Morphometric characteristics of the ultrastructure of endocrine cells in the rat gastric mucosa during chronic toluene intoxication

I n t r o d u c t i o n . Chronic exposure to industrial toxicants such as toluene is a significant pathogenic factor, however, its effect on the regulatory systems of the gastrointestinal tract, in particular, on the diffuse endocrine system of the stomach, has been insufficiently studied.

A i m . To investigate alterations in endocrine cells (enterochromaffin-like (ECL) and gastrin-producing (G) cells) of the gastric mucosa (GM) of rats following chronic intoxication with toluene vapors using a combination of morphological, morphometric, and ultrastructural methods.

M a t e r i a l s  a n d  m e t h o d s . Experimental animals (48 outbred sexually mature rats) were exposed to toluene vapor inhalation at a concentration 10 times the maximum permissible concentration, for 4 hours/day, 5 days/ week, over a period of 60 days. Tissue samples (pyloric GM) were collected on days 1, 7, 30, and 60 after toxicant exposure. The control group consisted of intact animals. Electron microscopic examination and morphometric analysis of the ultrastructure of ECL and G cells (areas of secretory granules (Ssg), the Golgi complex (Sgc), mitochondria (Sm), and parameters of nuclear chromatin) were performed.

R e s u l t s . In the early stages of the study (days 1 and 7), experimental animals showed signs of functional exhaustion and degranulation of ECL and G cells: Ssg and Sgc decreased by almost two-fold, Sm decreased by 32–35%, destruction of mitochondrial cristae was observed, and the proportion of heterochromatin in the nucleus increased. At the later stages (days 30 and 60), activation of reparative processes was observed: an increase in the number of organelles responsible for biosynthesis and secretion, the appearance of mitochondria with densified matrix, and normalization of the chromatin ratio.

C o n c l u s i o n . Chronic toluene intoxication induces nonspecific ultrastructural changes in gastric endocrine cells, characterized by degranulation and dysregeneratory processes during the acute period, and by the activation of intracellular repair mechanisms during the long-term period. The severity of changes depends on the duration of toxicant exposure.

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