Effects of cadmium exposure on the ultrastructural pathology of different pulmonary cells, leukocyte count, and activity of glutathione peroxidase and lactate dehydrogenase in relation to free radical production in Uromastyx aegyptius.
Animal studies on the toxicity of heavy metals have been widely used as model to simulate the impacts of environmental pollution on the human health. In the present study the authors hypothesized that cadmium exposure inducts changes in reactive oxygen species (ROS) and that may be involved in the pathogenesis of lung diseases. The pathological changes of different pulmonary cells of ROS-cadmium-dependent effects were investigated in relation to the activity of lactate dehydrogenase (LDH) and glutathione peroxidase (GPx). Twelve animals were randomly assigned to two groups, control and experimental. The experimental group underwent ingestion of cadmium mixed with diet (200 mg/kg) for 7 weeks. Following the treatment conditions for each group, blood samples were collected and animals were sacrificed and the lung was isolated. Ultrastructure examination showed that cadmium resulted in desquamated pneumocyte type II with degenerated surfactant materials, thickened alveolar wall, and thickening of alveolar septum due to proliferation of endothelial cells lining the pulmonary capillaries as a result of an active transmigration. t-test results showed that cadmium caused a significant (p < .05) rise in leukocytes, lymphocytes, neutrophils, and monocytes, which was a sign for chemotactic activity that enhanced transmigration from pulmonary microcirculation into inflammated tissue. In addition, lung tissue FR production, LDH, and GPx activities increased significantly (p < .05) from the baseline control of 88.17+/-17.70, 183.49+/-29.50, and 4466.79+/-1190.32 to 129.67+/-14.49.14 (Carr U), 339.17+/-75.28 (U/L), and 5943.08+/-695 (U/L) respectively, in the cadmium-treated group. Based on the results of the present study, it can be concluded that long-term cadmium exposure (ingestion mixed with food) results in cadmium deposition in the tissue of the vasculature of the lungs, such as pulmonary capillary endothelial, which induced the buildup of ROS, a possible proposed new mechanism that explains lung inflammation.
Al-Johany
A M
AM
Department of Zoology, College of Science, King Saud University, Riyadh, Saudi Arabia. ajohany@ksu.edu.sa
Haffor
A S
AS
D000821:Animal Feed; D000818:Animals; D019187:Cadmium Compounds / Q000633:toxicity*; D004785:Environmental Pollutants / Q000633:toxicity*; D005609:Free Radicals / Q000378:metabolism*; D005979:Glutathione Peroxidase / Q000378:metabolism*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism*; D007958:Leukocyte Count; D007962:Leukocytes / Q000187:drug effects* / Q000473:pathology; D008116:Lizards; D008168:Lung / Q000187:drug effects* / Q000201:enzymology / Q000648:ultrastructure; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects; D011650:Pulmonary Alveoli / Q000187:drug effects / Q000648:ultrastructure; D018675:Toxicity Tests
D019187:Cadmium Compounds; D004785:Environmental Pollutants; D005609:Free Radicals; D007770:L-Lactate Dehydrogenase; D005979:Glutathione Peroxidase