Pathogenesis of the crosstalk between reproductive function and stress in animals - part 2: Prolactin, thyroid, inflammation and oxidative stress.

Stress has a significant impact on reproductive health and fertility in both humans as well as various animal species. In particular, chronic stress can disrupt the delicate balance of the hormonal system that regulates reproductive function, leading to a variety of reproductive disorders and fertility issues. Beside the action of the hypothalamic-pituitary-adrenal (HPA) system and the sympatho-adrenomedullary system (SAM), other subsequent mechanisms have been incriminated. Thus, stress has also been associated with increased prolactin level, resulting in an inhibition of the hypothalamo-pituitary-gonadal (HPG) system leading to several reproductive disorders. Thyroid function is inhibited during chronic stress, and therefore considered an important regulator of reproductive function. Thus, and in particular by interfering with the HPA system, stress-induced immune dysregulation can have adverse effects on reproduction. In addition, oxidative stress and inflammation have been proposed as potential mechanisms by which chronic stress affects reproductive function. This is caused by an increase in reactive oxygen species (ROS) production that has a harmful effect on cells. Furthermore, inflammation can lead to tissue damage and scarring, which can affect fertility. The present review completes the complex mechanism linking stress and reproduction through the current knowledge in various animal species in a comparative point of view.