradish peroxidase was used. This is ESR evidence that the Forrester-Hepburn mechanism can occur under mild conditions, depending on the experimental details. This technique can also be used to test for other artifact mechanisms. We investigated the known ene reaction of DBNBS and tryptophan in more detail. We found that a strong artifact signal is induced by light; however, with atypically long incubations, we found that the artifact is also formed thermally. ","PeriodicalId":505743,"journal":{"name":"Free radical biology & medicine","volume":" ","pages":"1497-1505"},"PeriodicalIF":0.0,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3859841/pdf/nihms-523110.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31578114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mass spectrometry evidence for formation of estrogen-homocysteine conjugates: estrogens can regulate homocysteine levels. 雌激素-同型半胱氨酸缀合物形成的质谱证据:雌激素可以调节同型半胱氨酸水平。

IF 7.4

Free radical biology & medicine Pub Date : 2013-12-01 Epub Date: 2013-08-06 DOI: 10.1016/j.freeradbiomed.2013.07.041

Nilesh W Gaikwad

{"title":"Mass spectrometry evidence for formation of estrogen-homocysteine conjugates: estrogens can regulate homocysteine levels.","authors":"Nilesh W Gaikwad","doi":"10.1016/j.freeradbiomed.2013.07.041","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2013.07.041","url":null,"abstract":"Homocysteine (HCys), a sulfur-containing amino acid, is formed during the metabolism of methionine. An imbalance between the rate of production and the use of HCys during methionine metabolism can result in an increase in the plasma and urinary levels of HCys. HCys has been shown to be toxic to vascular endothelial cells through several pathways. Many earlier clinical studies have revealed an association between plasma HCys and cardiovascular and other diseases. In contrast, estrogens are suggested to lower the risk of cardiovascular disease. Several studies indicate that estrogen metabolites could be responsible for cardiovascular protection. It has been demonstrated that electrophilic estrogen quinones, E1(E2)-2,3-Q and E1(E2)-3,4-Q, can alkylate DNA as well as form conjugates with glutathione. I hypothesize that estrogen quinones generated in situ by oxidative enzymes, metal ions, or molecular oxygen can interact with HCys to form conjugates. This in turn could lower the levels of toxic HCys as well as quenching the reactive estrogen quinones, resulting in cardiovascular protective effects. To test the feasibility of a protective estrogen-HCys pathway, estrogen quinones were treated with HCys. Tandem mass spectrometry analysis of the assay mixture shows the formation of estrogen-HCys conjugates. Furthermore, incubation of catechol estrogens with myeloperoxidase (MPO) in the presence of HCys resulted in the formation of respective estrogen-HCys conjugates. The identities of estrogen-HCys conjugates in MPO assay extracts were confirmed by comparing them to pure synthesized estrogen-HCys standards. I propose that through conjugation estrogens could chemically regulate HCys levels; moreover these conjugates could be used as potential biomarkers in determining health. ","PeriodicalId":505743,"journal":{"name":"Free radical biology & medicine","volume":" ","pages":"1447-1454"},"PeriodicalIF":7.4,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.freeradbiomed.2013.07.041","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31642857","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: 29

Diet-derived advanced glycation end products or lipofuscin disrupts proteostasis and reduces life span in Drosophila melanogaster. 饮食来源的晚期糖基化终产物或脂褐素破坏黑腹果蝇的蛋白质平衡并缩短寿命。

IF 7.4

Free radical biology & medicine Pub Date : 2013-12-01 Epub Date: 2013-08-30 DOI: 10.1016/j.freeradbiomed.2013.08.186

Eleni N Tsakiri, Kalliopi K Iliaki, Annika Höhn, Stefanie Grimm, Issidora S Papassideri, Tilman Grune, Ioannis P Trougakos

