Opioids in Inducing Cell Apoptosis: A Mini Review
Keywords:
Apoptosis, heroin, methadone, morphine, opioidsAbstract
Opioids are opium-like drugs which are commonly used as analgesics to treat moderate to severe pain. Apoptosis is a type of programmed cell death to remove unnecessary or damaged cells in an organism. Recently, the ability of opioids to induce apoptosis especially in cancer cell lines has gained the interest of many researchers. This fascinating finding has led to more testing of different kinds of opioids against different kinds of cancer cell lines in the course to search for the potential anticancer drugs. This review provides current information about opioids and apoptosis, and more importantly the compilations of researches over the years on how opioids are related to apoptotic cells death.References
Ripamonti CI, Bandieri E, Roila F. Management of cancer pain: ESMO Clinical Practice Guidelines. Annals of Oncology. 2011;22.
Inturrisi CE. Clinical pharmacology of opioids for pain. The Clinical journal of pain. 2002;18(4 Suppl):S3-13.
Drug Enforcement Administration. Drugs of Abuse – 2015 Edition: A DEA Resource Guide 2015. Available from: https://www.dea.gov/pr/multimedialibrary/publications/drug_of_abuse.pdf#page=38
National Institute on Drug Abuse. Research Report Series: Prescription Drug Abuse. Available from: https://www.drugabuse.gov/sites/default/files/rxreportfinalprint.pdf.
Akhgari M, Etemadi-Aleagha A, Jokar F. Street Level Heroin, an Overview on Its Components and Adulterants. Neuropathology of Drug Addictions and Substance Misuse. 2016;1(Chapter 81):867-77.
Stoelting RK, Miller RD. Chapter 10: Opioids. Basics of Anesthesia: Churchill Livingstone, Elsevier Inc; 2007.
National Institute on Drug Abuse (NIDA). The Neurobiology of Drug Addiction 2007. Available from: https://www.drugabuse.gov/sites/default/files/1922-the-neurobiology-of-drug-addiction.pdf
Loris AC. Opioids - mechanisms of action 1996. Available from: https://www.nps.org.au/australianprescriber/articles/opioids-mechanisms-of-action#authors.
Ghelardini C, Di Cesare Mannelli L, Bianchi E. The pharmacological basis of opioids. Clinical cases in mineral and bone metabolism: the official journal of the Italian Society of Osteoporosis, Mineral Metabolism, and Skeletal Diseases. 2015;12(3):219-21.
Kam PCA, Ferch NI. Apoptosis: mechanisms and clinical implications. Anaesthesia. 2000;55:1081-93.
Martin SJ. Apoptosis: suicide, execution or murder? Trends in cell biology. 1993;3(5):141-4.
Archana M, Bastian, Yogesh T, Kumaraswamy K. Various methods available for detection of apoptotic cells- A review. Indian Journal of Cancer. 2013;50(3):274-83.
Zhao H. Extrinsic and Intrinsic Apoptosis Signal Pathway Review Apoptosis and Medicine, InTech 2012.
Elmore S. Apoptosis: a review of programmed cell death. Toxicologic pathology. 2007;35(4):495-516.
Kischkel F, Hellbardt S, Behrmann I, Germer M, Pawlita M, Krammer P, et al. Cytotoxicitydependent APO-1 (Fas/CD95)- associated proteins form a death-inducing signaling complex (DISC) with the receptor. Embo J. 1995;14:5579–88.
Du C, Fang M, Li Y, Li L, Wang X. Smac, a mitochondrial protein that promotes cytochrome c-dependent caspase activation by eliminating IAP inhibition. Cell. 2000;102(1):33-42.
van Loo G, van Gurp M, Depuydt B, Srinivasula SM, Rodriguez I, Alnemri ES, et al. The serine protease Omi/HtrA2 is released from mitochondria during apoptosis. Omi interacts with caspase-inhibitor XIAP and induces enhanced caspase activity. Cell death and differentiation. 2002;9(1):20-6.
Garrido C, Galluzzi L, Brunet M, Puig PE, Didelot C, Kroemer G. Mechanisms of cytochrome c release from mitochondria. Cell death and differentiation. 2006;13(9):1423-33.
Schimmer AD. Inhibitor of apoptosis proteins: translating basic knowledge into clinical practice. Cancer research. 2004;64(20):7183-90.
Joza N, Susin SA, Daugas E, Stanford WL, Cho SK, Li CY, et al. Essential role of the mitochondrial apoptosis-inducing factor in programmed cell death. Nature. 2001;410(6828):549-54.
