Oxidative stress

Abstract

Considerable evidence implicates oxidative stress in the pathophysiology of many complications of human pregnancy, and this topic has now become a major focus of both clinical and basic science research. Oxidative stress arises when the production of reactive oxygen species overwhelms the intrinsic anti-oxidant defences. Reactive oxygen species play important roles as second messengers in many intracellular signalling cascades aimed at maintaining the cell in homeostasis with its immediate environment. At higher levels, they can cause indiscriminate damage to biological molecules, leading to loss of function and even cell death. In this chapter, we will review how reactive oxygen species are generated and detoxified in the human placenta, and what roles they may play at homeostatic concentrations. We will then consider their involvement in normal placental development, and in complications ranging from miscarriage to pre-eclampsia and premature rupture of the membranes.

Fig. 1

The principal reactive oxygen species, their potential origins and detoxification pathways. NADPH, nicotinamide adenine dinucleotide phosphate.

Fig. 2

How reactive oxygen species may be generated within the syncytiotrophoblast, and the principal consequences for the function of the tissue. CHOP, C/EBP homologous protein; NADPH, nicotinamide adenine dinucleotide phosphate; ROS, reactive oxygen species; UPR, unfolded protein response.