{"title":"Diet-derived advanced glycation end products or lipofuscin disrupts proteostasis and reduces life span in Drosophila melanogaster.","authors":"Eleni N Tsakiri, Kalliopi K Iliaki, Annika Höhn, Stefanie Grimm, Issidora S Papassideri, Tilman Grune, Ioannis P Trougakos","doi":"10.1016/j.freeradbiomed.2013.08.186","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2013.08.186","url":null,"abstract":"Advanced glycation end product (AGE)-modified proteins are formed by the nonenzymatic glycation of free amino groups of proteins and, along with lipofuscin (a highly oxidized aggregate of covalently cross-linked proteins, sugars, and lipids), have been found to accumulate during aging and in several age-related diseases. As the in vivo effects of diet-derived AGEs or lipofuscin remain elusive, we sought to study the impact of oral administration of glucose-, fructose-, or ribose-modified albumin or of artificial lipofuscin in a genetically tractable model organism. We report herein that continuous feeding of young Drosophila flies with culture medium enriched in AGEs or in lipofuscin resulted in reduced locomotor performance and in accelerated rates of AGE-modified proteins and carbonylated proteins accumulation in the somatic tissues and hemolymph of flies, as well as in a significant reduction of flies health span and life span. These phenotypic effects were accompanied by reduced proteasome peptidase activities in both the hemolymph and the somatic tissues of flies and higher levels of oxidative stress; furthermore, oral administration of AGEs or lipofuscin in flies triggered an upregulation of the lysosomal cathepsin B, L activities. Finally, RNAi-mediated cathepsin D knockdown reduced flies longevity and significantly augmented the deleterious effects of AGEs and lipofuscin, indicating that lysosomal cathepsins reduce the toxicity of diet-derived AGEs or lipofuscin. Our in vivo studies demonstrate that chronic ingestion of AGEs or lipofuscin disrupts proteostasis and accelerates the functional decline that occurs with normal aging. ","PeriodicalId":505743,"journal":{"name":"Free radical biology & medicine","volume":" ","pages":"1155-1163"},"PeriodicalIF":7.4,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.freeradbiomed.2013.08.186","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31702785","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: 53

The effects of intermittent hypoxia on redox status, NF-κB activation, and plasma lipid levels are dependent on the lowest oxygen saturation. 间歇性缺氧对氧化还原状态、NF-κB活化和血脂水平的影响依赖于最低氧饱和度。

IF 7.4

Free radical biology & medicine Pub Date : 2013-12-01 Epub Date: 2013-08-31 DOI: 10.1016/j.freeradbiomed.2013.08.180

Miguel Quintero, María Del Carmen Gonzalez-Martin, Victoria Vega-Agapito, Constancio Gonzalez, Ana Obeso, Ramon Farré, Teresa Agapito, Sara Yubero

{"title":"The effects of intermittent hypoxia on redox status, NF-κB activation, and plasma lipid levels are dependent on the lowest oxygen saturation.","authors":"Miguel Quintero, María Del Carmen Gonzalez-Martin, Victoria Vega-Agapito, Constancio Gonzalez, Ana Obeso, Ramon Farré, Teresa Agapito, Sara Yubero","doi":"10.1016/j.freeradbiomed.2013.08.180","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2013.08.180","url":null,"abstract":"Obstructive sleep apnea syndrome (OSAS) is described as repetitive obstructions of the upper airways during sleep, causing concomitant episodes of systemic hypoxia and associated cardiovascular and metabolic pathologies. The mechanisms generating these pathologies are controversial. Because recurrent hypoxia is the element of inadequate respiration that leads to the pathology, experimental models of OSAS consist in the exposure of the animals to intermittent hypoxia (IH) by cycling O2 percentages in their habitats. A proposed mechanism linking the IH of OSAS to pathologies is the increased production of reactive oxygen species (ROS). However, it has been argued that many patients seem to lack oxidative stress and that, to augment ROS in IH animals, intense hypoxia, seldom encountered in patients, has to be applied. To solve the controversy, we have exposed rats to two intensities of IH (cycles of 10 or 5% O2, 40s, and then 21% O2, 80s; 8h/day, 15 days). We then measured reduced and oxidized glutathione and lipid peroxide levels, aconitase and fumarase activities, and ROS-disposal enzyme activity in liver, brain, and lung. Liver levels of nuclear NF-κB-p65 and plasma C-reactive protein (CRP), as well as lipid levels, were also assessed. Lowest hemoglobin saturations were 91.7 ± 0.8 and 73.5 ± 1.4%. IH caused tissue-specific oxidative stress related to hypoxic intensity. Nuclear NF-κB-p65 and lipid content in the liver and CRP in the plasma all increased with IH intensity, as did both plasma triglycerides and cholesterol. We conclude that IH, even of moderate intensity, causes oxidative stress probably related to the pathologies encountered in OSAS patients.","PeriodicalId":505743,"journal":{"name":"Free radical biology & medicine","volume":" ","pages":"1143-1154"},"PeriodicalIF":7.4,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.freeradbiomed.2013.08.180","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31705522","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: 41

