Lead Exposure Influences Serum Biomarkers, Hepatocyte Survival, Bone Marrow Hematopoiesis, and the Reproductive Cycle in Japanese Quails.

Lead toxicity has been a hallmark issue of toxicology over the last decades. However, predictive and non-robust models did not provide complete data on low-dose lead interaction with the organism at different functional levels (e.g., blood-serum-liver-bone marrow-bursa fabricii-reproductive system axis). Japanese quails are an animal model with a strong immune system, making them suitable for the thorough assessment of in vivo chronic lead toxicity. In this study, we have exposed Japanese quails via water ingestion to 0.25 and 0.5 μg/mL lead(II) chloride (PbCl2) for 20 days and assessed blood cells, serum biomarkers, hepatocyte survival, bone marrow hematopoiesis, bursa fabricii, and lead accumulation in eggs. Blood cells passed through morphological alterations (loss and inversion of the erythrocyte nucleus, multiple erythrocyte and thrombocyte aggregation, lymphocyte degradation, and blast cell infiltration). In the serum, PbCl2 increased the activity of creatine kinase (CK) and lactate dehydrogenase (LDH); increased the level of cholesterol, sodium, creatinine, and urea; and reduced the level of proteins, triglycerides, chloride, potassium, calcium, and alkaline phosphatase (ALP) activity (P < 0.05). Liver tissue of the exposed animals exhibited apparent death of hepatocytes. In the bone marrow, macrophages and heterophils contained a vast number of the infiltrated/uptaken granules upon PbCl2 exposure. Ultimately, PbCl2 exposure elicited a series of events observed first in the blood and serum parameters and later translated to the hematopoietic centers.