title: Acrylamide-induced prenatal programming of intestine structure in guinea pig.
abstract: Potential effects of prenatal administration of acrylamide (ACR) on postnatal development of the small intestine were not examined experimentally yet. The aim of this study was to establish changes of morphological parameters of the small intestine damaged by prenatal action of ACR in guinea pigs. The 3 mg/kg body weight of ACR was given in drinking water every day during the last 35 days of the pregnancy in guinea pigs. The histomorphometry of the duodenum and jejunum was determined. Immunohistochemical staining with anti cadherin antibody was performed. Maternal treatment with ACR led to the decrease of the expression of cadherin in the epithelium. Maternal ACR treatment increased the number of total, divided and inactive crypt, and the number of damaged villi in the duodenum and jejunum of newborn guinea pigs. The thickness of myenteron and submucosa, mucosa fractal dimension and the depth of crypts in the duodenum were increased by ACR. Additionally, in offspring born by mothers administered with ACR the decrease of villi epithelium thickness and active crypt number was observed. Moreover, ACR decreased goblet cells and inact villi number in the duodenum, mucosa thickness and crypts width in the jejunum. Intestine absorptive surface was affected by ACR in the jejunum as well. Results of measurements showed that maternal ACR treatment had negative influence on small intestine histomorphometry. ACR acting prenatally influenced small intestine nervous plexuses that became enlarged by 2.5 times compared with the control group. In conclusion, our results showed the negative impact of maternal ACR treatment on histological structure, integrity and innervation of small intestine wall as well as on absorptive function of small intestine mucosa.
authors.affiliation: Department of Animal Physiology, Faculty of Veterinary Medicine, University of Life Sciences in Lublin, Lublin, Poland. ewarst@interia.pl.
authors.forename: E
authors.initials: E
authors.lastname: Tomaszewska
authors.forename: P
authors.initials: P
authors.lastname: Dobrowolski
authors.forename: I
authors.initials: I
authors.lastname: Puzio
authors.forename: L
authors.initials: L
authors.lastname: Prost
authors.forename: P
authors.initials: P
authors.lastname: Kurlak
authors.forename: P
authors.initials: P
authors.lastname: Sawczuk
authors.forename: B
authors.initials: B
authors.lastname: Badzian
authors.forename: M
authors.initials: M
authors.lastname: Hulas-Stasiak
authors.forename: K
authors.initials: K
authors.lastname: Kostro
mesh_terms: D020106:Acrylamide / Q000633:toxicity*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D024042:Collagen Type I / Q000378:metabolism; D024061:Collagen Type III / Q000378:metabolism; D004386:Duodenum / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D005260:Female; D006168:Guinea Pigs; D007408:Intestinal Absorption / Q000187:drug effects; D007413:Intestinal Mucosa / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D007583:Jejunum / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008297:Male; D008431:Maternal-Fetal Exchange; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects
chemical_list: D024042:Collagen Type I; D024061:Collagen Type III; D020106:Acrylamide