Nrf2 is essential for the expression of lipocalin-prostaglandin D synthase induced by prostaglandin D2. Nrf2对于前列腺素D2诱导的脂钙素-前列腺素D合成酶的表达至关重要。

IF 7.4

Free radical biology & medicine Pub Date : 2013-12-01 Epub Date: 2013-09-09 DOI: 10.1016/j.freeradbiomed.2013.08.192

Kyun Ha Kim, Ruxana T Sadikot, Lei Xiao, John W Christman, Michael L Freeman, Jefferson Y Chan, Yu-Kyoung Oh, Timothy S Blackwell, Myungsoo Joo

{"title":"Nrf2 is essential for the expression of lipocalin-prostaglandin D synthase induced by prostaglandin D2.","authors":"Kyun Ha Kim, Ruxana T Sadikot, Lei Xiao, John W Christman, Michael L Freeman, Jefferson Y Chan, Yu-Kyoung Oh, Timothy S Blackwell, Myungsoo Joo","doi":"10.1016/j.freeradbiomed.2013.08.192","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2013.08.192","url":null,"abstract":"Nrf2 is a transcription factor that protects against inflammatory diseases, but the underlying mechanism of this effect remains unclear. Here, we report that Nrf2 uses lipocalin-prostaglandin D synthase (L-PGDS) as a mechanism for suppressing inflammation. Exogenously added prostaglandin D2 (PGD2) induced L-PGDS expression in bone-marrow-derived macrophages (BMDMs), suggesting a positive feedback loop between L-PGDS expression and PGD2. Unlike lipopolysaccharide (LPS)-induced L-PGDS expression, PGD2-mediated expression was independent of MAPK, PU.1, or TLR4. Sequence analysis located a putative Nrf2 binding site in the murine L-PGDS promoter, to which Nrf2 bound when treated with PGD2. Chemical activation, or overexpression, of Nrf2 was sufficient to induce L-PGDS expression in macrophages, BMDMs, or lungs of Nrf2-knockout (KO) mice, but treatment with PGD2 failed to do so, suggesting a pivotal role for Nrf2 in the expression of L-PGDS. Consistent with this, expression of Nrf2 in the lungs of Nrf2-KO mice was sufficient to induce the expression of L-PGDS and to reduce neutrophilic lung inflammation elicited by LPS. Furthermore, expression of L-PGDS in mouse lungs decreased neutrophilic infiltration, ameliorating lung inflammation in mice. Together, our results show that Nrf2, activated by PGD2, induced L-PGDS expression, resulting in decreased inflammation. We suggest that the positive feedback induction of L-PGDS by PGD2 is part of the mechanism by which Nrf2 regulates inflammation. ","PeriodicalId":505743,"journal":{"name":"Free radical biology & medicine","volume":" ","pages":"1134-1142"},"PeriodicalIF":7.4,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.freeradbiomed.2013.08.192","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31727108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 20

Evaluation of long-term vitamin E insufficiency or excess on bone mass, density, and microarchitecture in rodents. 评估长期维生素E不足或过量对啮齿动物骨量、密度和微结构的影响。

IF 7.4

Free radical biology & medicine Pub Date : 2013-12-01 Epub Date: 2013-09-16 DOI: 10.1016/j.freeradbiomed.2013.09.004

Urszula T Iwaniec, Russell T Turner, Brenda J Smith, Barbara J Stoecker, Allison Rust, Bo Zhang, Vihas T Vasu, Kishorchandra Gohil, Carroll E Cross, Maret G Traber

