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Reappraisal of xenobiotic-induced, oxidative stress-mediated cellular injury in chronic pancreatitis: a systematic review.

Abstract

AIM

To reappraise the hypothesis of xenobiotic induced, cytochrome P450-mediated, micronutrient-deficient oxidative injury in chronic pancreatitis.

METHODS

Individual searches of the Medline and Embase databases were conducted for each component of the theory of oxidative-stress mediated cellular injury for the period from 1(st) January 1990 to 31(st) December 2012 using appropriate medical subject headings. Boolean operators were used. The individual components were drawn from a recent update on theory of oxidative stress-mediated cellular injury in chronic pancreatitis.

RESULTS

In relation to the association between exposure to volatile hydrocarbons and chronic pancreatitis the studies fail to adequately control for alcohol intake. Cytochrome P450 (CYP) induction occurs as a diffuse hepatic and extra-hepatic response to xenobiotic exposure rather than an acinar cell-specific process. GSH depletion is not consistently confirmed. There is good evidence of superoxide dismutase depletion in acute phases of injury but less to support a chronic intra-acinar depletion. Although the liver is the principal site of CYP induction there is no evidence to suggest that oxidative by-products are carried in bile and reflux into the pancreatic duct to cause injury.

CONCLUSION

Pancreatic acinar cell injury due to short-lived oxygen free radicals (generated by injury mediated by prematurely activated intra-acinar trypsin) is an important mechanism of cell damage in chronic pancreatitis. However, in contemporary paradigms of chronic pancreatitis this should be seen as one of a series of cell-injury mechanisms rather than a sole mediator.

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  • Authors+Show Affiliations

    Ajith K Siriwardena, Hepatobiliary Surgery Unit, Manchester Royal Infirmary, Manchester M13 9WL, United Kingdom.

    Source

    World journal of gastroenterology 20:11 2014 Mar 21 pg 3033-43

    MeSH

    Acinar Cells
    Animals
    Antioxidants
    Cytochrome P-450 Enzyme System
    Enzyme Induction
    Glutathione Transferase
    Hepatocytes
    Humans
    Inhalation Exposure
    Micronutrients
    Oxidative Stress
    Pancreatitis, Chronic
    Superoxide Dismutase
    Xenobiotics

    Pub Type(s)

    Journal Article
    Review
    Systematic Review

    Language

    eng

    PubMed ID

    24659895

    Citation

    Siriwardena, Ajith K.. "Reappraisal of Xenobiotic-induced, Oxidative Stress-mediated Cellular Injury in Chronic Pancreatitis: a Systematic Review." World Journal of Gastroenterology, vol. 20, no. 11, 2014, pp. 3033-43.
    Siriwardena AK. Reappraisal of xenobiotic-induced, oxidative stress-mediated cellular injury in chronic pancreatitis: a systematic review. World J Gastroenterol. 2014;20(11):3033-43.
    Siriwardena, A. K. (2014). Reappraisal of xenobiotic-induced, oxidative stress-mediated cellular injury in chronic pancreatitis: a systematic review. World Journal of Gastroenterology, 20(11), pp. 3033-43. doi:10.3748/wjg.v20.i11.3033.
    Siriwardena AK. Reappraisal of Xenobiotic-induced, Oxidative Stress-mediated Cellular Injury in Chronic Pancreatitis: a Systematic Review. World J Gastroenterol. 2014 Mar 21;20(11):3033-43. PubMed PMID: 24659895.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Reappraisal of xenobiotic-induced, oxidative stress-mediated cellular injury in chronic pancreatitis: a systematic review. A1 - Siriwardena,Ajith K, PY - 2013/09/19/received PY - 2013/11/05/revised PY - 2013/12/03/accepted PY - 2014/3/25/entrez PY - 2014/3/25/pubmed PY - 2015/4/14/medline KW - Cellular injury KW - Chronic pancreatitis KW - Cytochrome P450 KW - Oxidative stress KW - Xenobiotics SP - 3033 EP - 43 JF - World journal of gastroenterology JO - World J. Gastroenterol. VL - 20 IS - 11 N2 - AIM: To reappraise the hypothesis of xenobiotic induced, cytochrome P450-mediated, micronutrient-deficient oxidative injury in chronic pancreatitis. METHODS: Individual searches of the Medline and Embase databases were conducted for each component of the theory of oxidative-stress mediated cellular injury for the period from 1(st) January 1990 to 31(st) December 2012 using appropriate medical subject headings. Boolean operators were used. The individual components were drawn from a recent update on theory of oxidative stress-mediated cellular injury in chronic pancreatitis. RESULTS: In relation to the association between exposure to volatile hydrocarbons and chronic pancreatitis the studies fail to adequately control for alcohol intake. Cytochrome P450 (CYP) induction occurs as a diffuse hepatic and extra-hepatic response to xenobiotic exposure rather than an acinar cell-specific process. GSH depletion is not consistently confirmed. There is good evidence of superoxide dismutase depletion in acute phases of injury but less to support a chronic intra-acinar depletion. Although the liver is the principal site of CYP induction there is no evidence to suggest that oxidative by-products are carried in bile and reflux into the pancreatic duct to cause injury. CONCLUSION: Pancreatic acinar cell injury due to short-lived oxygen free radicals (generated by injury mediated by prematurely activated intra-acinar trypsin) is an important mechanism of cell damage in chronic pancreatitis. However, in contemporary paradigms of chronic pancreatitis this should be seen as one of a series of cell-injury mechanisms rather than a sole mediator. SN - 2219-2840 UR - https://www.unboundmedicine.com/medline/citation/24659895/full_citation L2 - http://www.wjgnet.com/1007-9327/full/v20/i11/3033.htm DB - PRIME DP - Unbound Medicine ER -