44.3.1 Arsenic Interaction with Selenium
An arsenic interaction with selenium seems to have occurred in a toxicity test conducted with endangered larval razorback sucker (Table 44.1).85 The study involved exposing larvae to several food treatments and water treatments at locations near Grand Junction, CO. This discussion will be limited to one water treatment and two food treatments: nauplii of brine shrimp (reference food) or natural zooplankton collected from a low-selenium wetland (termed HTEW: Horsethief east wetland) located near the Colorado River, but up-gradient from irrigation activities.
Selenium residues in razorback sucker larvae after 10 days of exposure were 6.3–6.7 àg/g in the brine shrimp treatment and 6.1–7.0 àg/g in the HTEW treatment. However, survival was very different between the two food treatments: 87% in the brine shrimp treatment, but 15–20% in the HTEW treatment. The difference may have been due in part to the selenium concentrations in food at 10 days of exposure because the brine shrimp treatment had lower selenium concentrations (3.2 àg/g) than the HTEW treatment (5.0 àg/g). Nevertheless, selenium concentrations in both food treatments were above the selenium dietary toxic threshold (3 àg/g),96,97 and whole-body residues in larvae from both food treatments were above the whole-body adverse effect threshold (4 àg/g).55,69,73,75,88,98–101
The same scenario occurred at day 30 in razorback sucker larvae fed the brine shrimp treatment, where whole-body residues were 5.2 àg/g, and in larvae fed the HTEW treatment, where whole- body residues were 8.2 àg/g. Survival of larvae was different between the food treatments: 81–83%
in the brine shrimp treatment, but 0–10% in the HTEW treatment. Considering that the whole- body residues were somewhat similar, and selenium concentrations in food were relatively close, but survival was very different between the food treatments, it seems that the selenium residue in larvae fed the brine shrimp treatment was somehow inactivated from having a toxic effect, whereas in the HTEW treatment no inactivation occurred.
Hamilton et al.86 discussed the potential confounding factors, such as difference between zooplankton and nauplii of brine shrimp (i.e., caloric content, nutrition value, trace element content, suitability as fish food), and concluded that an interaction probably occurred between arsenic and selenium in the brine shrimp treatment. Arsenic concentrations in brine shrimp nauplii were 24 àg/g, and in the HTEW treatment they were 6 àg/g. Arsenic concentrations in brine shrimp nauplii were not elevated sufficiently to cause dietary toxicity102 but may have ameliorated the toxic stress of dietary selenium. Arsenic compounds have been shown to protect against the toxicity of a variety of forms of selenium including selenite, selenocystine, and selenomethionine.93 The protective effect of arsenic has been observed in rats, dogs, swine, cattle, and birds.93 In general, arsenic exposure in water or diet protected against dietary selenium toxicity,103–110 but combined arsenic and selenium waterborne exposure did not.111,112 Dubois et al.104 and Klug et al.105 reported that the toxicity of selenite, selenomethionine, selenocystine, and seleniferous grain was reduced in rats by exposure to arsenic as either arsenite or arsenate, but not as arsenic sulfides. Klug et al.106 exposed rats for 12 weeks to arsenic in water and selenium in the diet and reported that arsenic protected against selenium-induced mortality, reduced growth, and reduced feeding, even though selenium residues were increased in liver (28%), kidney (141%), and muscle (52%) compared to exposure to only
© 2003 by CRC Press LLC Table 44.1 Interactive Effects of Nutritional Factors and Other Elements on Selenium Toxicity in Fish
Species, Age
Form of Se, Dietary (Conc.)
Interactive Factor
Observation
Period Effects Ref.
Rainbow trout, juvenile Sodium selenite (5 or 10 ppm) Low (0.8%) vs.
elevated (24%) carbohydrate
Juvenile through 16 weeks
Excess dietary carbohydrate enhanced selenium toxicity (reduced body weight, enlarged glycogen-filled livers, food avoidance)
57
Chinook salmon, swim-up larvae
Diets with clean fishmeal fortified with seleno-D,L- methionine vs. fishmeal using selenium-laden western mosquitofish (5.3–9.6 ppm)
Organic forms of selenium or trace elements or nutritional factors
Swim-up through 90 days
Fish growth reduced at slightly lower selenium concentrations and in shorter exposure period fed diets with fishmeal using selenium-laden western mosquitofish compared to clean fishmeal fortified with seleno-D,L-methionine
69
Razorback sucker, larvae Natural zooplankton from selenium-contaminated sites vs. brine shrimp from a commercial source (6–7 ppm)
Elevated arsenic in nauplii of brine shrimp (24 ppm) vs.
