Effects of acute alcohol intoxication on the respiration and dehydrogenase activity of rat pancreatic acini

The exocrine function of pancreatic acini cells is a highly energy-intensive process. A cell always needs to maintain a stable level of ATP balancing between states of activation and rest. Low-energy is one of the possible mechanisms contributing to the development of pancreatic diseases. The most commonly encountered disease of the pancreas is acute pancreatitis. It is known that excessive alcohol consumption causes the development of pancreatitis. The pathogenesis of this disease is linked to the cellular loss of energy, but the mechanism of alcohol’s effect on the mitochondria in pancreatic acini is unclear. This study’s main aim is to assess the impact of acute alcohol administration on the mitochondrial function of rat pancreatic acini. Wistar rats were administered ethanol (6 g/kg body weight) by oral gavage for 3 h before the experiment. A suspension of isolated pancreatic acini was obtained following collagenase digestion. Respiration of isolated pancreatic acini was studied with a Clark electrode. The maximal respiration rate was studied at different concentrations of protonophore FCCP (0.5–2 μM) in solutions containing glucose combined with oxidative substrates (pyruvate and glutamine, monomethyl-succinate or dimethyl-α-ketoglutarate). Dehydrogenase activity was measured by colorimetric method. Ethanol administration caused a significant increase in the activity of pyruvate dehydrogenase. It was confirmed that FCCP induced an increase in the respiration rate of pancreatic acinar cells in each experimental group. The addition of 1.5 μM FCCP reduced the respiration rate of pancreatic acini during the oxidation of glucose and monomethyl succinate or dimethyl-α-ketoglutarate, but not during the oxidation of glucose, pyruvate and glutamine substrates. The administration of ethanol had no impact on the basal or FCCP-uncoupled respiration of isolated pancreatic acini. The observed data are consistent with the findings of other researchers. However, alcohol exposure is not sufficient to cause mitochondrial damage in pancreatic acinar cells. In conclusion, acute ethanol administration does not cause mitochondrial dysfunction in the pancreas of rats but causes an increase in pyruvate dehydrogenase activity.