Effects of water quality and fish size on toxicity of methiocarb, a carbamate pesticide, to rainbow trout

The acute toxicity of methiocarb in juvenile rainbow trout (Oncorhynchus mykiss, 3.25±0.79g) was evaluated in glass aquaria under static conditions. Nominal concentrations of methiocarb in the toxicity test ranged from 1.25 to 7.50mgL(-1). The concentrations of methiocarb that killed 50% of the rainbow trout within 24-h (24-h LC(50)), 48-h LC(50), 72-h LC(50), and 96-h LC(50) were 5.43±0.19, 5.04±0.18, 4.95±0.19, and 4.82±0.21mgL(-1) (95% confidence limits), respectively. Mortality of fish increased with increasing water temperature. Increasing alkalinity from 19mgL(-1) as CaCO(3) to 40, 60, or 90mgL(-1) as CaCO(3) significantly decreased mortality of fish. Total hardness ranging from 50mgL(-1) as CaCO(3) to 147mgL(-1) as CaCO(3) did not affect mortality of fish exposed to methiocarb. Fish exposed to methiocarb had histological alterations such as lamellar edema, separation of epidermis from lamellae, and lamellar fusion. Methiocarb exposed fish had necrosis between molecular and granular layer of cerebellum where Purkinje cells present. Results indicate that alkalinity, temperature, and fish size affect methiocarb toxicity of rainbow trout.     

Temperature-induced changes in pentachlorophenol chronic toxicity to early ufe stages of rainbow trout

Temperature was a controlling factor in pentachlorophenol (PCP) toxiciiy to rainbow trout (Salmo gairdnen). Eggs of frout exposed to PCP from fertilization to hatch showed elevated mortality and reduced weight at hatch. The effects on hatch weight were greatest in the cold regime (6°C) compared to (the warm (10°C). Continued PCP exposure after hatch resulted in significantly elevated mortality, reduced growth rates and reduced yolk sac resorption efficiency, and these effects were again greatest in the cold regime (6°C) compared to the warm (15°C). In contrast, during 4 wk of feeding after yolk sac resorption, PCP-induced mortality was unaffected by temperature but growth rates were reduced to the greatest extent in the warm regime (20°C) compared to the cold (12°C). The potential biomass of 1000 newly fertilized eggs at hatch, after yolk sac resorption, and after 4 wk of feeding was calculated from observed mortality and wet weights. The overall production of fish in the warm regime was reduced relative to controls at estimated threshold PCP concentrations of about 10 μg/l. In contrast, final biomass of fish in a cold regime was higher than control biomass at 10 μg/l and the estimated threshold of adverse effect was 20 μg/l. Although fish in a warm regime appeared to be affected at a lower concentration of PCP than those in the cold regime, the overall response to; the highest PCP concentration was similar. Trout exposed to PCP during the egg stage were far more sensitive to PCP than were those exposed only after hatch.     

Acute and chronic toxicity studies with monochlorobenzene in rainbow trout

The toxicity of monochlorobenzene (CB) was investigated in rainbow trout following acute intraperitoneal (i.p.) administration and chronic exposure via the water in a continuously flowing system for 15 or 30 days.In the acute study overt toxicity and hepatotoxicity were monitored over a 96-h time period. Variables measured to assess toxicity included weight changes, liver weight to body weight ratios, behavioral changes, alanine aminotransferase activity (GPT), sulfobromophthalein (BSP) retention, total plasma protein concentration and liver histopathology. In the chronic study the same measures of toxicity were followed as well as food consumption and alkaline phosphatase (AP) activity.Upon acute i.p. exposure the toxicant (9.8 mmol/kg) caused behavioral changes in the fish which were consistent with the known anesthetic properties of CB in mammals. Elevations in BSP retention and GPT activity, and histopathology indicated that CB was hepatotoxic in fish.The LC₅₀ of CB in trout exposed via the water for 96 h was 4.7 mg/l. Chronic exposure of trout to 2 or 3 mg/l CB resulted in similar behavioral changes as seen in the acute study. Liver toxicity was evident from elevations in GPT activity. BSP retention and AP activity appeared to be affected by the nutritional status of the trout as much as by the CB treatment. After 30 days of exposure to 3 mg/l CB, trout appeared to have developed some tolerance to the toxic effects.     

