**1. Introduction**

Aerobic life inherently depends on oxygen, which is essential for a controlled oxidation of molecules containing carbon, subsequently leading to the release of energy. Nevertheless, aerobic cells, including spermatozoa, are persistently counteracting the so-called Oxygen Paradox: while oxygen is crucial to sustain aerobic life, it is simultaneously toxic to the cell survival [1]. Normal aerobic metabolism leads to the generation of by-products called free

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radicals (FR) [2, 3], which, under physiological conditions, are necessary for a normal cell function [4]. On the other hand, if FR concentrations become too high, either because of their overgeneration or due to low levels of antioxidant defense mechanisms, oxidative stress (OS) emerges with unpredictable consequences on the cell behavior and survival [5].

Oxidative stress has been implicated in the pathogenesis of a variety of human diseases such as atherosclerosis, cancer, diabetes, liver damage, AIDS, Parkinson's disease and health complications associated with premature birth [6]. In the meantime, seminal OS is believed to be one of the main factors in the pathogenesis of sperm dysfunction in male sub- or infertility [7–9]. Several intrinsic and extrinsic factors have the ability to promote reactive oxygen species (ROS) generation in the testicular as well as post-testicular (e.g. epididymal) environment, resulting in defective spermatogenesis and altered sperm function [9]. As expected, approximately 25% of infertile patients exhibit higher ROS levels in semen as opposed to fertile men [7, 10–12].

Although the origin of ROS generation in semen and their roles in male reproduction have only recently been uncovered, numerous questions still remain unanswered, thus offering multiple strategies for future research. As such, the role of free radicals and oxidative stress in fertility and subfertility is an area requiring continuous scientific attention.
