Tributyltin chloride exposure to post-ejaculatory sperm reduces motility, mitochondrial function and subsequent embryo development.

Context: Male exposure to environmental toxicants can disrupt spermatogenesis and sperm function. However, consequences of environmentally relevant organotin exposure to post-ejaculatory mammalian spermatozoa on fertility are poorly understood.

Aims: Determine the consequences of tributyltin chloride (TBT) exposure on post-ejaculatory sperm function and subsequent embryo development.

Methods: Frozen-thawed bovine sperm were exposed to TBT (0.1-100nM) for 90min (acute) and 6h (short-term) followed by quantification of multiple sperm kinematics via computer aided sperm analysis. JC-1 dye was used to measure mitochondrial membrane potential. Sperm were then exposed to TBT for 90min in non-capacitating conditions, washed several times by centrifugation and applied to gamete co-incubation for in vitro embryo production to the blastocyst stage.

Key Results: 100nM TBT decreased total motility (88 vs 79%), progressive motility (80 vs 70%) curvilinear velocity and beat-cross frequency for 90min with similar phenotypes at 6h (P <0.05). Sperm mitochondrial membrane potential was lower in 10 and 100nM groups after 6h (P ≤0.05). Embryos fertilised from TBT-exposed sperm had reduced cleavage rate (80 vs 62%) and 8-16 cell morula development (55 vs 24%) compared to development from unexposed sperm.

Conclusions: Exposure of post-ejaculatory mammalian sperm to TBT alters sperm function through lowered motility and mitochondrial membrane potential. Fertilisation of oocytes with TBT-exposed sperm reduces embryo development through mechanisms of paternal origin.

Implications: Acute and short-term environmental exposure of post-ejaculatory sperm to organotins and endocrine disrupting chemicals such as TBT contribute to idiopathic subfertility and early embryo loss.