Glutathione Deficiency Decreases Tissue Ascorbate Levels in Newborn Rats： Ascorbate Spares Glutathione and Protects [1991]; Alton Meister, Cornell University;_WJD_2016-0913_V001R01_IR93_IR94_

Glutathione Deficiency Decreases Tissue Ascorbate Levels in Newborn Rats： Ascorbate Spares Glutathione and Protects [1991]; Alton Meister, Cornell University;_WJD_2016-0913_V001R01_IR93_IR94_
Source (資訊來源):
http://www.jstor.org/stable/2357111?seq=1#page_scan_tab_contents
Info cited on 2016-09-13-WD2 (資訊引用於 中華民國105年9月13日) by 湯偉晉 (WeiJin Tang)
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2016-09-13
Glutathione Deficiency Decreases Tissue Ascorbate Levels in Newborn Rats: Ascorbate Spares Glutathione and Protects

Glutathione Deficiency Decreases Tissue Ascorbate Levels in Newborn Rats: Ascorbate Spares Glutathione and Protects

Glutathione Deficiency Decreases Tissue Ascorbate Levels in Newborn Rats: Ascorbate Spares Glutathione and Protects
Johannes Mrtensson and Alton Meister
Proceedings of the National Academy of Sciences of the United States of America
Vol. 88, No. 11 (Jun. 1, 1991), pp. 4656-4660
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/2357111
Page Count: 5

Abstract
Glutathione deficiency in newborn rats, produced by administration of L-buthionine-(S,R)-sulfoximine, a transition-state inactivator of γ-glutamylcysteine synthetase, decreases ascorbate levels of kidney, liver, brain, and lung. These tissues, especially their mitochondria, undergo severe damage and the animals die within a few days. When glutathione levels are markedly decreased, ascorbate levels decrease leading to formation of dehydroascorbate, which is degraded. Ascorbate has high antioxidant activity, but it (and other antioxidants such as α-tocopherol) must be maintained in reduced forms. These studies show in vivo that an important function of glutathione is to maintain tissue ascorbate. Administration of large doses of ascorbate (but not of dehydroascorbate) to buthionine sulfoximine-treated newborn rats decreases mortality, leads to normal levels of ascorbate, and spares glutathione. Newborn rats given lower doses of buthionine sulfoximine develop cataracts that, as shown previously, can be prevented by giving glutathione monoester; as found here, such cataracts can be partially prevented by administration of high doses of ascorbate or dehydroascorbate. Ascorbate spares glutathione indicating that these compounds have similar antioxidant actions. Ascorbate may have reductive functions that are not efficiently performed by glutathione. Although glutathione normally functions to maintain ascorbate, α-tocopherol, and other cellular components in reduced states, ascorbate can serve as an essential antioxidant in the presence of severe glutathione deficiency.

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Glutathione Depletion Induces Giant DNA and High-Molecular-Weight DNA Fragmentation Associated with Apoptosis through Lipid Peroxidation and Protein Kinase C Activation in C6 Glioma Cells [1999];_WJD_2016-0913_V001R01_IR92_

Glutathione Depletion Induces Giant DNA and High-Molecular-Weight DNA Fragmentation Associated with Apoptosis through Lipid Peroxidation and Protein Kinase C Activation in C6 Glioma Cells [1999];_WJD_2016-0913_V001R01_IR92_
Source (資訊來源):
http://www.sciencedirect.com/science/article/pii/S0003986198910670
Info cited on 2016-09-13-WD2 (資訊引用於 中華民國105年9月13日) by 湯偉晉 (WeiJin Tang)
Glutathione Depletion Induces Giant DNA and High-Molecular-Weight DNA Fragmentation Associated with Apoptosis through Lipid Peroxidation and Protein Kinase C Activation in C6 Glioma Cells [1999];_WJD_2016-0913_V001R01_IR92_
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2016-09-13
Archives of Biochemistry and Biophysics
Volume 363, Issue 1, 1 March 1999, Pages 33-42