Acute toxicity modeling of rainbow trout and silver sea bream exposed to waterborne metals

Of three proposed acute toxicity models, the uptake-depuration (UD) model, the time-integrated concentration (TIC) model, and the concentration-time (CT) model are derived and verified with acute toxicity data to estimate the internal residues of waterborne metals in fish as a function of a few constants and variables. The main factors are the exposure time, the external exposure concentration, the bioconcentration factor (BCF), and the depuration rate constant (k2). The UD model is based on the concept of residue levels at the cell membrane well correlating with the whole-body concentrations, whereas the TIC and the CT models are based on the idea of irreversible inhibition of the enzyme acetylcholinesterase (AChE) governing the metal acute toxicity in that metals in the entire fish or in the aqueous phase can be described by the critical area under the time-concentration curve that is associated with a critical TIC of toxicant in the target tissue. A highly significant correlation (r2 > 0.9) was found between predictions and LC50(t) data for both the TIC and the CT models, indicating successfully describe 4- to 18-d LC50(t) data of arsenic (As), cobalt (Co), copper (Cu), and Co/Cu mixture in rainbow trout (Oncorhyuchus mykiss) and of Cu in fingerlings and subadults of silver sea bream (Sparus sarba). The time-dependent lethal internal concentration at the site of action that causes 50% mortality is also predicted for a given compound and species. It concludes that the TIC and the CT models can be applied to regulate the acute toxicity and to estimate incipient LC50 values and internal residues of waterborne metals in fish.     

Trophic transfer and dietary toxicity of Cd from the oligochaete to the rainbow trout

Dietary toxicity of metals on fish is often studied using commercial pellet food, and there is a lack of investigation on the toxicity of metals that are biologically incorporated into the natural food from the aquatic environment. In this study, we investigated the toxicity of dietborne Cd from the oligochaete Lumbriculus variegatus to the rainbow trout Oncorhynchus mykiss. The oligochaete worms were exposed to waterborne Cd (0.1, 5, 20, and 200 microgL(-1)) for 1 week and the fish were fed this food exclusively (daily ration=3.5% body wet weight) for 1 month. Cd concentrations in the worms averaged 0.1, 0.6, 2.2, and 30.3 microgg(-1) wet weight respectively, whereas the whole fish accumulated 0.002, 0.005, 0.019, and 0.387 microg Cd g(-1) wet weight respectively, after feeding upon control or Cd-contaminated worms for 4 weeks. Highest concentrations of Cd were retained in the gut, followed by the kidney and liver of the fish, with the latter two increasing over time; however, gut tissue accounted for >80% of whole body Cd burdens at all times. The trophic transfer efficiency of Cd was low (0.9-6.4%) although higher than in previous studies using Cd-spiked commercial diets, and was only weakly correlated to the internal Cd storage in the worms. The level of Cd in the contaminated worms did not affect Cd trophic transfer efficiency, but was reduced over the dietary exposure period. Dietborne Cd did not interfere with whole body Ca uptake from the water or alter plasma [Ca], but reduced growth by 50% in the trout exposed to the highest Cd dose. Cd stored in the metallothionein-like proteins of the fish gut tissue increased while that in the heat-denaturable proteins was reduced, suggesting detoxification over time. This study suggests a higher bioavailability and toxicity of Cd from the natural diets than from the commercial diets used in previous studies.     

Intercalibration study in the evaluation of toxicity with rainbow trout hepatocytes

An intercalibration exercise was carried out evaluating the transferability and reproducibility of the rainbow trout hepatocyte cytotoxicity test. First, rainbow trout hepatocytes were plated in 96-well microplates, packed at 4°C, and sent to eight different laboratories. Each laboratory was instructed to initiate 24-h exposure on two blind samples, one of which was toxic. Second, five laboratories were trained to perform the hepatocyte cytotoxicity test independently with their own fish source. Afterward, they were invited to evaluate toxicity of three samples: reference toxicant (KCl), toxic, and nontoxic industrial effluent. The labs were instructed to evaluate cell viability with either propidium iodide exclusion test or with neutral red uptake assay. These two assays were proposed to accommodate laboratories' constraints (i.e., available spectrophotometers or fluorometers, microplate vs tube centrifuges). Results showed all groups were able to identify toxic sample (i.e., KCl) from nontoxic one. Cytotoxic concentration at which 50% of hepatocytes are killed (CC50) varied between 70–131 mM, when cell viability was determined with PI test, while CC50 values varied between 82–118 mM with NRU assay. These values were in the same range as data obtained in our laboratory during an in-house intercalibration exercise. Moreover, 4/5 of the independent laboratories could correctly classify toxicity of the (3) samples. The rainbow trout hepatocyte cytotoxicity assessment test does, therefore, appear to be reproducible and transferable to other laboratories, producing statistically similar classifications and results for measurement endpoints such as identification of nontoxic samples, lowest observable effect concentration, and CC50 values. ©1999 John Wiley & Sons, Inc. Environ Toxicol 14: 429–437, 1999     

