CONCLUSION: Acetylsalicylic acid (aspirin, ASA) in a therapeutic dose prevents lipid peroxidation and damage of cell organelles in pancreatic tissue of rats chronically fed with ethanol. In contrast, higher ASA dosages lead to enhanced biochemical and morphological signs of pancreatic damage different from findings in rats fed by ethanol alone. METHODS: Two groups of rats received 20% alcohol as drinking fluid plus a diet containing either 6 (S6) or 10 g/kg (S10) ASA. Two control groups received no ASA (CA) and neither ASA nor alcohol (CW), respectively. Feeding was performed by the interrupted feeding regimen with four 18-h periods of food and fluid withdrawal weekly. After 7 mo, pancreatic tissue was examined by light and electron microscopy. In pancreas homogenates, the contents of malondialdehyde (MDA), protein, trypsinogen, lipase, pancreatic secretory trypsin inhibitor, acid phosphatase (AcPh), cathepsin B, beta-glucuronidase, and desoxyribonucleic acid were determined. RESULTS: In the pancreas of group CA, we found a 100% increase of MDA compared with group CW, increased fat deposition, as well as damaged mitochondria (Mito) and endoplasmic reticula (ER) in acinar cells, decreased protein content, decreased AcPh activity, and unchanged secretory parameters. The ASA-fed groups showed MDA contents indistinguishable from group CW. Protein and secretory parameters were decreased. Lysosomal enzymes were decreased in S6, but in S10, they were always higher than in group S6 and mostly as high as in group CW. Fat deposits were as frequent as in group CA. Mito and ER were mostly well preserved, but more autophagosomes and residual bodies occurred, particularly in group S10.
CONCLUSION:Acetylsalicylic acid (aspirin, ASA) in a therapeutic dose prevents lipid peroxidation and damage of cell organelles in pancreatic tissue of rats chronically fed with ethanol. In contrast, higher ASA dosages lead to enhanced biochemical and morphological signs of pancreatic damage different from findings in rats fed by ethanol alone. METHODS: Two groups of rats received 20% alcohol as drinking fluid plus a diet containing either 6 (S6) or 10 g/kg (S10) ASA. Two control groups received no ASA (CA) and neither ASA nor alcohol (CW), respectively. Feeding was performed by the interrupted feeding regimen with four 18-h periods of food and fluid withdrawal weekly. After 7 mo, pancreatic tissue was examined by light and electron microscopy. In pancreas homogenates, the contents of malondialdehyde (MDA), protein, trypsinogen, lipase, pancreatic secretory trypsin inhibitor, acid phosphatase (AcPh), cathepsin B, beta-glucuronidase, and desoxyribonucleic acid were determined. RESULTS: In the pancreas of group CA, we found a 100% increase of MDA compared with group CW, increased fat deposition, as well as damaged mitochondria (Mito) and endoplasmic reticula (ER) in acinar cells, decreased protein content, decreased AcPh activity, and unchanged secretory parameters. The ASA-fed groups showed MDA contents indistinguishable from group CW. Protein and secretory parameters were decreased. Lysosomal enzymes were decreased in S6, but in S10, they were always higher than in group S6 and mostly as high as in group CW. Fat deposits were as frequent as in group CA. Mito and ER were mostly well preserved, but more autophagosomes and residual bodies occurred, particularly in group S10.