Li L, Luo X, Wang X. Endonuclease G is an apoptotic DNase when released from mitochondria. Nature. 2001;412:95–9.
Enari M, Sakahira H, Yokoyama H, Okawa K, Iwamatsu A, Nagata S. A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD. Nature. 1998;391(6662):43-50.
Beesoo R, Neergheen-Bhujun V, Bhagooli R, Bahorun T. Apoptosis inducing lead compounds isolated from marine organisms of potential relevance in cancer treatment. Mutation research. 2014;768:84-97.
Koff JL, Ramachandiran S, Bernal-Mizrachi L. A time to kill: targeting apoptosis in cancer. International journal of molecular sciences. 2015;16(2):2942-55.
Ichim G, Tait SWG. A fate worse than death: apoptosis as an oncogenic process. Nature Reviews/ Cancer. 2016;16:539-48.
Klener P, Jr., Andera L, Klener P, Necas E, Zivny J. Cell death signalling pathways in the pathogenesis and therapy of haematologic malignancies: overview of apoptotic pathways. Folia biologica. 2006;52(1-2):34-44.
Bottone MG, Santin G, Aredia F, Bernocchi G, Pellicciari C, Scovassi AI. Morphological Features of Organelles during Apoptosis: An Overview. Cells. 2013;2(2):294-305.
Ziegler U, Groscurth P. Morphological features of cell death. News in physiological sciences: an international journal of physiology produced jointly by the International Union of Physiological Sciences and the American Physiological Society. 2004;19:124-8.
Chaabane W, User SD, El-Gazzah M, Jaksik R, Sajjadi E, Rzeszowska-Wolny J, et al. Autophagy, apoptosis, mitoptosis and necrosis: interdependence between those pathways and effects on cancer. Archivum immunologiae et therapiae experimentalis. 2013;61(1):43-58.
Wong A. Synthetic Opium: The Occurrence,Bioactivity, Biosynthesis and Synthesis of Oxycodone. Chemistry. 2008;150.
Klockgether-Radke AP. [F. W. Serturner and the discovery of morphine. 200 years of pain therapy with opioids]. Anasthesiologie, Intensivmedizin, Notfallmedizin, Schmerztherapie : AINS. 2002;37(5):244-9.
Schmitz R. Friedrich Wilhelm Serturner and the discovery of morphine. Pharmacy in history. 1985;27(2):61-74.
Freye E, Levy JV. Opioids in Medicine: A Comprehensive Review on the Mode of Action and the use of Analgesics in Different Pain States: Springer; 2008.
Gupta M, Singh J, Sood S, Arora B. Mechanism of antinociceptive effect of nimodipine in experimental diabetic neuropathic pain. Methods and findings in experimental and clinical pharmacology. 2003;25(1):49-52.
Hsiao PN, Chang MC, Cheng WF, Chen CA, Lin HW, Hsieh CY, et al. Morphine induces apoptosis of human endothelial cells through nitric oxide and reactive oxygen species pathways. Toxicology. 2009;256(1-2):83-91.
Zhang Y, Chen Q, Yu L-C. Morphine: A Protective or Destructive Role in Neurons? The Neuroscientist. 2008;14(6):561-70.
Ries RK, Fiellin DA, Miller SC, Saitz R. Principles of Addiction Medicine. Fourth ed: Lippincott Williams & Wilkins; 2009.
Smith HS. Opioid metabolism. Mayo Clinic proceedings. 2009;84(7):613-24.
Maneckjee R, Minna JD. Opioids Induce While Nicotine Suppresses Apoptosis in Human Lung Cancer Cells. Cell Growth & Differentiation. 1994;5:1033-40.
Singhal PC, Kapasi AA, Reddy K, Franki N, Gibbons N, Ding G. Morphine promotes apoptosis in Jurkat cells. Journal of leukocyte biology. 1999;66(4):650-8.
Deling Yin MW, Ying Zhang, Sarah Whaley, Junying Miao,Kenneth Ferslew, Jing Zhao, Charles Stuart. Morphine promotes Jurkat cell apoptosis through pro-apoptotic FADD/P53 and anti-apoptotic PI3K/Akt/NF-nB pathways. Journal of Neuroimmunology 2006;174:101-7.
Yin D, Mufson R, Wang R, Shi Y. Fas-mediated cell death promoted by opioids. Nature. 1999;397(6716):218.
Rytomaa M, Martins LM, Downward J. Involvement of FADD and caspase-8 signalling in detachment-induced apoptosis. Current biology : CB. 1999;9(18):1043-6.