low arsenic in zooplankton (6 ppm)
5-day-old through 30 days
Elevated arsenic in brine shrimp counteracted selenium to prevent toxic effects, whereas low arsenic in zooplankton did not. Similar selenium residues in larvae but greatly different effects
86
Atlantic salmon, fry Organic selenium in fish (unknown)
Dietary copper (500 ppm)
Fry through 12 weeks
Reduced growth, depleted energy stores, and selenium-copper antagonism
115, 116 Pearl dace (adult)
Yellow perch (~2 g) Northern pike (~35 g)
Natural zooplankton exposed to waterborne selenium (6, 100 ppb)
Mercury-contaminated lakes
3, 6, and 8 weeks Dietary selenium, but not waterborne selenium, reduced mercury uptake in fish; at elevated concentrations, selenium reduced survival of yellow perch but not pearl dace
118–120
Yellow perch (adult) Northern pike (adult)
Selenite uptake in the food chain (5 ppb in water)
Mercury-contaminated lakes
Adults for 1–2 years
Reduced mercury residues below level of human health, but selenium reduced fish survival and reproduction
122–125
selenium in the diet (no arsenic exposure). Klug et al.106 concluded that arsenic counteracted selenium toxicity in some way other than increasing selenium elimination. Levander and Argrett107 also showed that arsenic protected against selenosis in rats and that selenium residues were increased in carcass over animals in the selenium-only exposure. Others have concluded that arsenic exposure increased the elimination of selenium in bile in short-term (1–10 h) injection experiments.90–93 In a reciprocal manner, selenium has been reported to reduce arsenic-induced teratogenic deformities in hamsters.113
Considering that (1) the whole-body residues of larvae were elevated in the brine shrimp and HTEW dietary treatments, (2) selenium concentrations in both diet treatments were above the selenium dietary toxicity threshold, (3) arsenic concentrations in the brine shrimp treatment were elevated (24 àg/g) and in the HTEW treatment were low (6.0 àg/g), (4) survival was high in the brine shrimp treatments but low in the HTEW treatment, and (5) no confounding factors seemed to be present between the two dietary treatments such as caloric content, nutritional value, trace element content (other than arsenic), and suitability as fish food, it seems likely that arsenic interacted with selenium in the fish larvae and inhibited mortality in larvae fed the brine shrimp treatment but did not inhibit mortality in the HTEW treatment.86 These results were similar to observations of Klug et al.106 and Levander and Argrett.107
44.3.2 Copper Interaction with Selenium
Lorentzen et al.114 and Berntssen et al.115,116 both reported that elevated dietary copper reduced concentrations of selenium in liver of Atlantic salmon. Lorentzen et al.114 suggested that reduced selenium concentrations were due to the formation of insoluble copper–selenium complexes in the intestinal lumen, reducing selenium bioavailability or the excretion of copper–selenium complexes from the liver through the bile. Berntssen et al.116 reported that dietary copper exposure significantly reduced selenium concentrations in intestine and liver, which in turn reduced glutathione concen- trations (selenium is a component of glutathione). However, dietary copper did not affect antioxidant glutathione peroxidase enzyme activity. In contrast, Hilton and Hodson57 reported that increasing dietary selenium exposure of rainbow trout significantly increased copper concentrations in liver.
They speculated that dietary selenium interfered with copper transport or excretion.
44.3.3 Mercury Interaction with Selenium
Perhaps one of the most published interactions between inorganic elements is that between mercury and selenium. Pelletier117 reviewed the literature for aquatic organisms and concluded that many authors reported simultaneous bioaccumulation of mercury and selenium, but there was no evidence of natural joint bioaccumulation of mercury and selenium in fishes, crustaceans, and mollusks. He noted that many results were unrelated and sometimes contradictory.
A series of experiments by Rudd, Turner, and others118–120 investigated the ability of selenium to ameliorate the toxic effects on fish inhabiting a mercury-contaminated lake in the English- Wabigoon River system in Ontario, Canada. They conducted enclosure experiments in the lake and reported that selenium additions reduced mercury accumulation in fish. Selenium interfered with mercury mobilization through the food web rather than mercury accumulation directly from water.
They cautioned that selenium amelioration of mercury should be approached with caution because selenium readily and efficiently accumulated in the food organisms and fish, especially through the food chain, and recommended that selenium additions be limited to 1 àg/L. Klaverkamp et al.121 reported that exposure of northern pike (Esox lucius) to waterborne selenium at 1 àg/L reduced mercury accumulation in carcass, but exposure to 100 àg/L selenium increased mercury accumu- lation in carcass.
Another series of experiments in mercury-contaminated lakes in Sweden also tested the ame- liorating effects of selenium.122–124 Like the studies by Rudd, Turner, and others, these studies also
confirmed that selenium readily reduces mercury accumulation in fish, but selenium bioaccumulated in fish via the food chain if waterborne selenium concentrations were > 3–5 àg/L. Fish kills of yellow perch (Perca flavescens) occurred in 4 of the 11 lakes in their study, which prompted Lindqvist et al.,125 who reviewed mercury concerns in the Swedish environment, to recommend against the use of the selenium amelioration technique in mercury-contaminated lakes.