Pathophysiological Events Associated With Pancreatitis in Response to Tobacco: An In Vitro Comparative Study With Ethanol in Primary Acinar Cell Culture.
Cuvinte cheie
Abstract
OBJECTIVE
The aim of this study was to comparatively analyze the effects of different concentrations of cigarette smoke condensate (CSC, a standardized tobacco extract) and ethanol on intracellular enzyme activation, cell necrosis, alteration of cytosolic calcium concentration ([Ca]c), and amylase secretion in pancreatic acinar cells.
METHODS
The effects of CSC (1 μg/mL to 0.4 mg/mL) and ethanol (10-100 mM) on intracellular enzyme activity, cell necrosis, and [Ca]c were measured by fluorescence assays in isolated pancreatic acinar cells. Amylase secretion was evaluated by spectrophotometry. Supramaximal concentrations of cholecystokinin (10-100 nM) were used as positive control.
RESULTS
Neither CSC nor ethanol induced trypsin or elastase activation. Both CSC (0.1-0.4 mg/mL) and ethanol (10-75 mM) significantly increased [Ca]c. Amylase secretion was increased only in CSC-treated cells (0.3 and 0.4 mg/mL). After 60 minutes, CSC (0.3 and 0.4 mg/mL) significantly increased acinar cell necrosis at a similar percentage to that induced by cholecystokinin. Ethanol did not induce any significant cell necrosis.
CONCLUSIONS
Cigarette smoke condensate induces acinar cell injury and increases [Ca]c and amylase secretion, independently of intracellular enzyme activation, suggesting that tobacco could induce several main early events of pancreatitis in pancreatic acinar cells. However, ethanol only induces increases [Ca]c, having no effect on cell injury, amylase secretion, or intracellular enzyme activation.
