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

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 Fats (it = 12) by two successive daily injections of 55 mg/kg streptozotocin, while control animals solution (it = 10) were injected with it buffer solution hyperglycaemia Was confirmed by blood glucose levels greater than I I mmol/L. T study female rats were made pregnant and, on day 15 of gestation, the rats were sacrificed, and the feature. placentas and membranes dissected oil( Of the Uterine horns. Following morphological examination, the fetuses, placentas and membranes were homogenized, and used to measure COX activities and prostaglandin (PG) E, and PGF(2 alpha) levels. Results. - Fetuses front diabetic mothers exhibited significantly (P<0.05) shorter crown-to-rump) lengths, lower body weights and heavier placental weight.,;. The activity of COX-I in the fetuses, placentas and membranes front diabetic mothers represented I small percentage of total COX activity compared with that of COX-2. The presence of a COX-I inhibitor in the control and diabetic rats was investigaed and found to be negative. The activity of COX-2 in malformed fetuses front diabetic mothers was significantly lower (P<0.05) compared with non-malformed fetuses from control and diabetic mothers. The mean level of PGE(2) in fetuses from diabetic mothers wits significantly (P<0.05) lower than that ill controls. In contrast, the big-est increases in PGF(2 alpha) were observed in the malformed diabetic fetuses, placentas and membranes. Conclusion. - The increased production of of PGF(2 alpha) 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(2 alpha) are causally related to, or simply coincidental with, fetal malformation. (C) 2009 Published by Elsevier Masson SAS.