Physiological levels of reactive oxygen species (ROS) play an important regulatory role through various signaling transduction pathways in folliculogenesis, oocyte maturation, endometrial cycle, luteolysis, implantation, embryogenesis, and pregnancy. Persistent and elevated generation of ROS leads to a disturbance of redox potential that in turn causes oxidative stress (OS). Our literature review captures the role of ROS in modulating a range of physiological functions and pathological processes affecting the female reproductive life span and even thereafter (i.e., menopause). The role of OS in female reproduction is becoming increasingly important, as recent evidence suggest that it plays a part in conditions such as polycystic ovarian disease, endometriosis, spontaneous abortions, preeclampsia, hydatidiform mole, embryopathies, preterm labor, and intrauterine growth retardation. OS has been implicated in different reproductive scenarios and is detrimental to both natural and assisted fertility. Many extrinsic and intrinsic conditions exist in assisted reproduction settings that can be tailored to reduce the toxic effects of ROS. Laboratory personnel should avoid procedures that are known to be deleterious, especially when safer procedures that can prevent OS are available. Although antioxidants such as folate, zinc, and thiols may help enhance fertility, the available data are contentious and must be evaluated in controlled studies with larger populations.