{"title":"Evaluation of long-term vitamin E insufficiency or excess on bone mass, density, and microarchitecture in rodents.","authors":"Urszula T Iwaniec, Russell T Turner, Brenda J Smith, Barbara J Stoecker, Allison Rust, Bo Zhang, Vihas T Vasu, Kishorchandra Gohil, Carroll E Cross, Maret G Traber","doi":"10.1016/j.freeradbiomed.2013.09.004","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2013.09.004","url":null,"abstract":"High dietary α-tocopherol levels reportedly result in osteopenia in growing rats, whereas α-tocopherol deficiency in α-tocopherol transfer protein-knockout (α-TTP-KO) mice results in increased cancellous bone mass. Because osteoporosis is a disease associated primarily with aging, we hypothesized that age-related bone loss would be attenuated in α-TTP-KO mice. Cancellous and cortical bone mass and microarchitecture were assessed using dual-energy X-ray absorptiometry and micro-computed tomography in 2-year-old α-TTP-KO and wild-type (WT) male and female mice fed dl-α-tocopherol acetate. In contrast to our expectations, differences in cancellous bone were not detected between WT and α-TTP-KO mice of either gender, and α-TTP-KO males had lower (p<0.05) cortical bone mass than WT males. We therefore evaluated bone mass, density, and microarchitecture in proximal femur of skeletally mature (8.5-month-old) male Sprague-Dawley rats fed diets containing low (15 IU/kg diet), adequate (75 IU/kg diet), or high (500 IU/kg diet) dl-α-tocopherol acetate for 13 weeks. Low dietary α-tocopherol did not increase bone mass. Furthermore, no reductions in cancellous or cortical bone mass were detected with high dietary α-tocopherol. Failure to detect increased bone mass in aged α-TTP-KO mice or bone changes in skeletally mature rats fed either low or high levels of α-tocopherol does not support the hypothesis that α-tocopherol has a negative impact on bone mass, density, or microarchitecture in rodents.","PeriodicalId":505743,"journal":{"name":"Free radical biology & medicine","volume":" ","pages":"1209-1214"},"PeriodicalIF":7.4,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.freeradbiomed.2013.09.004","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31746855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 19

Control of pathogen growth and biofilm formation using a urinary catheter that releases antimicrobial nitrogen oxides. 利用释放抗菌氮氧化物的导尿管控制病原体生长和生物膜形成。

IF 7.4

Free radical biology & medicine Pub Date : 2013-12-01 Epub Date: 2013-09-29 DOI: 10.1016/j.freeradbiomed.2013.09.012

Hiroaki Kishikawa, Anette Ebberyd, Ute Römling, Annelie Brauner, Petra Lüthje, Jon O Lundberg, Eddie Weitzberg

{"title":"Control of pathogen growth and biofilm formation using a urinary catheter that releases antimicrobial nitrogen oxides.","authors":"Hiroaki Kishikawa, Anette Ebberyd, Ute Römling, Annelie Brauner, Petra Lüthje, Jon O Lundberg, Eddie Weitzberg","doi":"10.1016/j.freeradbiomed.2013.09.012","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2013.09.012","url":null,"abstract":"Antibacterial nitrogen oxides including nitric oxide are formed from nitrite under acidic conditions. In a continuous-flow model of the urinary bladder we used the retention cuff of an all-silicone Foley catheter as a depot for export of nitrogen oxides. The cuff was filled with sodium nitrite (50mM) and an acidic buffer solution (pH 3.6) and the growth of nine common uropathogens in the surrounding artificial urine was measured along with biofilm formation on the catheter surface. In experiments with control catheters (NaCl) bacteria grew readily and biofilm developed within hours in five of nine strains. In contrast, with test catheters bacterial counts were markedly reduced and biofilm formation by Pseudomonas aeruginosa, Klebsiella pneumoniae, and Enterobacter cloace was prevented, whereas Escherichia coli and Staphylococcus aureus were unaffected. We conclude that antibacterial nitrogen oxides generated in the retention cuff of a urinary catheter diffuse into urine and prevent the growth of urinary pathogens and biofilm formation. Although promising, future studies will reveal if this novel approach can be clinically useful for the prevention of catheter-associated urinary tract infections. ","PeriodicalId":505743,"journal":{"name":"Free radical biology & medicine","volume":" ","pages":"1257-1264"},"PeriodicalIF":7.4,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.freeradbiomed.2013.09.012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31774428","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: 28

Reactive oxygen species exacerbate autoimmune hemolytic anemia in New Zealand Black mice. 活性氧加重新西兰黑鼠自身免疫性溶血性贫血。

IF 7.4

Free radical biology & medicine Pub Date : 2013-12-01 Epub Date: 2013-10-02 DOI: 10.1016/j.freeradbiomed.2013.09.021

Tasuku Konno, Noriyuki Otsuki, Toshihiro Kurahashi, Noriko Kibe, Satoshi Tsunoda, Yoshihito Iuchi, Junichi Fujii

