Chronic morphine treatment induces oxidant and apoptotic damage in the mice liver

Payabvash, Seyedmehdi; Beheshtian, Azadeh; Salmasi, Amirali; Kiumehr, Saman; Ghahremani, Mohammad Hossein; Tavangar, Seyed Mohammad; Sabzevari, Omid; Dehpour, Ahmad Reza

doi:10.1016/j.lfs.2006.05.008

Cited by 61 publications

(58 citation statements)

References 44 publications

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“…Opioid peptides are up regulated in diseases states such as liver dysfunction, endotoxic shock, trauma and cholestasis (7,11,14). Morphine administration is shown to induce oxidative stress and increase superoxide dismutase and catalase activities and apoptosis in liver tissue (32). Furthermore, several studies implicate a role for opioid peptides in total cholesterol, VLDL and low-density lipoprotein (LDL) cholesterol dysregulation (5).…”

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confidence: 99%

Naltrexone attenuates endoplasmic reticulum stress induced hepatic injury in mice

Moslehi

Nabavizadeh

Dehpou

et al. 2014

Acta Physiologica Hungarica

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Endoplasmic reticulum (ER) stress provides abnormalities in insulin action, inflammatory responses, lipoprotein B100 degradation and hepatic lipogenesis. Excess accumulation of triglyceride in hepatocytes may also lead to disorders such as non-alcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). Opioid peptides are involved in triglyceride and cholesterol dysregulation, inflammation and cell death. In this study, we evaluated Naltrexone effects on ER stress induced liver injury. To do so, C57/BL6 mice received saline, DMSO and Naltrexone, as control groups. ER stress was induced by tunicamycin (TM) injection. Naltrexone was given before TM administration. Liver blood flow and biochemical serum analysis were measured. Histopathological evaluations, TNF-α measurement and Real-time RT-PCR were also performed. TM challenge provokes steatosis, cellular ballooning and lobular inflammation which significantly reduced in Naltrexone treated animals. ALT, AST and TNF-α increased in the TM group and improved in the Naltrexone plus TM group. Triglyceride and cholesterol levels decreased in TM treated mice with no increase in Naltrexone treated animals. In the Naltrexone plus TM group, gene expression of Bax/Bcl-2 ratio and caspase3 significantly lowered compared with the TM group. In this study, we found that Naltrexone had a notable alleviating role in ER stress induced steatosis and liver injury.

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confidence: 99%

Naltrexone attenuates endoplasmic reticulum stress induced hepatic injury in mice

Moslehi

Nabavizadeh

Dehpou

et al. 2014

Acta Physiologica Hungarica

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“…Many studies have demonstrated that morphine may decrease the incidence, development or spread of certain cancers, because it has been associated with downregulation of developmental processes and cell activity, including tumor growth retardation. Payabvash et al (Payabvash et al, 2006) found that morphine inhibited mice liver cancer growth. Also, morphine has been demonstrated to decrease growth of human breast cancer cells in vitro (Hatzoglou et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Exogenous Morphine Inhibits Human Gastric Cancer MGC-803 Cell Growth by Cell Cycle Arrest and Apoptosis Induction

Qin

Chen²,

Li³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Morphine is not only an analgesic treating pain for patients with cancer but also a potential anticancer drug inhibiting tumor growth and proliferation. To gain better insight into the involvement of morphine in the biological characteristics of gastric cancer, we investigated effects on progression of gastric carcinoma cells and the expression of some apoptosis-related genes including caspase-9, caspase-3, survivin and NF-κB using the MGC-803 human gastric cancer cell line. The viability of cells was assessed by MTT assay, proliferation by colony formation assay, cell cycle progression and apoptosis by flow cytometry and ultrastructural alteration by transmission electron microscopy. The influences of morphine on caspase-9, caspase-3, survivin and NF-κB were evaluated by semi-quantitative RT-PCR and Western blot. Our data showed that morphine could significantly inhibit cell growth and proliferation and cause cell cycle arrest in the G2/M phase. MGC-803 cells which were incubated with morphine also had a higher apoptotic rate than control cells. Morphine also led to morphological changes of gastric cancer cells. The mechanism of morphine inhibiting gastric cancer progression in vitro might be associated with activation of caspase-9 and caspase-3 and inhibition of survivin and NF-κB.