Chen Q, Cui J, Zhang Y, Yu LC. Prolonged morphine application modulates Bax and Hsp70 levels in primary rat neurons. Neuroscience letters. 2008;441(3):311-4.
National Institute on Drug Abuse (NIDA). Drug Facts: Heroin2014 August 1, 2016 Available from: https://www.drugabuse.gov/publications/drugfacts/heroin.
Ciccarone D. Heroin in brown, black and white: Structural factors and medical consequences in the US heroin market. International Journal of Drug Policy. 2009;20(3):277-82.
Coleman MD. Human Drug Metabolism: An Introduction. John Wiley & Sons. 2010;Second edition:288.
Zovko A, Criscuolo CL. The pharmacological effects of diacetylmorphine (heroin) after diffusion through the blood–brain barrier. 2009.
Contestabile A. Cerebellar granule cells as a model to study mechanisms of neuronal apoptosis or survival in vivo and in vitro. Cerebellum. 2002;1(1):41-55.
Tan M, Li Z, Ma S, Luo J, Xu S, Lu A, et al. Heroin activates Bim via c-Jun N-terminal kinase/c-Jun pathway to mediate neuronal apoptosis. Neuroscience. 2013;233:1-8.
Gerlach R. A Brief Overview on the Discovery of Methadone. INDRO eV Munster. 2004.
Krantz MJ, Mehler PS. Treating opioid dependence. Growing implications for primary care. Arch Intern Med. 2004;164(3):277-88.
Fainsinger R, Schoeller T, Bruera E. Methadone in the management of cancer pain: a review. Pain. 1993;52(2):137-47.
Bruera E, Fainsinger R, Moore M, Thibault R, Spoldi E, Ventafridda V. Local toxicity with subcutaneous methadone. Experience of two centers. Pain. 1991;45(2):141-3.
Ferrari A, Coccia C, Bertolini A, Sternieri E. Methadone--metabolism, pharmacokinetics and interactions. Pharmacological Research. 2004;50(6):551-9.
Garrido MJ, Troconiz IF. Methadone: a review of its pharmacokinetic/pharmacodynamic properties. Journal of pharmacological and toxicological methods. 1999;42(2):61-6.
Nilsson MI, Widerlov E, Meresaar U, Anggard E. Effect of urinary pH on the disposition of methadone in man. European journal of clinical pharmacology. 1982;22(4):337-42.
Dole V, Nyswander M. Heroin addiction--a metabolic disease. Arch Intern Med. 1967;120(1):19-24.
Leppert W. The role of methadone in cancer pain treatment--a review. The International Journal Of Clinical Practice. 2009;63(7):1095-109.
Friesen C, Roscher M, Alt A, Miltner E. Methadone, commonly used as maintenance medication for outpatient treatment of opioid dependence, kills leukemia cells and overcomes chemoresistance. Cancer research. 2008;68(15):6059-64.
Perez-Alvarez S, Cuenca-Lopez MD, de Mera RM, Puerta E, Karachitos A, Bednarczyk P, et al. Methadone induces necrotic-like cell death in SH-SY5Y cells by an impairment of mitochondrial ATP synthesis. Biochimica et biophysica acta. 2010;1802(11):1036-47.
Friesen C, Roscher M, Hormann I, Fichtner I, Alt A, Hilger RA, et al. Cell death sensitization of leukemia cells by opioid receptor activation. Oncotarget. 2013;4(5):677-90.
Friesen C, Hormann I, Roscher M, Fichtner I, Alt A, Hilger R, et al. Opioid receptor activation triggering downregulation of cAMP improves effectiveness of anti-cancer drugs in treatment of glioblastoma. Cell cycle. 2014;13(10):1560-70.
Downloads
Published
Issue
Section
License
JBCS Publication Ethics
JBCS is committed to ensure the publication process follows specific academic ethics. Hence, Authors, Reviewers and Editors are required to conform to standards of ethical guidelines.
Authors
Authors should discuss objectively the significance of research work, technical detail and relevant references to enable others to replicate the experiments. JBCS do not accept fraudulent or inaccurate statements that may constitute towards unethical conduct.
Authors should ensure the originality of their works. In cases where the work and/or words of others have been used, appropriate acknowledgements should be made. JBCS do not accept plagiarism in all forms that constitute towards unethical publishing of an article.
This includes simultaneous submission of the same manuscript to more than one journal. Corresponding author is responsible for the full consensus of all co-authors in approving the final version of the paper and its submission for publication.
