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.

Morpho-functional alterations in lymphocytes and erythrocytes of Japanese quail due to prolonged in vivo exposure to heavy metal complexes.

BACKGROUND: Lead and cadmium are significant environmental pollutants that cause pathophysiological responses in many organs. Heavy metal absorption into many tissues is very fast due to a pronounced affinity for metallothioneins. METHOD: Japanese quail were exposed to different concentrations of metals (cadmium 0.20 mg/L and lead 0.25 and 0.50 mg/L) for 20 days. Erythrocytes (normal and hemolyzed) and lymphocytes (normal and altered) were monitored in this study. The analysis observed the percentage of normal and altered cells, as well as erythrocyte surface area. Cell counts were analyzed using light microscopy, while surface area and cytological changes in cells and nuclei were analyzed using licensed software. RESULTS: Different concentrations of metals have caused erythrocyte hemolysis as well as structural and morphological alterations in lymphocytes. Destruction of cell and nucleus membrane, changes in cell size, erythrocyte denucleation and reduced erythrocyte surface area were observed. Cadmium has caused erythrocyte hemolysis (29.30 %) and lymphocyte damage (92.10 %). Higher doses of lead resulted in greater damage to lymphocytes (63 %). Also, treatment with higher dose of lead produced a higher percentage of hemolyzed erythrocytes (19.20 %) in comparison to lower dose (9.90 %). CONCLUSION: The toxicity of heavy metals leads to reduced maturation of the blast, which causes the appearance of immature cells in peripheral circulation and severe destruction of blood cell membranes. Erythrocyte hemolysis can lead to anemia, while lymphocyte damage can lead to lymphocytopenia.