Oxygen Radical Production Precedes Alcohol-Induced Acute Pancreatitis in Rats

Wittel, Uwe A.; Bachem, Max G.; Siech, Marco

doi:10.1097/00006676-200305000-00018

Cited by 19 publications

(11 citation statements)

References 25 publications

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“…It was reported earlier that reactive oxygen species (ROS) generated in pancreatic acinar cells play an important role in chronic ethanol-induced pancreatitis (Norton et al, 1998;Szuster-Ciesielska et al, 2001;Wittel et al, 2003;). Further, ethanol-induced augmented ROS production has been implicated with lipid peroxidation (Takabayashi et al, 1995;Kono et al, 2001) which induces either apoptosis or necrosis depending on its extent (Andican et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Aqueous extract of black tea (Camellia sinensis) prevents ethanol+cholecystokinin-induced pancreatitis in a rat model

et al. 2006

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Section: Discussionmentioning

confidence: 99%

Aqueous extract of black tea (Camellia sinensis) prevents ethanol+cholecystokinin-induced pancreatitis in a rat model

et al. 2006

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“…A premature activation of digestive enzymes caused by an imbalance of trypsinogen and trypsinogen-inhibiting capacity [40] and a colocalization of digestive and lysosomal enzymes [41] as well as direct injury by ethanol metabolites (fatty acid ethyl esters) via the nonoxidative pathway [42] and intra-acinar oxidative stress through free oxygen radicals [43] are factors discussed in the literature. Singh et al [44] showed an increased activity of trypsinogen and a parallel decreased trypsin-inhibiting capacity in pancreata of rats chronically fed with the LDC alcohol diet.…”

Section: Discussionmentioning

confidence: 99%

Chronic Alcohol Intake Increases the Severity of Pancreatitis Induced by Acute Alcohol Administration, Hyperlipidemia and Pancreatic Duct Obstruction in Rats

et al. 2010

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“…The clinical experience that alcohol is mostly consumed together with fat-enriched meals led to the experimental design of this study. Alcohol caused already a certain amount of free radical production in vivo (31). Alcohol has recently been found to cause cellular damage by free oxygen radicals in the gastrointestinal mucosa (6), in the liver (22,28), and in the pancreas (19).…”

Section: Discussionmentioning

confidence: 99%

Stimulation of stellate cells by injured acinar cells: a model of acute pancreatitis induced by alcohol and fat (VLDL)

Siech

Zhou

Zhou³

et al. 2009

American Journal of Physiology-Gastrointestinal and Liver Physi

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MG. Stimulation of stellate cells by injured acinar cells: a model of acute pancreatitis induced by alcohol and fat (VLDL). Am J Physiol Gastrointest Liver Physiol 297: G1163-G1171, 2009. First published September 24, 2009 doi:10.1152/ajpgi.90468.2008.-Mechanisms leading to acute pancreatitis after a fat-enriched meal combined with excess alcohol are incompletely understood. We have studied the effects of alcohol and fat (VLDL) on pancreatic acinar cell (PAC) function, oxidative stress, and repair mechanisms by pancreatic stellate cells (PSC) leading to fibrogenesis. To do so, PAC (rat) were isolated and cultured up to 24 h. Ethanol and/or VLDL were added to PAC. We measured PAC function (amylase, lipase), injury (lactic dehydrogenase), apoptosis (TUNEL, Apo2.7, annexin V binding), oxidative stress, and lipid peroxidation (conjugated dienes, malondialdehyde, chemoluminescence); we also measured PSC proliferation (bromodeoxyuridine incorporation), matrix synthesis (immunofluorescence of collagens and fibronectin, fibronectin immunoassay), and fatty acids in PAC supernatants (gas chromatography). Within 6 h, cultured PAC degraded and hydrolyzed VLDL completely. VLDL alone (50 g/ml) and in combination with alcohol (0.2, 0.5, and 1% vol/vol) induced PAC injury (LDL, amylase, and lipase release) within 2 h through generation of oxidative stress. Depending on the dose of VLDL and alcohol, apoptosis and/or necrosis were induced. Antioxidants (Trolox, Probucol) reduced the cytotoxic effect of alcohol and VLDL. Supernatants of alcohol/VLDL-treated PAC stimulated stellate cell proliferation and extracellular matrix synthesis. We concluded that, in the presence of lipoproteins, alcohol induces acinar cell injury. Our results provide a biochemical pathway for the clinical observation that a fat-enriched meal combined with excess alcohol consumption can induce acinar cell injury (acute pancreatitis) followed by repair mechanisms (proliferation and increased matrix synthesis in PSC).ethanol; free radicals; pancreas THE MECHANISM OF ALCOHOLIC PANCREATITIS is incompletely understood. Despite the fact that about 40% of acute pancreatitis and 70% of chronic pancreatitis in humans are induced by alcohol, most alcoholics will never be affected by any of these diseases. As calculated by Ammann et al. (1), only 5% of all alcohol abusers will develop alcoholic pancreatitis. Interestingly enough, this can also be observed in setups with animals where acute pancreatitis cannot be induced by alcohol itself (8,15,25). Therefore, additional factors accompanying alcohol intake must be coresponsible for the induction of the disease. Some of these cofactors such as stimulation of pancreatic secretion and/or obstruction of pancreatic outflow have been experimentally observed by us and others (8,12,25,26).Clinical experience has taught us that a large number of patients presenting an acute event of alcoholic pancreatitis have drunk lots of alcohol together with an opulent (fat enriched) meal the day before onset of the disease. In the present ...

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Oxygen Radical Production Precedes Alcohol-Induced Acute Pancreatitis in Rats

Cited by 19 publications

References 25 publications

Aqueous extract of black tea (Camellia sinensis) prevents ethanol+cholecystokinin-induced pancreatitis in a rat model

Aqueous extract of black tea (Camellia sinensis) prevents ethanol+cholecystokinin-induced pancreatitis in a rat model

Chronic Alcohol Intake Increases the Severity of Pancreatitis Induced by Acute Alcohol Administration, Hyperlipidemia and Pancreatic Duct Obstruction in Rats

Stimulation of stellate cells by injured acinar cells: a model of acute pancreatitis induced by alcohol and fat (VLDL)

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