Author(s):
Amaral, Alexandra 
; Lourenço, Bárbara ; Marques, Mónica ; Ramalho-Santos, J.
Date: 2013
Persistent ID: http://hdl.handle.net/10316/25646
Origin: Estudo Geral - Universidade de Coimbra
Document details
Mitochondria functionality and sperm quality
Description
Although mitochondria are best known for being the eukaryotic cell powerhouses, these organelles participate in various cellular functions besides ATP production, such as calcium homoeostasis, generation of reactive oxygen species (ROS), the intrinsic apoptotic pathway and steroid hormone biosynthesis. The aim of this review was to discuss the putative roles of mitochondria in mammalian sperm function and how they may relate to sperm quality and fertilisation ability, particularly in humans. Although paternal mitochondria are degraded inside the zygote, sperm mitochondrial functionality seems to be critical for fertilisation. Indeed, changes in mitochondrial integrity/functionality, namely defects in mitochondrial ultrastructure or in the mitochondrial genome, transcriptome or proteome, as well as low mitochondrial membrane potential or altered oxygen consumption, have been correlated with loss of sperm function (particularly with decreased motility). Results from genetically engineered mouse models also confirmed this trend. On the other hand, increasing evidence suggests that mitochondria derived ATP is not crucial for sperm motility and that glycolysis may be the main ATP supplier for this particular aspect of sperm function. However, there are contradictory data in the literature regarding sperm bioenergetics. The relevance of sperm mitochondria may thus be associated with their role in other physiological features, particularly with the production of ROS, which in controlled levels are needed for proper sperm function. Sperm mitochondria may also serve as intracellular Ca2C stores, although their role in signalling is still unclear. Part of the work in the authors’ laboratory was funded by FEDER and COMPETE, via FCT (Fundac¸a˜o para a Cieˆncia e Tecnologia), Portugal in grants PTDC/EBB-EBI/101114/2008, PTDC/EBB-EBI/120634/2010 and PTDC/QUI-BIQ/120652/ 2010. Center for Neuroscience and Cell Biology (CNC) funding is also supported by FCT (PEst-C/SAU/LA0001/2011). A Amaral is the recipient of a post-doctoral fellowship from FCT (SFRH/BPD/63120/2009).
Although mitochondria are best known for being the eukaryotic cell powerhouses, these organelles participate in various cellular functions besides ATP production, such as calcium homoeostasis, generation of reactive oxygen species (ROS), the intrinsic apoptotic pathway and steroid hormone biosynthesis. The aim of this review was to discuss the putative roles of mitochondria in mammalian sperm function and how they may relate to sperm quality and fertilisation ability, particularly in humans. Although paternal mitochondria are degraded inside the zygote, sperm mitochondrial functionality seems to be critical for fertilisation. Indeed, changes in mitochondrial integrity/functionality, namely defects in mitochondrial ultrastructure or in the mitochondrial genome, transcriptome or proteome, as well as low mitochondrial membrane potential or altered oxygen consumption, have been correlated with loss of sperm function (particularly with decreased motility). Results from genetically engineered mouse models also confirmed this trend. On the other hand, increasing evidence suggests that mitochondria derived ATP is not crucial for sperm motility and that glycolysis may be the main ATP supplier for this particular aspect of sperm function. However, there are contradictory data in the literature regarding sperm bioenergetics. The relevance of sperm mitochondria may thus be associated with their role in other physiological features, particularly with the production of ROS, which in controlled levels are needed for proper sperm function. Sperm mitochondria may also serve as intracellular Ca2C stores, although their role in signalling is still unclear. Part of the work in the authors’ laboratory was funded by FEDER and COMPETE, via FCT (Fundac¸a˜o para a Cieˆncia e Tecnologia), Portugal in grants PTDC/EBB-EBI/101114/2008, PTDC/EBB-EBI/120634/2010 and PTDC/QUI-BIQ/120652/ 2010. Center for Neuroscience and Cell Biology (CNC) funding is also supported by FCT (PEst-C/SAU/LA0001/2011). A Amaral is the recipient of a post-doctoral fellowship from FCT (SFRH/BPD/63120/2009).
Document Type
Article
Language English
Language English
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