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“…This conclusion also derived from findings related to chronic morphine administration in latent pain situations, where morphine's cytotoxic effects may be partially associated with apoptosis induction [36]. Again, we see the double-edged sword in morphine physiology and regulation, however, the specific mechanisms by which morphine influences tumor growth are far from being fully understood.…”

Section: Apoptotic and Transcriptional Effects Of Morphine Administramentioning

confidence: 67%

“…Researchers recently have proposed a protective role for morphine against tumor growth and metastasis through induction of apoptosis in tumor cells [36,37]. This conclusion also derived from findings related to chronic morphine administration in latent pain situations, where morphine's cytotoxic effects may be partially associated with apoptosis induction [36].…”

Section: Apoptotic and Transcriptional Effects Of Morphine Administramentioning

confidence: 98%

Endogenous morphine/nitric oxide-coupled regulation of cellular physiology and gene expression: Implications for cancer biology

Stefano

Kream

Mantione

et al. 2008

Seminars in Cancer Biology

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Cancer is a simplistic, yet complicated, process that promotes uncontrolled growth. In this regard, this unconstrained proliferation may represent primitive phenomena whereby cellular regulation is suspended or compromised. Given the new empirical evidence for a morphinergic presence and its profound modulatory actions on several cellular processes it is not an overstatement to hypothesize that morphine may represent a key chemical messenger in the process of modulating proliferation of diverse cells. This has been recently demonstrated by the finding of a novel opiate-alkaloid selective receptor subtype in human multilineage progenitor cells (MLPC). Adding to the significance of morphinergic signaling are the findings of its presence in plant, invertebrate and vertebrate cells, which also have been shown to synthesize this messenger as well. Interestingly, we and others have shown that some cancerous tissues contain morphine. Furthermore, in medullary histolytic reticulosis, which is exemplified by cells having hyperactivity, the mu3 (μ 3 ) opiate select receptor was not present. Thus, it would appear that morphinergic signaling has inserted itself in many processes taking a long time to evolve, including those regulating the proliferation of cells across diverse phyla.Keywords endogenous morphine; μ 3 opiate receptor; nitric oxide; stem cell; cancer * Corresponding Author: Dr. George B. Stefano, Neuroscience Research Institute, SUNY College at Old Westbury, P.O. Box 210, Old Westbury, NY 11568, USA Tel: 001-516-876-2732; Fax: 001-516-876-2727; Email: gstefano@sunynri.org. Email addresses: gstefano@sunynri.org (GB Stefano); rmkream@sunynri.org (RM Kream); kmantione@sunynri.org (KJ Mantione); msheehan@sunynri.org (M Sheehan); patcad@sunynri.org (P Cadet); zhuwei@sunynri.org (W Zhu); tbilfinger@notes.cc.sunysb.edu (TV Bilfinger); esch@fh-coburg.de (T Esch) Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptSemin Cancer Biol. Author manuscript; available in PMC 2009 June 1. Historical Context and Clinical ImplicationsMorphine and chemically related opiate alkaloids represent time-tested analgesic principles for management of severe pain associated with metastatic disease [1,2]. A substantial body of accumulated evidence, however, documents a cadre of cellular/physiological effects associated with pharmacological administration of morphine and related opiate alkaloids that lie outside the realm of anti-nociception and appear to be mediated by indirect and/or "non-traditional" mechanisms. Notably, complementary studies have monitored ...

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Chronic morphine treatment induces oxidant and apoptotic damage in the mice liver

Cited by 61 publications

References 44 publications

Naltrexone attenuates endoplasmic reticulum stress induced hepatic injury in mice

Naltrexone attenuates endoplasmic reticulum stress induced hepatic injury in mice

Exogenous Morphine Inhibits Human Gastric Cancer MGC-803 Cell Growth by Cell Cycle Arrest and Apoptosis Induction

Endogenous morphine/nitric oxide-coupled regulation of cellular physiology and gene expression: Implications for cancer biology

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