Introduction

Male factor infertility is a contributing factor in roughly 40% of infertile couples in the USA [1]. It is also thought to be the sole cause in about half of these cases [2]. Several conditions have been described as potential causes for male infertility including varicocele, leukocytospermia, genital infection, and idiopathic infertility, as well as exposure to environmental factors such as smoking and pollutants. These clinical conditions have been linked to oxidative stress (OS), which occurs when there is an imbalance between reactive oxygen species (ROS) and antioxidants in the body.

ROS are reactive molecules that contain oxygen, which includes oxidizing free radicals that are necessary for normal biological functions. When produced in excess, ROS can cause sperm damage and may lead to selective cell death (apopto-sis) [3]. Spermatozoa are particularly susceptible to oxidative damage because of their lack of an antioxidant defense system outside of the cytoplasm, which is mostly lost during the maturation process [4] . When the sperm cytoplasm is retained as cytoplasmic droplets, higher OS is to be expected due to ROS-producing enzymes in the cytoplasm [5] . Another source of ROS is leukocytes in the seminal fluid. Oxidative damage can affect the lipids of the sperm plasma membrane, as well as the sperm DNA. This type of damage does not only affect sperm function but also lead to negative consequences with the developing embryo and pregnancy rates [6],

In this chapter, we review recent literature and research to assess the current knowledge regarding the impact of OS on male infertility. Also discussed are the mechanisms behind oxidative damage and its contribution to the pathogenesis of male infertility.

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