Biochemical cellular damage indicators and in situ cell death in chronic alcohol consumption: Pseudomonas aeruginosa induced pneumonia rat model

Abstract

In this study, our aim was to investigate whether cellular alterations occurred in liver and lung tissue in presence of chronic alcohol ingestion and Pseudomonas aeruginosa pneumonia related to oxidative stress and in situ cell death. Male wistar rats were divided into five groups: the sham group fed by normal solid diet, two control groups; one fed by normal liquid diet, and the other fed by liquid diet plus ethanol, two pneumonia groups induced by Pseudomonas aeruginosa; one fed by normal liquid diet, and the other fed by liquid diet plus ethanol. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelling analysis was performed to confirm in situ cell death. Serum alanine amino transferase and lactate dehydrogenase activities, and tissue and serum malondialdehyde levels, paraoxonase, arylesterase activities, and tissue caspase-3 activities were determined. Serum alanine amino transferase activities of both ethanol given groups were higher than the other groups (p<0.05). Liver malondialdehyde level was increased in ethanol with pneumonia group (p<0.05). Lung malondialdehyde levels were not different among groups. Terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelling positive cell ratio in the liver was higher in both ethanol given groups and normal liquid diet with pneumonia group than sham and control group fed by normal liquid diet. Liver and lung caspase-3 activities were not different among groups. Although serum paraoxonase activities were lower in both pneumonia groups, it was not statistically significant. It may be interpreted as growing infection during chronic ethanol ingestion that causes increased liver damage through oxidative stress.