अमूर्त

Intratracheal administration of diesel exhaust particles causes male reproductive toxicity and enhances liver cytochrome P450 1A1 activity.

Hiromi Izawa, Misato Fukuyama-Osawa

Diesel Exhaust Particles (DEPs) contain Polycyclic Aromatic Hydrocarbons (PAHs) and the Aryl hydrocarbon Receptor (AhR) is closely involved in the endocrine disrupting action of PAHs. Activation of the AhR is thought to cause various effects such as reproductive dysfunction. In our previous studies, Subcutaneous (SC) administration of DEPs to male mice caused reproductive toxicity and increased hepatic Cytochrome P450 1A1 (CYP1A) enzyme activity, as an indirect index of AhR activity. Air pollutants in the environment enter the body through the airways. In this study, we examined the effect of Intratracheally (IT) administered DEP on spermatogenesis and hepatic CYP1A1 in male mice. The amount of DEP administered IT in this study was lower than that administered SC in previous studies. The result showed that similar to SC, IT administered DEP decreased daily sperm production and hepatic CYP1A1 activity significantly. Thus, DEP toxicity was suggested to be more pronounced with IT administration than with SC administration.