Prenatal diclofenac sodium exposure and sertoli cells: A light and electron microscopic evaluation

Abstract

Developing technology and global free trade have together created a consumer society in the field of health, and this has in turn increased the consumption of drugs. The use of non-steroidal anti-inflammatory drugs (NSAIDs), with their toxic effects, has also increased considerably in recent years. The teratogenic potential of these drugs during pregnancy, their effects on fetal organs, fetal growth, and their neonatal and long-term effects in children all require consideration. NSAIDs given to pregnant women cross the placenta and may cause adverse embryo-fetal and neonatal effects, depending on the type of drug administered, the dose and length of treatment, and the duration of pregnancy. Placental transition continues in all cases, independently of gestational age. The half-life of these drugs is longer in the fetal circulation (14.7 hours) than in the maternal circulation (2.2 hours). The fetus is therefore more exposed to the deleterious effects of the drug. These effects result from the mechanisms of action of NSAIDs and physiological changes in drug pharmacokinetics in the gestational period. Diclofenac sodium (DS) is a commonly used NSAID among women of reproductive age. The use of these drugs during pregnancy is reported to be capable of leading to developmental disorders in both human and animal embryos, since they cross the placental barrier and affect the fetus. This drug inhibits the biosynthesis of prostaglandins, cross the placental barrier, get into fetal circulation, and exhibit toxic effects in organs such as the brain, kidney, ovary and testis. Sertoli cells are the somatic cells of the testis with an important role in spermatogenesis and testis formation. In this context; this chapter discusses in detail the effects of the prostaglandin synthesis inhibitor DS on the development of Sertoli cells in terms of light and electron microscopy, particularly its use during pregnancy, and is intended to contribute to the current scientific literature.