This study measured the dietary selenium requirement of rainbow trout and their response to excessive levels of dietary selenium. A dietary selenium level of 0.07 microgram/g dry feed with a waterborne selenium level of 0.4 +/- 0.2 microgram/liter and a dietary vitamin E level of 0.4 IU/g dry diet was sufficient to prevent frank selenium deficiency symptoms. Maximal plasma GSH.px activity was obtained at a dietary selenium level between 0.15 and 0.38 microgram/g dry feed which is less than the average selenium concentration of commercial diets. Chronic dietary selenium toxicity occurred at 13 microgram selenium/g dry feed. Major effects of selenium toxicity were reduced growth rate, poor feed efficiency and a high number of mortalities. No histopathological lesions or significant deviation in the investigated blood parameters or liver somatic index were detected in trout raised on diets containing 13 microgram selenium/g dry feed. Tissue selenium analysis indicated that trout can maintain homeostasis with dietary selenium levels up to 1.25 microgram/g dry feed. The selenium uptake and accumulation in tissues of trout reared on diets containing in excess of 3 microgram/g dry feed may ultimately be toxic to trout if maintained over long periods of time.

Rainbow trout, Salmo gairdneri, were fed purified diets with zinc concentrations ranging from deficient to excessive (1, 90, 590 μg Zn∙g−1) and simultaneously exposed to a range of waterborne [Zn] (7, 39, 148, 529 μg Zn∙L−1). After 1 wk, fish fed the deficient diet, at ambient waterborne [Zn], had low plasma [Zn] which decreased further during the 16-wk experiment. Growth ceased after 12 wk; hematocrit and plasma protein were depressed. Both whole body [Zn] and body burden decreased by 16 wk, but most other elements were elevated. Increasing waterborne [Zn] alone increased plasma [Zn], whole body [Zn], and growth in a graded manner and normalized hematocrit, plasma protein, and other whole body elements. Increasing dietary [Zn] to 90 μg Zn∙g−1 at ambient waterborne [Zn] prevented depression of plasma [Zn] and permitted normal growth and whole body [Zn]. Zinc uptake from water, probably across the gills, was independent of uptake from the diet since at any dietary [Zn], increasing the waterborne [Zn] resulted in increased whole body [Zn]. Even when dietary [Zn] was adequate, the waterborne contribution was as high as 57%, and 100% when the dietary [Zn] was deficient. There were no toxic effects on any of the variables measured.

Effects of dietaryascorbic acid oaa chronic lead toxicity to young rainbow trout (SaBmo gatriineri). Can. 1. Fish. Aquat, Newly hatched rainbow trout (Salmo gairdneri) exposed to waterborne lead and receiving diets deficient in. or supplemented with, ascorbic acid, developed classical symptoms of iead toxicity and ascorbic acid deficiency. Those exposed to lead showed elevated blood lead concentrations, inhibition of erythrocyte &amino levulinic acid dehydratase, darkening of the tail regions and spinal curvatures. Those receiving ascorbate deficient diets showed depletion of carcass, liver, kidney, and brain ascorbic acid concentrations plus spinal curvatures. Fish subjected to both treatments simultaneously showed no evidence of an enhancement of aacorbate deficiency symptoms by exposure to lead or enhancement or reduction of lead toxicity symptoms by ascorbate deficient or supplemented diets, respectively. These results demonstrate that, although aspects of lead toxicity in fish resemble ascorbic acid deficiency, there is no metabolic interaction between the two factors. . 1980. Effects of dietary ascorbic acid on chronic lead toxicity to young rainbow trout (Salmo gairdvleri). Can. J. Fish. Aquat. Sci. 37: 17@%76. Bes truites arcen-ciel (Salmo gairdneri) nouvellement ecloses exposks A du plomb contenu dans I'eau et recevant des regimes dkficients en acide ascorbique ou avec supplkment cle cet acide dkveloppe~st les syrnptcmes slassiques de toxicitk par B e plornb et de deficience d'acide ascorbique. Ees truites exposees au plomb msntrent une plus forte concentration de plomb sanguin, inhibition de la 6-amia101evuIinique acide ddshydratase des Crythroeytes, assombrissement de la rdgion caudale et courbatures de I'epine dorsale. Les truites nourries A des regimes pauvres en ascsrbates montreiat un Cpuisement des concentrations d'acide ascorbique dans le squelette, fuie, rein et cerveau, en plus de courbatures de 1'Cpine dorsale. Les poissons soumis simultandment aux deux traitements ne rnontrent pas de signe d'aggravation des sympt6mes de dCficience d'ascorbates causCe par exposition au plomb, ou augmentation ou reduction des symptames de toxicit6 par le plomb causee par des rigimes dam lesquels les ascorbates sont deficients ou ont Cte ajoutks respectivement. Ces resultats demontrent que, bien que les aspects de la toxicite par le pBomb chez les poissons ressemblent 2i une deficience d'acide ascorbique, il n'y a pas d'interastion rn6tabolique entre les deux facteurs.

Juvenile rainbow trout were reared for 24 wk on practical-type diets formulated with fish meals derived from coho salmon (Oncorhynchus kisutch) taken from Lake Michigan, Lake Ontario, and the Pacific Ocean. Levels of contaminants (DDT, chlordane, dieldrin, mirex, and PCBs) increased 10-fold from control and Pacific Ocean salmon-based diets to Lake Ontario salmon-based diets. Rainbow trout accumulated contaminants in direct proportion to dietary levels. However, there were no significant differences in the final body weights, feed to gain ratios, or mortality rates of the trout reared on the different test diets. No signs of abnormal behavior or any indication of histopathological abnormalities were observed in any of the fish. There were no signs of thyroid hyperplasia or any significant decline in serum T3 or T4 levels with increasing dietary contaminant levels. Therefore, rainbow trout do not appear to have been affected by the uptake and accumulation of contaminants. However, the trout did not appear to regulate their body burden of contaminants; this ultimately could prove to be toxic and may adversely affect the ability of these fish to reproduce and survive. The final concentrations of mirex and PCBs in the Lake Ontario-fed fish exceeded the allowed limits to protect human health; therefore, fish meals produced from Lake Ontario salmon are unsuitable as a source of feed for aquaculture of rainbow trout intended for human consumption.

A variety of biochemical techniques have been used to assess the response of fish to contaminants. These techniques may provide valuable tools for determining the degree of impact on real fish populations of contaminant exposure and for identifying areas of contamination. Many of these techniques have not proven useful because they were not sensible, sensitive, or specific. This paper reviews the use of erythrocyte δ-amino levulinic acid dehydratase (ALAD) activity to indicate lead exposure of fish, both in the laboratory and in field surveys of Great Lakes fish. The enzyme has proven to be a reliable tool in laboratory studies of lead effects on rainbow trout (Salmo gairdneri). The field survey demonstrated that ALAD activity is a suitable indicator of lead exposure of lake trout (Salvelinus namaycush) but that more research is required to confirm its applicability to other species.