Regular Article

Glutathione Depletion Induces Giant DNA and High-Molecular-Weight DNA Fragmentation Associated with Apoptosis through Lipid Peroxidation and Protein Kinase C Activation in C6 Glioma Cells

Glutathione Depletion Induces Giant DNA and High-Molecular-Weight DNA Fragmentation Associated with Apoptosis through Lipid Peroxidation and Protein Kinase C Activation in C6 Glioma Cells

Glutathione Depletion Induces Giant DNA and High-Molecular-Weight DNA Fragmentation Associated with Apoptosis through Lipid Peroxidation and Protein Kinase C Activation in C6 Glioma Cells

Author links open the overlay panel. Numbers correspond to the affiliation list which can be exposed by using the show more link.
Yoshihiro Higuchi a, 1, Shigeru Matsukawa b
a Department of Pharmacology, Kanazawa University School of Medicine, Kanazawa, Ishikawa, 920-8640, Japan
b The Central Research Laboratories, Fukui Medical School, Matsuoka, Fukui, 910-1193, Japan
Received 29 June 1998, Revised 30 November 1998, Available online 6 April 2002
doi:10.1006/abbi.1998.1067

Abstract
Glutathione (GSH) depletion caused byl-buthionine-(S,R)-sulfoximine (BSO) induced apoptosis that was recognized by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick endo-labeling (TUNEL), nuclear DNA staining with fluorescence dye, and internucleosomal DNA fragmentation in C6 rat glioma cells. The BSO-induced cell death was associated with caspase-3 activation. Lipid peroxidation and protein kinase C (PK-C) activation were observed during the apoptosis of C6 cells, and these events were inhibited by antioxidants and iron chelators without affecting BSO-induced GSH depletion. Furthermore, approximately 2 Mbp giant DNA fragments were observed in the BSO-treated cells. The giant DNA fragmentation were followed by approximately 30–700 kbp and then less than 100 kbp, including internucleosomal DNA fragmentations. Such serial DNA degradation was prevented by the antioxidants, the iron chelators, and the PK-C inhibitors. These results suggest that during apoptosis induced by GSH-depletion caused by BSO, reactive oxygen species endogenously produced cause lipid peroxidation and that the lipid peroxidation induced PK-C activation, processes which are thought to be involved in the giant DNA, high-molecular-weight DNA, and the internucleosomal DNA fragmentations.
Keywords

apoptosis; reactive oxygen species (ROS); giant DNA fragments; glutathione; lipid peroxidation; protein kinase C
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☆
Davies, K. T. A.
1
To whom correspondence should be addressed at Department of Pharmacology, Kanazawa University School of Medicine, 13-1 Takara-machi, Kanazawa, Ishikawa 920-8640, Japan. Fax: +81-76-234-4227. E-mail:higuchi@kenroku.kanazawa-u.ac.jp.
Copyright © 1999 Academic Press. All rights reserved.
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Avian Influenza A(H7N9) Virus Infection in Pregnant Woman, China, 2013 [2014]; antifibrotic therapy (glutathione) (抗纖維化治療(穀胱甘肽))

Avian Influenza A(H7N9) Virus Infection in Pregnant Woman, China, 2013 [2014]; antifibrotic therapy (glutathione) (抗纖維化治療(穀胱甘肽));_WJD_2016-0903_V001R01_IR93_
Source (資訊來源):
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3901503/
Info cited on 2016-09-03-WD6 (資訊引用於 中華民國105年9月3日) by 湯偉晉 (WeiJin Tang)
Source (資訊來源):
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3901503/pdf/13-1109.pdf
Info cited on 2016-09-03-WD6 (資訊引用於 中華民國105年9月3日) by 湯偉晉 (WeiJin Tang)

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2016-09-03
Emerg Infect Dis. 2014 Feb; 20(2): 333–334.
doi:  10.3201/eid2002.131109
PMCID: PMC3901503
Avian Influenza A(H7N9) Virus Infection in Pregnant Woman, China, 2013