Reviewers
Reviewers of JBCS treat manuscripts received for review as confidential documents. Therefore, Reviewers must ensure the confidentiality and should not use privileged information and/or ideas obtained through peer review for personal advantage.
Reviews should be conducted based on academic merit and observations should be formulated clearly with supporting arguments. In cases where selected Reviewer feels unqualified to review a manuscript, Reviewer should notify the editor and excuse himself from the review process in TWO (2) weeks time from the review offer is made.
In any reasonable circumstances, Reviewers should not consider to evaluate manuscripts if they have conflicts of interest (i.e: competitive, collaborative and/or other connections with any of the authors, companies, or institutions affiliated to the papers).
Editors
Editors should evaluate manuscripts exclusively based on their academic merit. JBCS strictly do not allow editors to use unpublished information of authors without the written consent of the author. Editors are required to take appropriate responsive actions if ethical complaints have been presented concerning a submitted manuscript or published paper.
CONFLICT OF INTEREST
Journal of Biomedical and Clinical Sciences requires authors to declare all competing interests in relation to their work. All submitted manuscripts must include a ‘competing interests section at the end of the manuscript listing all competing interests (financial and non-financial). Where authors have no competing interests, the statement should read ,The authors have declared that no competing interests exist. Editors may ask for further information relating to competing interests.
Editors and reviewers are also required to declare any competing interests and will be excluded from the peer review process if a competing interest exists. Competing interests may be financial or non-financial. A competing interest exists when the authors interpretation of data or presentation of information may be influenced by their personal or financial relationship with other people or organizations. Authors should disclose any financial competing interests but also any non-financial competing interests that may cause them embarrassment if they were to become public after the publication of the article.
HUMAN AND ANIMAL RIGHTS
All research must have been carried out within an appropriate ethical framework. If there is suspicion that work has not taken place within an appropriate ethical framework, Editors will follow the Misconduct policy and may reject the manuscript, and/or contact the author(s) institution or ethics committee. On rare occasions, if the Editor has serious concerns about the ethics of a study, the manuscript may be rejected on ethical grounds, even if approval from an ethics committee has been obtained.
Research involving human subjects, human material, or human data, must have been performed in accordance with the Declaration of Helsinki and must have been approved by an appropriate ethics committee. A statement detailing this, including the name of the ethics committee and the reference number where appropriate, must appear in all manuscripts reporting such research. Further information and documentation to support this should be made available to Editors on request.
Experimental research on vertebrates or any regulated invertebrates must comply with institutional, national, or international guidelines, and where available should have been approved by an appropriate ethics committee. The Basel Declaration outlines fundamental principles to adhere to when conducting research in animals and the International Council for Laboratory Animal Science (ICLAS) has also published ethical guidelines.
A statement detailing compliance with relevant guidelines (e.g. the revised Animals (Scientific Procedures) Act 1986 in the UK and Directive 2010/63/EU in Europe) and/or ethical approval (including the name of the ethics committee and the reference number where appropriate) must be included in the manuscript. The Editor will take account of animal welfare issues and reserves the right to reject a manuscript, especially if the research involves protocols that are inconsistent with commonly accepted norms of animal research. In rare cases, Editors may contact the ethics committee for further information.
INFORMED CONSENT
For all research involving human subjects, informed consent to participate in the study should be obtained from participants (or their parent or guardian in the case of children under 16) and a statement to this effect should appear in the manuscript, this includes to all manuscripts that include details, images, or videos relating to individual participants.
DATA SHARING POLICY
JBCS strongly encourages that all datasets on which the conclusions of the paper rely should be available to readers. We encourage authors to ensure that their datasets are either deposited in publicly available repositories (where available and appropriate) or presented in the main manuscript or additional supporting files, in machine-readable format (such as spreadsheets rather than PDFs) whenever possible
Authors who do not wish to share their data must state that data will not be shared, and give the reason.
COPYRIGHT NOTICE
The JBCS retains the copyright of published manuscripts under the terms of the Copyright Transfer Agreement. However, the journal permits unrestricted use, distribution, and reproduction in any medium, provided permission to reuse, distribute and reproduce is obtained from the Journal's Editor and the original work is properly cited.
While the advice and information in this journal are believed to be true and accurate on the date of its going to press, neither the authors, the editors, nor the publisher can accept any legal responsibility for any errors or omissions that may be made. The publisher makes no warranty, express or implied, with respect to the material contained herein.
Copyright (c) 2023 Journal of Biomedical and Clinical Sciences (JBCS)
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
