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dc.contributor.authorChauvigné, Françoiseng
dc.contributor.authorBoj, Mónicaeng
dc.contributor.authorFinn, Roderick Nigeleng
dc.contributor.authorCerdà, Joaneng
dc.description.abstractReactive oxygen species (ROS), particularly hydrogen peroxide (H2O2), cause oxidative cell damage and inhibit sperm function. In most oviparous fishes that spawn in seawater (SW), spermatozoa may be exposed to harmful ROS loads associated with the hyperosmotic stress of axonemal activation and ATP synthesis from mitochondrial oxidative phosphorylation. However, it is not known how marine spermatozoa can cope with the increased ROS levels to maintain flagellar motility. Here, we show that a marine teleost orthologue of human aquaporin-8, termed Aqp8b, is rapidly phosphorylated and inserted into the inner mitochondrial membrane of SW-activated spermatozoa, where it facilitates H2O2 efflux from this compartment. When Aqp8b intracellular trafficking and mitochondrial channel activity are immunologically blocked in activated spermatozoa, ROS levels accumulate in the mitochondria leading to mitochondrial membrane depolarisation, the reduction of ATP production, and the progressive arrest of sperm motility. However, the decreased sperm vitality underlying Aqp8b loss of function is fully reversed in the presence of a mitochondria-targeted antioxidant. These findings reveal a previously unknown detoxification mechanism in spermatozoa under hypertonic conditions, whereby mitochondrial Aqp8b-mediated H2O2 efflux permits fuel production and the maintenance of flagellar motility.en_US
dc.publisherNature Publishing Groupen_US
dc.rightsAttribution-NonCommercial-NoDerivs CC BY-NC-NDeng
dc.subjectReproductive biologyeng
dc.titleMitochondrial aquaporin-8-mediated hydrogen peroxide transport is essential for teleost spermatozoon motilityen_US
dc.typePeer reviewed
dc.typeJournal article
dc.source.journalScientific Reports

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Except where otherwise noted, this item's license is described as Attribution-NonCommercial-NoDerivs CC BY-NC-ND