Activities of cyclooxygenases, and levels of prostaglandins E2 And F2α, in fetopathy associated with experimental diabetic gestation

Abstract Aim The present study investigated the cyclooxygenase (COX) pathway to elucidate any changes that may be involved in the mechanism(s) underlying diabetic fetopathy. Methods Diabetes was induced in female rats ( n =12) by two successive daily injections of 55mg/kg streptozotocin, while control animals ( n =10) were injected with a buffer solution; hyperglycaemia was confirmed by blood glucose levels greater than 11mmol/L. The study female rats were made pregnant and, on day 15 of gestation, the rats were sacrificed, and the fetuses, placentas and membranes dissected out of the uterine horns. Following morphological examination, the fetuses, placentas and membranes were homogenized, and used to measure COX activities and prostaglandin (PG) E 2 and PGF 2α levels. Results Fetuses from diabetic mothers exhibited significantly ( P P 2 in fetuses from diabetic mothers was significantly ( P 2α were observed in the malformed diabetic fetuses, placentas and membranes. Conclusion The increased production of PGF 2α probably proceeds, at least in part, independently of the COX pathway and via the isoprostane route. However, it is unclear whether the relatively high levels of PGF 2α are causally related to, or simply coincidental with, fetal malformation.