Avian Influenza A(H7N9) Virus Infection in Pregnant Woman, China, 2013

Avian Influenza A(H7N9) Virus Infection in Pregnant Woman, China, 2013
Xian Qi,1 Lunbiao Cui,1 Ke Xu,1 Bin Wu, Fenyang Tang, Changjun Bao, Yefei Zhu, Ming-hao Zhou, and Hua Wangcorresponding author
Jiangsu Provincial Center for Disease Control and Prevention, Nanjing, China
corresponding authorCorresponding author.
Address for correspondence: Hua Wang, Jiangsu Provincial Center for Disease Control and Prevention, 172 Jiangsu Rd, Nanjing 210009, China; email: nc.cdcsj@auh
Author information ▼ Article notes ▼ Copyright and License information ►
Keywords: influenza virus, avian influenza A(H7N9) virus, influenza, viruses, pregnant woman, China
To the Editor: In February 2013, human infection with reassortant avian influenza A(H7N9) virus occurred in eastern China. A total of 135 laboratory-confirmed cases and 44 deaths among case-patients have been reported as of August 11, 2013. Unlike infection with other H7 subtype viruses (e.g., H7N2, H7N3, and H7N7), which often cause mild-to-moderate-human disease (1), infection with H7N9 subtype virus caused severe pneumonia and acute respiratory distress syndrome in most laboratory-confirmed case-patients (2,3). Pregnant women are particularly susceptible to severe complications from influenza (seasonal and pandemic), and have an increased risk for maternal death (4).

On March 30, 2013, a 25-year-old pregnant woman came to the outpatient department of a hospital in Zhenjiang, Jiangsu Province, China. She had cough and fever (temperature 38.0°C), which had begun 2 days earlier. She also reported mild myalgia and mild sore throat. The patient had no any underlying medical conditions and was at 17 weeks gestation, as estimated by ultrasound. On April 5, she was admitted to the respiratory department of the hospital with a temperature of 39.9°C, a leukocyte count of 7.9 ×109 cells/L, and a lymphocyte count of 0.7 × 109 cells/L.

On April 6, she was transferred to the intensive care unit because of shortness of breath, respiratory failure, and loss of consciousness. She was given mechanical ventilation, broad-spectrum antimicrobial drugs, oseltamivir, gamma-globulin, antifibrotic therapy (glutathione) (抗纖維化治療(穀胱甘肽)), and nutritional support. Oseltamivir (150 mg/d, 2 times/d) had been administered during April 6–12. A chest radiograph showed extensive infiltrates of both lungs.

On April 21, she regained consciousness, and her condition stabilized over the next few days. On April 23, she was extubated, transferred to the common ward, and given nasal oxygen supplementation and antimicrobial and antifibrotic drug therapy. Her condition improved gradually, and on May 14 she was discharged in good health without fetal abnormality.

The fetus was monitored daily by using ultrasound to check the heart rate; fetal heart rate and activity were normal during hospitalization. The fetus continued to grow appropriately and was delivered by cesarean section at 35 weeks’ gestation on July 17 (length 48 cm, weight 3,300 g, and Apgars scores of 9 at 1 min and 10 at 5 min). The clinical timeline for the case-patient is shown in the Figure.

Figure
Figure
Clinical timeline for a pregnant woman infected with avian influenza A(H7N9) virus, China, 2013. ICU, intensive care unit; RT-PCR, reverse transcription PCR.
The patient and her husband lived in a house with her husband’s parents. No live poultry were present in the residential district, but the husband’s parents worked as pork butchers in a live animal market ≈500 m from the residential district. Several kinds of live poultry (e.g., chicken, duck, pigeon, and quail) were sold in the market. During the 2 weeks before illness onset, the patient did not have contact with persons known to be febrile. However, during that time, she visited the live animal market once. Eighteen potential close contacts of the patient were identified (15 health care workers and 3 household members). Respiratory symptoms did not develop in any of these contacts during a 7-day surveillance period.