Dietary vanadium toxicity in juvenile rainbow trout: a preliminary study

A growth-feeding trial was conducted in which duplicate groups (70 fish/tank) of juvenile rainbow trout (initial weight 2.9 g/fish) were fed semi-purified test diets supplemented with from 0 to 10 g vanadium (as sodium orthovanadate)/kg diet for 12 wk at 15°C. All levels of supplemented vanadium (determined levels 10.2 to 8960 mg vanadium/kg diet) significantly reduced growth and feeding response in the trout. At high levels of dietary vanadium (> 493 mg/kg), feed avoidance and increased mortalities were apparent in the trout. The vanadium retention factor (carcass vanadium/total amount of vanadium consumed) and carcass concentration factor (carcass vanadium concentration/dietary vanadium content) increased in relation to the dietary vanadium level indicating a bioaccumulation of vanadium in this fish. This is in direct contrast to the apparently low bioaccumulation of waterborne vanadium in trout. The minimum dietary vanadium toxicity level could not be determined; however, it is probably less than 10 mg vanadium/kg diet. The major biochemical and/or physiological effect of vanadium in the trout would appear to be increased ‘in vivo’ lipid oxidation.     

The toxicity and metabolism of the pyrethroids cis-and trans-cypermethrin in rainbow trout,Salmo gairdneri

1. The toxicity of cis-and trans-cypermethrin to rainbow trout was investigated and the concentrations of the two isomers in brain associated with toxic signs (excitability and loss of equilibrium) were determined. cis-Cypermethrin and trans-cypermethrin were equally toxic and showed similar brain levels associated with toxic signs (cis:0.25 μg/g, mean (range 0.07-0-53); trans:0.17 μg/g (0-07-0-31)).

2. Orally administered cypermethrin was less toxic than predicted, probably due to poor intestinal uptake. Toxicity was due to absorption via the gills of unchanged pyrethroid excreted from the intestine into the water.

3. The metabolism of the radiolabelled insecticides, [¹⁴C-cyclopropyl]- and [¹⁴C-benzyl]-cis- and trans-cypermethrin has been investigated in vivo and in vitro.

4. The principal route of elimination in vivo was the bile, with 20-28% dose excreted as biliary metabolites in 24h. No difference in the rates of elimination of the cis and trans isomers was observed.

5. cis-Cypermethrin was metabolized primarily to the glucuronide of 4′-hydroxy-cypermethrin (80% total bile radioactivity), together with dichlorovinyldimethyl-cyclopropanecarboxylic acid and its glucuronide, 3-(4-hydroxyphenoxy)benzoic acid (4′-hydroxy-3BPA) and its ester and ether glucuronides, 3-phenoxybenzoyl glucuronide and 4′-hydroxy-3BPA sulphate were detected. trans-Cypermethrin was metabolized to the same products, but with only 36% as 4′-hydroxy-cypermethrin glucuronide.     

Subcellular partitioning links BLM‐based toxicokinetics for assessing cadmium toxicity to rainbow trout

The purpose of this article was to develop an integrated‐scale toxicological model to investigate the impact of cadmium (Cd) toxicity on rainbow trout (Oncorhynchus mykiss) based on recent published experimental data. This model was generated from three different types of functional relationship: biotic ligand model (BLM), damage assessment model (DAM), and subcellular partitioning model (SPM), both of key toxicological determinants involved and of functional connections between them. Toxicokinetic parameters of uptake rate constant (k₁) and elimination rate constant (k₂) in gill, liver, and subcellular fractions were derived. A negative correlation between gill binding fraction of Cd and bioaccumulation factor was found. Detoxifying ability (% detoxified in liver metabolically detoxified pool (MDP)) and k₂ were negatively correlated, indicating that increasing % detoxified in MDP can compensate for lower k₂. This finding suggests a potential tradeoff between the abilities of elimination and detoxification for Cd. Yet, compensation between the ability to eliminate Cd and the ability to recover Cd‐induced damage was not found. However, changes in k₂ and recovery rate constant (k_r) can shift the dynamics of Cd susceptibility probability. This analysis implicates that once k₂ is determined experimentally, the values of k_r and % detoxified in MDP can be predicted by the proposed k₂?k_r and k₂?% detoxified relationships. This study suggests that the mechanistic linking of BLM‐based DAM and SPM can incorporate the organ‐ and cell‐scale exposure experimental data to investigate the mechanisms of ecophysiological response for aquatic organisms exposed to metal stressors. © 2010 Wiley Periodicals, Inc. Environ Toxicol, 2011.     

