Rat tight junction proteins are disrupted after subchronic exposure to okadaic acid

Okadaic acid (OA), a lipophilic phycotoxin distributed worldwide, causes diarrheic shellfish poisoning and even leads to tumor formation. Currently, the consumption of contaminated seafood is the most likely cause of chronic OA exposure, but there is a serious lack of relevant data. Here, the Sprague-Dawley rats were exposure to OA by oral administration at 100 mu g/kg body weight, and the tissues were collected and analyzed to assess the effect of subchronic OA exposure. The results showed that subchronic OA administration disturbed colonic mucosal integrity and induced colitis. The colonic tight junction proteins were disrupted and the cell cycle of colonic epithelial cells was accelerated. It is inferred that disruption of the colonic tight junction proteins might be related to the development of chronic diarrhea by affecting water and ion transport. Moreover, the accelerated proliferation of colonic epithelial cells indicated that subchronic OA exposure might promote the restitution process of gut barrier or induce tumor promoter activity in rat colon.

Automated summary

In this study, Sprague-Dawley rats were exposed to subchronic oral administration of Okadaic acid (OA). The results showed that OA disrupted colonic mucosal integrity, induced colitis, and might contribute to chronic diarrhea by affecting water and ion transport. Additionally, subchronic OA exposure possibly promoted the restitution process of gut barrier or induced tumor promoter activity in rat colon.