Lead (Pb) becomes a global public health concern for its high toxicology. Birds are sensitive to environmental pollution and Pb contamination exerts multiple negative influences on bird life. Pb also impacts on avian reproductive system. Thus, in this study, we attempted to determine toxicological effects and possible mechanistic pathways of Pb on avian testicular development by using the model species-Japanese quail (Coturnix japonica). Male quail chicks of 1-week-old were exposed to 0, 50, 500, and 1000 ppm Pb concentrations in drinking water for 5 weeks when reaching sexual maturation. The results showed that high Pb doses (500 and 1000 ppm) induced testis atrophy and cloacal gland shrinkage. Microstructural damages of both hypothalamus and testis indicated the disruption of the hypothalamus-pituitary-gonadal (HPG) axis by Pb exposure. The decrease of gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH) and follicle-stimulating hormone (FSH) and testosterone (T) may also imply HPG axis disruption. Moreover, excess testicular oxidative damages featured by increasing reactive oxygen species (ROS) and malondialdehyde (MDA) and decreasing catalase (CAT), glutathione (GSH), superoxide dismutase (SOD), glutathione-S-transferase (GST), and total antioxidant capacity (T-AOC) indicated increasing risks of reproductive dysfunction by Pb. Furthermore, increasing apoptosis and upregulation of gene expression associated with cell death suggested testicular abnormal development. In addition, molecular signaling involved with steroidogenesis in the testis was disturbed by Pb treatment. The study showed that Pb could impair testicular development and reproductive function by morphological and histological injury, hormone suppression, oxidative stress, cell death, and HPG axis disruption.