Abstract
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 (0.1–100 nM) for 90 min (acute) and 6 h (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 90 min 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 100 nM TBT decreased total motility (88 vs 79%), progressive motility (80 vs 70%) curvilinear velocity and beat-cross frequency for 90 min with similar phenotypes at 6 h (P < 0.05). Sperm mitochondrial membrane potential was lower in 10 and 100 nM groups after 6 h (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.
Subject
Developmental Biology,Endocrinology,Genetics,Molecular Biology,Animal Science and Zoology,Reproductive Medicine,Biotechnology
Cited by
5 articles.
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