Histochemical changes of the lung tissue in experimental chronic alcoholic intoxication



  • Alexey Lazko Astrakhan State Medical University, Astrakhan, Russia
  • Larisa Udochkina Astrakhan State Medical University, Astrakhan, Russia https://orcid.org/0000-0001-5016-0633
  • Nina Losovskaya Alexandro-Mariinsky Regional Clinical Hospital, Astrakhan, Russia


lungs, chronic alcohol intoxication, alcohol dehydrogenase, succinate dehydrogenase, glucose-6-phosphate dehydrogenase, acid phosphatase, alkaline phosphatase, nonspecific esterases


Among organ systems in the human body affected by alcohol abuse, the lungs are particularly vulnerable to infections and injury. Chronic alcoholism causes alterations in host defence of the upper and lower airways, disruption of alveolar epithelial barrier integrity, alcohol-induced ciliary lesions and alveolar macrophages dysfunction. Currently with a spread of SARS-COV 2 infections which instantly destroys the lung tissue, the alcohol-induced lung damage issues acquire vital importance, as they might further increase severity of lesions of lung tissue in the infected alcohol abusers.Recent investigations suggest that the effect of the chronic excessive alcohol consumption and SARS-COV 2 infection on the lungs might have similar and thus synergizing mechanisms. Therefore the mechanism of the lung tissue lesions in chronic alcohol intoxication need to be scrutinized, including the time-line of their development, to be able to develop more effective preventive measures. The objective of the study is to assess histochemical changes in the lung tissue of laboratory animals with chronic alcohol intoxication of different duration. Total of 48 outbred male white mice weighing 18-22 g were enrolled in the study. The experimental animals were exposed to alcohol for 1, 2 and 3 months by the semi-voluntary intake, using 20% alcohol as the only source of fluid, while control animals were getting drinking water. At the end of experiment the lung tissue of the mice was processed histologically and histochemically for alcoholic dehydrogenase (ADH), glucose-6-phasphate-dehydrogenae (G6PDH), alkaline (ALP) and acidic (AP) phosphatases, nonspecific esterase (NE) and succinate dehydrogenase (SDH). Image analysis of the histological slides was performed using Image Pro Plus software. Statistical differences were assessed using paired t-test. Chronic alcohol consumption causes metabolic lesions in the alveolar epithelium and endothelium of alveolar capillaries revealed by an increase in the activity of ADH, G6PD and NE paralleled with a decrease in the total SDH activity of the respiratory portion of the lungs in a time-related pattern. High activity of alkaline phosphatase was noted in endothelial cells of lung capillaries. Thus, under conditions of chronic intoxication, ethanol disturbs cell metabolism, as evidenced by the changes of the enzymatic activity in the lung tissue which leads to inhibition of oxygen-dependent metabolic processes and activation of reserve mechanisms for compensating of energy deficits.