Abstract:
Chronic toxic hepatitis (CTH) in pregnant women represents a significant risk factor for impaired fetal development due to the
liver’s central role in metabolic regulation and detoxification. The gastrointestinal tract (GIT), which undergoes complex
morphogenesis during gestation, is particularly vulnerable to disruptions in maternal homeostasis. This study investigates the
morphological and morphometric alterations in the GIT of offspring born to mothers with experimentally induced CTH, aiming
to elucidate the potential mechanisms and long-term consequences of such exposure.
Using a controlled animal model, pregnant rats were subjected to chronic carbon tetrachloride (CCl₄)-induced hepatotoxicity to
simulate maternal CTH. Postnatal offspring were examined at day 21, with comparative histological and morphometric analyses
conducted on gastric, small intestinal, and colonic tissues. Histopathological evaluation revealed significant structural
abnormalities, including mucosal atrophy, glandular degeneration in the stomach, shortened and widened intestinal villi, and
reduced crypt depth in the colon. Morphometric assessments demonstrated a statistically significant decrease in villus height
(control: 450 ± 25 µm vs. CTH: 320 ± 30 µm, p < 0.01), crypt depth (control: 120 ± 10 µm vs. CTH: 85 ± 8 µm, p < 0.05), and
overall mucosal thickness (control: 200 ± 15 µm vs. CTH: 150 ± 12 µm, p < 0.01), indicating compromised epithelial integrity
and absorptive capacity.
These findings suggest that maternal CTH disrupts normal GIT development in offspring, likely due to a combination of metabolic
disturbances, oxidative stress, and impaired nutrient exchange. The observed changes may predispose affected individuals to
gastrointestinal dysfunction, malabsorption syndromes, and increased susceptibility to enteric infections later in life. This study
highlights the need for further research into therapeutic strategies to mitigate the developmental impact of maternal liver disease
on fetal organ systems.
