Triclocarban (TCC) is a broad-spectrum antimicrobial widely used in various personal care products, textiles, and children’s toys.
    TCC has potential reproductive and developmental toxicity in animals. However, little is known regarding the effect of TCC on
    human sperm function. In this study, an in vitro assay was used to investigate the effects of TCC on normal human spermatozoa and
    the possible underlying mechanisms involved. Semen from healthy male donors was collected and cultured in complete Biggers,
    Whitten and Whittingham (BWW) and low-sugar BWW media, followed by treatment with TCC at concentrations of 0, 0.1 μmol l−1,
    1 μmol l−1, 10 μmol l−1, and 100 μmol l−1 for 4 h. TCC was found to reduce the sperm total motility and progressive motility.
    Moreover, the sperm kinematic parameters, straight-line velocity (VSL), average path velocity (VAP), and curvilinear velocity (VCL)
    were affected in a dose-dependent manner. After treatment with TCC at the lowest effective concentration of 10 μmol l−1, TCC
    caused a significant decrease in mitochondrial adenosine triphosphate (ATP) production and mitochondrial membrane potential
    (MMP) and a significant increase in reactive oxygen species (ROS), similar to the observations with the positive control carbonyl
    cyanide 4-(trifluoromethoxy) phenylhydrazone (FCCP), suggesting that TCC may decrease sperm motility by affecting the oxidative
    phosphorylation (OXPHOS) pathway. In a sugar-free and low-sugar BWW culture environment, TCC enhanced the damaging effect
    on sperm motility and ATP, MMP, and lactate decreased significantly, suggesting that TCC may also affect the glycolytic pathway
    that supplies energy to spermatozoa. This study demonstrates a possible mechanism of TCC toxicity in spermatozoa involving both
    the OXPHOS and glycolysis pathways.

Keywords: Keywords: ATP; energy metabolism; human sperm; motility; triclocarban

Full Text |