Ammonia detoxifying mechanisms of rainbow trout altered by dietary dieldrin

Abstract

Dietary dieldrin dosages of 14, 43, 143 and 430 μg/kg body weight per day for 240 days altered ammonia detoxifying mechanisms and brain amino acid metabolism of rainbow trout. These dosages corresponded to 0.36, 1.08, 3.6, and 10.8 μg dieldrin/g food, respectively. Whole-body dieldrin residues in fish from the lowest 3 dosage groups were comparable to those found in fish from the aquatic environment. The brain concentrations of amino acids associated with ammonia detoxifying mechanisms, aspartate, glutamate and alanine, were significantly altered, as were the enzymes related to their metabolism. Brain glutamate dehydrogenase (GDH) activity was decreased by all doses of dieldrin, whereas liver GDH and brain glutamine synthetase activities were stimulated by all treatment doses. Brain ammonia concentrations increased in the groups given the 2 highest dosages. Mitochondrial morphology in liver cells was significantly altered by dieldrin treatment as determined by electron microscopy. Since GDH is an intramitochondrial enzyme, examination by electron microscopy gave further evidence that dieldrin significantly altered mitochondrial metabolism. A possible mode of action of dieldrin was proposed which suggests that dieldrin inhibits or decreases brain GDH activity followed by ammonia intoxication after liver GDH and brain glutamine synthetase activities are exceeded. The ammonia detoxifying mechanisms of fish seemed to be very sensitive to dieldrin; the “no-effect” dosage was below 14 μg/kg body weight per day (0.36 μg/g food).