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Journal of Environmental Pathology, Toxicology and Oncology

Published 4 issues per year

ISSN Print: 0731-8898

ISSN Online: 2162-6537

The Impact Factor measures the average number of citations received in a particular year by papers published in the journal during the two preceding years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) IF: 2.4 To calculate the five year Impact Factor, citations are counted in 2017 to the previous five years and divided by the source items published in the previous five years. 2017 Journal Citation Reports (Clarivate Analytics, 2018) 5-Year IF: 2.8 The Immediacy Index is the average number of times an article is cited in the year it is published. The journal Immediacy Index indicates how quickly articles in a journal are cited. Immediacy Index: 0.5 The Eigenfactor score, developed by Jevin West and Carl Bergstrom at the University of Washington, is a rating of the total importance of a scientific journal. Journals are rated according to the number of incoming citations, with citations from highly ranked journals weighted to make a larger contribution to the eigenfactor than those from poorly ranked journals. Eigenfactor: 0.00049 The Journal Citation Indicator (JCI) is a single measurement of the field-normalized citation impact of journals in the Web of Science Core Collection across disciplines. The key words here are that the metric is normalized and cross-disciplinary. JCI: 0.59 SJR: 0.429 SNIP: 0.507 CiteScore™:: 3.9 H-Index: 49

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Inhibition of Prostacyclin Release by Cigarette Smoke Extract in Endothelial Cells is not Related to Enhanced Superoxide Generation and NADPH-Oxidase Activation

Volume 25, Issue 3, 2006, pp. 585-596
DOI: 10.1615/JEnvironPatholToxicolOncol.v25.i3.30
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ABSTRACT

Exposure of human umbilical endothelial cells (ECs) to cigarette smoke extract (CSE) activated the NADPH-oxidase enzyme and increased the production of superoxide (O2) as well as reactive oxygen species (ROS). CSE also inhibited the prostacyclin (PGI2) formation by ECs. Preincubation of ECs with diphenylene iodonium (DPI), the inhibitor of NADPH oxidase, blocked the increase of O2 production, but neither lowered the ROS level nor prevented the inhibition of PGI2 formation in CSE-treated cells. Preincubation of ECs with a medium supplemented with 1 mM vitamin C did not decrease, but rather increased the O2 production in CSE-treated cells. However, adding 1 mM glutathione (GSH) to vitamin C decreased the O2 production, indicating that vitamin C was overwhelmed by the prooxidant in CS, and GSH enhanced the recycling process and spared vitamin C. The ROS level remained high in CSE-treated cells even after preincubation with vitamin C or vitamin C + GSH compared to the control cells. These results are discussed in light of the possible decrease of antioxidant enzyme activities in CSE-treated cells and the increase of cellular hydrogen peroxide (H2O2) generated from the CSE, which cause an imbalance between oxidizing species and the antioxidants producing oxidative stress in CSE-treated cells. These results demonstrate that CSE has a direct inhibitory effect on PGI2 formation and enhances the level of ROS in CSE-treated ECs, regardless of the activation of NADPH-oxidase.

CITED BY
  1. Barbieri Silvia S., Amadio Patrizia, Gianellini Sara, Zacchi Elena, Weksler Babette B., Tremoli Elena, Tobacco smoke regulates the expression and activity of microsomal prostaglandin E synthase‐1: role of prostacyclin and NADPH‐oxidase, The FASEB Journal, 25, 10, 2011. Crossref

  2. Fearon Ian M., Risk Factors, Oxidative Stress, and Cardiovascular Disease, in Systems Biology of Free Radicals and Antioxidants, 2014. Crossref

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