Four methods were used for laboratory diagnosis: real-time reverse transcription PCR, virus isolation, full-genome sequencing, and modified hemagglutination inhibition assays. Clinical samples tested were 2 throat swab specimens obtained from the patient on April 6 and 7, 38 paired serum samples obtained from the patient and close contacts during the acute and convalescent phases of infection, and 6 environmental samples (2 avian feces samples and 4 poultry cage specimens obtained from the live animal market that the patient visited). Throat swab specimens from patient were positive for the hemagglutinin (HA) and neuraminidase genes of avian influenza A (H7N9) virus. Of 6 environmental samples, 5 were positive for (H7N9) virus HA genes. No (H7N9) virus HA antibodies were detected from paired serum samples from all 18 close contacts.

Two virus strains were isolated: 1 from a patient specimen (A/Zhenjiang/1/2013) and 1 from a chicken cage specimen (A/environment/Zhenjiang/4/2013) (GenBank accession nos. KF007057-KF007064 and KF007009-KF007016, respectively). Genome comparison showed that isolates had a nucleotide identity of 96.8%–99.8%, indicating an amino acid identity of 98·2%–99·6%. Phylogenetic analysis showed that 5 genes (HA, nucleoprotein, neuraminidase, matrix, and nonstructural protein) of the 2 isolates belonged to the same clade. However, the 3 polymerase genes (polymerase basic 1, polymerase basic 2, and polymerase acidic) clustered in a different clade. These results suggested that the 2 strains originated from an independent reassortment mechanism and that the H7N9 subtype viruses had undergone genetic reassortment to generate multiple novel genotypes in China.

According to epidemiologic and clinical data for infections with avian influenza A(H7N9) virus, most patients with severe illness, including severe pneumonia and acute respiratory distress syndrome, were elderly men with underlying medical conditions (2,3). Our findings suggest that pregnancy might be a risk factor for clinically severe influenza in young women infected with H7N9 subtype virus.

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Acknowledgments
M.-h.Z. and H.W. were partially supported by the Innovation Platform for Public Health Emergency Preparedness and Response (NO.ZX201109); X.Q. was partially supported by the Natural Science Foundation of Jiangsu Province (BK20131450); and X.Q., L.C., and Y.Z. were partially supported by the Jiangsu Province Key Medical Talent Foundation (RC2011084, RC2011085, and RC2011191) and the 333 Projects of Jiangsu Province.

Suggested citation for this article: Qi X, Cui L, Xu K, Wu B, Tang F, Bao C, et al. Avian influenza A(H7N9) virus infection in pregnant woman, China, 2013 [letter]. Emerg Infect Dis [Internet]. 2014 Feb [date cited]. http://dx.doi.org/10.3201/eid2002.131109

1These authors contributed equally to this article.

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References
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2. Gao HN, Lu HZ, Cao B, Du B, Shang H, Gan JH, et al. Clinical findings in 111 cases of influenza a (H7N9) virus infection. N Engl J Med. 2013;368:2277–85 . 10.1056/NEJMoa1305584 [PubMed] [Cross Ref]
3. Gao R, Cao B, Hu Y, Feng Z, Wang D, Hu W, et al. Human infection with a novel avian-origin influenza A (H7N9) virus. N Engl J Med. 2013;368:1888–97 . 10.1056/NEJMoa1304459 [PubMed] [Cross Ref]
4. Siston AM, Rasmussen SA, Honein MA, Fry AM, Seib K, Callaghan WM, et al. Pandemic 2009 influenza A(H1N1) virus illness among pregnant women in the United States. JAMA. 2010;303:1517–25 . 10.1001/jama.2010.479 [PubMed] [Cross Ref]
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2016-09-03
Oseltamivir (Tamiflu) Uses, Dosage, Side Effects - Drugs.com
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