Mitochondrial Reactive Oxygen Species (ROS) Production Alters Sperm Quality

Abstract

Besides ATP production, mitochondria are key organelles in several cellular functions, such as steroid hormone biosynthesis, calcium homoeostasis, intrinsic apoptotic pathway, and the generation of reactive oxygen species (ROS). Despite the loss of the majority of the cytoplasm occurring during spermiogenesis, mammalian sperm preserves a number of mitochondria that rearrange in a tubular structure at the level of the sperm flagellum midpiece. Although sperm mitochondria are destroyed inside the zygote, the integrity and the functionality of these organelles seem to be critical for fertilization and embryo development. The aim of this review was to discuss the impact of mitochondria-produced ROS at multiple levels in sperm: the genome, proteome, lipidome, epigenome. How diet, aging and environmental pollution may affect sperm quality and offspring health-by exacerbating oxidative stress-will be also described.

Keywords: ROS impact on sperm quality; oxidative stress; sperm physiology.

Figure 1

The Mitochondrial Eve or Adam mechanism. Most literature hypothesizes that the zygote exclusively inherits maternal mitochondria so that paternal ones that enter into the zygote are eliminated by the involvement of the proteasome-autophagy-lysosome pathway (A). A second hypothesis that still sustains maternal inheritance expects a precocious elimination of paternal mtDNA from motile SPZ and a change in mitochondria morphology creating vacuolar organelles in order to provide energy for sperm motility (B). A third hypothesis does not exclude the paternal inheritance of mitochondria with an uneven distribution of these organelles inside the embryo (C).

Figure 2

The impact of ROS on sperm quality at multiple levels. A drafting view of the main exogenous insults and the dangerous effects on sperm cells.