Perchlorate uptake and effects on thyroid function in fish

Perchlorate salts occur in many forms including ammonium perchlorate and sodium perchlorate. Because perchlorate is used as an oxidizer in rocket propellants and explosives, contamination is common near military installations such as Longhorn Army Ammunition Plant. The toxicity of perchlorate involves the inhibition of iodine uptake by the thyroid follicular cells, thereby reducing thyroid hormone synthesis. This leads to an increase in the amount of TSH (thyrotropin-releasing hormone) and TRH (thyroid stimulating hormone) produced due to negative feedback. The continued stimulation of TSH on the thyroid follicular cells leads to hypertrophy, colloid depletion, and the formation of goiters. Thyroid hormones are important in metabolism, growth, development, and reproduction and have a permissive action on other tissues.

Although the mechanism of action of perchlorate is known in humans, amphibians, and rats and there are studies that have been conducted in fish and amphibians, not much is known about the effects of environmentally relevant concentrations of perchlorate. Since perchlorate is water soluble, fish and other aquatic organisms receive the greatest exposure to perchlorate in contaminated areas. The purpose of this project was to determine the uptake of perchlorate into mosquitofish and various tissues in the catfish and the effects on thyroid morphology and function in mosquitofish.

Mosquitofish were exposed to 0, 0.1, 1, 10, 100, and 1000 mg/L sodium perchlorate for 2, 10, and 30 d with 5 replicates per treatment group. Catfish were exposed to 100 mg/L sodium perchlorate for 5 d with 20 replicates. Tissue perchlorate concentrations in the catfish and mosquitofish were determined by extracting perchlorate from the tissues using accelerated solvent extraction with water, and then analyzing these extracts by ion chromatography. Histological slides of the mosquitofish thyroid follicles were analyzed for hypertrophy, hyperplasia, and colloid depletion. Whole body thyroxine (T4) concentrations in the mosquitofish were determined by radioimmimmunoassay (RIA).

Perchlorate did not bioconcentrate in the fish; tissue concentrations in the mosquitofish were 10 times less than the exposure concentration. The highest concentration of perchlorate in the catfish was found in the head, but this was 4 times less than the exposure concentration. Perchlorate also induced hyperplasia, hypertrophy, and colloid depletion in mosquitofish exposed to the highest concentrations (10, 100, and 1000 mg/L) of perchlorate for the longest time periods (10 and 30 d). T4 concentrations in the mosquitofish were also significantly decreased in fish exposed to perchlorate as compared to the controls in fish exposed to 1000 mg/L for 30 d.

At environmentally relevant concentration of perchlorate, there was little to no uptake of perchlorate into the whole body mosquitofish. Thyroid morphology and function were also only slightly modified by low doses of perchlorate. In contrast, exposure to high concentrations of perchlorate led to high concentrations of perchlorate in the various fish tissues, as well as disruptions in thyroid morphology and function. The results of this study are consistent with studies that have been conducted in humans, rats, amphibians, and other fish.