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      Growth Hormone-Releasing Hormone Antagonist JV-1-36 Suppresses Reactive Oxygen Species Generation in A549 Lung Cancer Cells

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          Abstract

          Growth hormone-releasing hormone (GHRH) and its receptors are expressed in a variety of human cancers, and have been involved in malignancies. GHRH antagonists (GHRHAnt) were developed to suppress tumor progression and metastasis. Previous studies demonstrate the involvement of reactive oxygen species (ROS) in cancer progression. Herein, we investigate the effect of a commercially available GHRH antagonist, namely JV-1–36, in the redox status of the A549 human cancer cell line. Our results suggest that this peptide significantly reduces ROS production in those cells in a time-dependent manner and counteracts H 2O 2-induced ROS. Our study supports the anti-oxidative effects of JV-1–36 and contributes in our knowledge towards the in vitro effects of GHRHAnt in cancers.

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          Reactive oxygen species in cancer.

          Geou-Yarh Liou, Peter Storz (2010)
          Elevated rates of reactive oxygen species (ROS) have been detected in almost all cancers, where they promote many aspects of tumour development and progression. However, tumour cells also express increased levels of antioxidant proteins to detoxify from ROS, suggesting that a delicate balance of intracellular ROS levels is required for cancer cell function. Further, the radical generated, the location of its generation, as well as the local concentration is important for the cellular functions of ROS in cancer. A challenge for novel therapeutic strategies will be the fine tuning of intracellular ROS signalling to effectively deprive cells from ROS-induced tumour promoting events, towards tipping the balance to ROS-induced apoptotic signalling. Alternatively, therapeutic antioxidants may prevent early events in tumour development, where ROS are important. However, to effectively target cancer cells specific ROS-sensing signalling pathways that mediate the diverse stress-regulated cellular functions need to be identified. This review discusses the generation of ROS within tumour cells, their detoxification, their cellular effects, as well as the major signalling cascades they utilize, but also provides an outlook on their modulation in therapeutics.
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            A tissue-scale gradient of hydrogen peroxide mediates rapid wound detection in zebrafish

            Philipp Niethammer, Clemens Grabher, A. Thomas Look … (2009)
            Barrier structures (e.g. epithelia around tissues, plasma membranes around cells) are required for internal homeostasis and protection from pathogens. Wound detection and healing represent a dormant morphogenetic program that can be rapidly executed to restore barrier integrity and tissue homeostasis. In animals, initial steps include recruitment of leukocytes to the site of injury across distances of hundreds of micrometers within minutes of wounding. The spatial signals that direct this immediate tissue response are unknown. Due to their fast diffusion and versatile biological activities, reactive oxygen species (ROS), including hydrogen peroxide (H2O2), are interesting candidates for wound-to-leukocyte signalling. We probed the role of H2O2 during the early events of wound responses in zebrafish larvae expressing a genetically encoded H2O2 sensor1. This reporter revealed a sustained rise in H2O2 concentration at the wound margin, starting ∼3 min after wounding and peaking at ∼20 min, which extended ∼100−200 μm into the tail fin epithelium as a decreasing concentration gradient. Using pharmacological and genetic inhibition, we show that this gradient is created by Dual oxidase (Duox), and that it is required for rapid recruitment of leukocytes to the wound. This is the first observation of a tissue-scale H2O2 pattern, and the first evidence that H2O2 signals to leukocytes in tissues, in addition to its known antiseptic role.
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              The Role of the Reactive Oxygen Species and Oxidative Stress in the Pathomechanism of the Age-Related Ocular Diseases and Other Pathologies of the Anterior and Posterior Eye Segments in Adults

              Malgorzata Nita, Andrzej Grzybowski (2016)
              The reactive oxygen species (ROS) form under normal physiological conditions and may have both beneficial and harmful role. We search the literature and current knowledge in the aspect of ROS participation in the pathogenesis of anterior and posterior eye segment diseases in adults. ROS take part in the pathogenesis of keratoconus, Fuchs endothelial corneal dystrophy, and granular corneal dystrophy type 2, stimulating apoptosis of corneal cells. ROS play a role in the pathogenesis of glaucoma stimulating apoptotic and inflammatory pathways on the level of the trabecular meshwork and promoting retinal ganglion cells apoptosis and glial dysfunction in the posterior eye segment. ROS play a role in the pathogenesis of Leber's hereditary optic neuropathy and traumatic optic neuropathy. ROS induce apoptosis of human lens epithelial cells. ROS promote apoptosis of vascular and neuronal cells and stimulate inflammation and pathological angiogenesis in the course of diabetic retinopathy. ROS are associated with the pathophysiological parainflammation and autophagy process in the course of the age-related macular degeneration.
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                Author and article information

                Journal
                Journal ID (nlm-journal-id): 101773223
                Journal ID (pubmed-jr-id): 50147
                Journal ID (nlm-ta): Endocrines
                Journal ID (iso-abbrev): Endocrines
                Title: Endocrines
                ISSN (Electronic): 2673-396X
                Publication date Nihms-submitted: 11 December 2022
                Publication date (Print): December 2022
                Publication date (Electronic): 09 December 2022
                Publication date PMC-release: 19 December 2022
                Volume: 3
                Issue: 4
                Pages: 813-820
                Affiliations
                School of Basic Pharmaceutical and Toxicological Sciences, College of Pharmacy, University of Louisiana Monroe, 1800 Bienville Drive, Monroe, LA 71201, USA
                Author notes

                Author Contributions: K.-T.K.: writing—original draft preparation, investigation, M.S.A.: investigation, formal analysis, writing—review and editing, K.A.: writing—review and editing, N.B.: visualization, supervision, funding acquisition, writing—review and editing. All authors have read and agreed to the published version of the manuscript.

                [* ]Correspondence: barabutis@ 123456ulm.edu ; Tel.: +1-(318)-342-1460; Fax: +1-(318)-342-1737
                Author information
                http://orcid.org/0000-0003-2964-3870
                http://orcid.org/0000-0001-8366-5099
                Article
                Manuscript ID: NIHMS1856743
                DOI: 10.3390/endocrines3040067
                PMC ID: 9762825
                PubMed ID: 36540765
                SO-VID: ae13f077-c929-4eeb-93ea-c06666917f69
                License:

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( https://creativecommons.org/licenses/by/4.0/).

                History
                Categories
                Subject: Article

                Keywords: inflammation,lung injury,endothelium,oxidative stress
                Data availability:
                Keywords: inflammation, lung injury, endothelium, oxidative stress

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