{"title":"Reactive oxygen species exacerbate autoimmune hemolytic anemia in New Zealand Black mice.","authors":"Tasuku Konno, Noriyuki Otsuki, Toshihiro Kurahashi, Noriko Kibe, Satoshi Tsunoda, Yoshihito Iuchi, Junichi Fujii","doi":"10.1016/j.freeradbiomed.2013.09.021","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2013.09.021","url":null,"abstract":"Elevated reactive oxygen species (ROS) and oxidative damage occur in the red blood cells (RBCs) of SOD1-deficient C57BL/6 mice. This leads to autoimmune responses against RBCs in aged mice that are similar to autoimmune hemolytic anemia (AIHA). We examined whether a SOD1 deficiency and/or the human SOD1 transgene (hSOD1) would affect phenotypes of AIHA-prone New Zealand Black (NZB) mice by establishing three congenic strains: those lacking SOD1, those expressing hSOD1 under a GATA-1 promoter, and those lacking mouse SOD1 but expressing hSOD1. Levels of intracellular ROS and oxidative stress markers increased, and the severity of the AIHA phenotype was aggravated by a SOD1 deficiency. In contrast, the transgenic expression of hSOD1 in an erythroid cell-specific manner averted most of the AIHA phenotype evident in the SOD1-deficient mice and also ameliorated the AIHA phenotype in the mice possessing intrinsic SOD1. These data suggest that oxidative stress in RBCs may be an underlying mechanism for autoimmune responses in NZB mice. These results were consistent with the hypothetical role of reactive oxygen species in triggering the autoimmune reaction in RBCs and may provide a novel approach to mitigating the progression of AIHA by reducing oxidative stress. ","PeriodicalId":505743,"journal":{"name":"Free radical biology & medicine","volume":" ","pages":"1378-1384"},"PeriodicalIF":7.4,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.freeradbiomed.2013.09.021","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31782542","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: 15

Epidemiology of selenium and type 2 diabetes: can we make sense of it? 硒和2型糖尿病的流行病学:我们能理解它吗?

IF 7.4

Free radical biology & medicine Pub Date : 2013-12-01 Epub Date: 2013-04-16 DOI: 10.1016/j.freeradbiomed.2013.04.003

Margaret P Rayman, Saverio Stranges

{"title":"Epidemiology of selenium and type 2 diabetes: can we make sense of it?","authors":"Margaret P Rayman, Saverio Stranges","doi":"10.1016/j.freeradbiomed.2013.04.003","DOIUrl":"https://doi.org/10.1016/j.freeradbiomed.2013.04.003","url":null,"abstract":"The potential of some selenoproteins to protect against oxidative stress led to the expectation that selenium would be protective against type 2 diabetes, and indeed in early in vivo and in vitro studies, selenium (as selenate) was shown to have antidiabetic and insulin-mimetic effects. However, more recently, findings from observational cross-sectional studies have raised concern that high selenium exposure may be associated with type 2 diabetes or insulin resistance, at least in well-nourished populations, though trial results have been inconsistent. Moreover, the largest trials that investigated the effects of selenium supplementation on diabetes endpoints have had cancer prevention as their primary outcome, casting doubt on the interpretation of posthoc analyses. Factors affecting serum/plasma selenium are not just location and level of disease-associated inflammation but the fact that higher concentrations of plasma selenoprotein P yet lower concentrations of glutathione peroxidase are found in type 2 diabetic patients than in normal subjects. From a public health perspective, selenium is marketed as a dietary supplement and is commonly added to multivitamin/mineral preparations that are consumed in many Western countries. Based on current evidence, however, the indiscriminate use of selenium supplements in individuals and populations with adequate-to-high selenium status cannot be justified and may increase risk. In conclusion, although there is a clear link between certain selenoproteins and glucose metabolism or insulin resistance, the relationship between selenium and type 2 diabetes is undoubtedly complex. It is possible that the relationship is U-shaped, with possible harm occurring both below and above the physiological range for optimal activity of some or all selenoproteins. ","PeriodicalId":505743,"journal":{"name":"Free radical biology & medicine","volume":" ","pages":"1557-1564"},"PeriodicalIF":7.4,"publicationDate":"2013-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.freeradbiomed.2013.04.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"31367867","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: 194