Quantitative morphological study of age-related features of structural restructuring of endothelial cells of arteries and veins of the prostate gland at ethanol intoxication

Abstract

Ethanol is one of the most common vascular toxins that directly damages endothelial cells and provokes microcirculatory disorders. The prostate gland, as a component of the male reproductive system, is highly sensitive to toxic influences, while its vascular bed is especially vulnerable to chronic ethanol exposure. Studying age-related remodeling of endotheliocytes under normal conditions and during ethanol intoxication is crucial for understanding the pathogenesis of prostate lesions. These data are also important for pediatric urology and surgery, since many pathological processes in adulthood originate from vascular dysfunctions developing at a younger age.

Аim - to investigate, using morphometric methods, the age-related features of structural remodeling of endothelial cells in the arterial and venous systems of the prostate gland in experimental animals exposed to prolonged ethanol intoxication.

Materials and methods. The study was conducted on 60 mature male white rats divided into four groups: intact animals aged 6 and 24 months, and ethanol-intoxicated rats of the same age. Histological preparations of the prostate gland were analyzed using hematoxylin-eosin and special stains (van Gieson, Mallory, Masson, toluidine blue, silver impregnation). Morphometric parameters included cell and nuclear area, nuclear-cytoplasmic index, and the proportion of damaged cells.

Results. In intact rats, age-related atrophic changes were observed in prostate endotheliocytes, with an 8.2% reduction in cell area and an 8.8% reduction in nuclear area. Chronic ethanol intoxication caused more pronounced alterations: in 6-month-old rats, cell area decreased by 28.1%, and in 24-month-old rats by 29.7%. The proportion of damaged endothelial cells in the arterial system increased 11.8-fold in young animals and 12.2-fold in older animals, while in the venous system the increase was 9.4-fold and 9.8-fold, respectively. Morphological examination revealed vascular wall thickening, intimal proliferation, mucoid swelling, fibrinoid necrosis, elastofibrosis, and dystrophic as well as necrobiotic changes of endotheliocytes, confirming endothelial dysfunction.

Conclusions. Prolonged ethanol exposure leads to age-dependent remodeling of prostate endothelial cells, manifested by cell atrophy, decreased nuclear size, imbalance of nuclear-cytoplasmic relationships, and a sharp increase in the proportion of damaged cells. The findings expand current understanding of endothelial dysfunction mechanisms in alcohol-related pathology and provide a morphological basis for developing preventive and therapeutic strategies for urogenital diseases, including in pediatric urology and surgery.

The experiments with laboratory animals were provided in accordance with all bioethical norms and guidelines.

The authors declare no conflict of interest.