Ammonium perchlorate-induced lesions in zebrafish kidneys
Ammonium perchlorate (AP) is a highly reactive chemical that is primarily used as a rocket propellant for military and aerospace industries. Widespread AP contamination has caused increased concern over its effect on biological systems. Perchlorate derived from AP, and other perchlorate species, inhibits iodide uptake by the thyroid follicles, thus impairing the production of thyroid hormones and disrupting the regulatory feedback mechanisms of the thyroid system. As a result, the secretion of thyroid-stimulating hormone (TSH) by the pituitary gland increases. Effects of AP on other physiological systems, such as the renal system, are not well understood. The mammalian and teleost kidney are both known to contain TSH and thyroid hormone receptors, as well as iodide transport mechanisms similar to those found in thyroid follicles. Therefore, the kidney is also a potential target of direct (association with iodide transporters) or indirect (decreased thyroid hormones and increased TSH) actions of perchlorate. This study examined the histopathological effects of AP on the zebrafish kidney. Adult zebrafish were exposed to water-borne perchlorate at concentrations of 18- ppm for eight weeks and 677-ppm for 4 weeks. At the end of the exposure period, the fish were processed for histological analyses of the trunk region of the kidney. The samples were then analyzed for increased presence of macrophage aggregates, focal granulomas, inflammation, and generating nephrons. Quantitative analysis was conducted by determining the relative average area covered by a lesion in randomly selected histological sections. The results indicated that exposure to AP at 18-ppm for eight weeks caused a significant increase in the incidence of renal macrophage aggregates when compared with the control fish. The other lesions showed no changes in incidence at any AP dose. The study also suggests a link between thyroid disruption and increases in renal macrophage aggregates.