The effect of feeding and fasting on ammonia toxicity in juvenile rainbow trout,Oncorhynchus mykiss

Present fresh water ammonia standards have been established using data collected from toxicity tests on unfed fish. Ammonia, however, is an unusual toxicant as it is produced as a metabolic waste following protein catabolism. The present research was conducted to investigate the relationship between feeding and ammonia toxicity in rainbow trout, Oncorhynchus mykiss. Results from these studies revealed that some fish fed to satiation have plasma ammonia levels greater than 30 microg/ml. This level was similar to the plasma ammonia levels in rainbow trout at the ammonia LC50 value calculated in the present experiments. Even though plasma ammonia in fed fish was elevated there was no significant difference between the 96 h LC50 values for fed and unfed fish (174 mg N per l) at pH 7.2. Feeding rates during these experiments decreased during the first 48 h of ammonia exposure, but increased again in the second 48 h at all but the highest ammonia level. Feeding rate never increased to the control level in ammonia exposed fish. In a second set of experiments feeding fish had a significantly higher 24 h LC50 level, 177 mg N per l, than fish fasted for 5 or 10 days, 135-143 mg N per l. No significant difference was noted however, between the 48 h LC50 values for fed and fasted fish. It was evident from these studies that feeding protects rainbow trout from ammonia toxicity during the first 24 h of exposure and that fasting exacerbates ammonia toxicity.     

The toxicity and metabolism of the pyrethroids cis- and trans-cypermethrin in rainbow trout, Salmo gairdneri

1. The toxicity of cis- and trans-cypermethrin to rainbow trout was investigated and the concentrations of the two isomers in brain associated with toxic signs (excitability and loss of equilibrium) were determined. cis-Cypermethrin and trans-cypermethrin were equally toxic and showed similar brain levels associated with toxic signs (cis:0.25 micrograms/g, mean (range 0.07-0.53); trans:0.17 micrograms/g (0.07-0.31]. 2. Orally administered cypermethrin was less toxic than predicted, probably due to poor intestinal uptake. Toxicity was due to absorption via the gills of unchanged pyrethroid excreted from the intestine into the water. 3. The metabolism of the radiolabelled insecticides, [14C-cyclopropyl]- and [14C-benzyl]-cis- and trans-cypermethrin has been investigated in vivo and in vitro. 4. The principal route of elimination in vivo was the bile, with 20-28% dose excreted as biliary metabolites in 24 h. No difference in the rates of elimination of the cis and trans isomers was observed. 5. cis-Cypermethrin was metabolized primarily to the glucuronide of 4'-hydroxy-cypermethrin (80% total bile radioactivity), together with dichlorovinyldimethylcyclopropanecarboxylic acid and its glucuronide, 3-(4-hydroxyphenoxy)benzoic acid (4'-hydroxy-3BPA) and its ester and ether glucuronides, 3-phenoxybenzoyl glucuronide and 4'-hydroxy-3BPA sulphate were detected. trans-Cypermethrin was metabolized to the same products, but with only 36% as 4'-hydroxy-cypermethrin glucuronide.     

Comparative toxicity of cis-cypermethrin in rainbow trout, frog, mouse, and quail

The synthetic alpha-cyano-phenoxybenzyl-containing pyrethroid insecticides act on the CNS of vertebrates and show a species-selective toxicity in the order fish greater than amphibians much greater than mammals greater than birds. Concentrations of [14C]cis-cypermethrin in the brains of representative members of each of these classes of chordates were measured at toxic signs (an onset of hyperactivity followed by seizures and loss of balance/equilibrium) as an indicator of target organ sensitivity. The concentration of cis-cypermethrin in brain, associated with toxic signs, in micrograms per gram (mean +/- SE) as determined by high-performance liquid chromatography was 0.08 +/- 0.03 (frog), 0.23 +/- 0.05 (trout), 1.71 +/- 0.33 (mouse), and 3.94 +/- 0.88 (quail). Trout brain was equally sensitive to the cis and trans isomers of cypermethrin. In both mouse and quail, some 90% of the radioactivity in the brain was parent pyrethroid. Trout and frog, however, afforded only 56 and 32%, respectively, of the brain 14C as cypermethrin, with the remaining radioactivity in both extractable and nonextractable metabolites, including 4'-hydroxy-cis-cypermethrin, which is potentially neuroactive. Following oral administration, cis-cypermethrin was readily absorbed and metabolized by quail. Intestinal uptake was far less rapid in trout and mouse, with unchanged cypermethrin dispersed in secreted bile, being readily eliminated from the intestines of fish. The uptake and metabolism of cis-cypermethrin and the brain sensitivities of these animals to the pyrethroid account for the observed differences in acute toxicity.     

Effects of salinity on the uptake, biotransformation, and toxicity of dietary seleno-L-methionine to rainbow trout.

Selenium (Se) is an element that has been of environmental concern in aquatic systems that drain arid regions heavily used for agricultural purposes. As hypersaline conditions are associated with these ecosystems, this study examined the effect of hypersaline water on the uptake, biotransformation, and toxicity of seleno-L-methionine (SeMe) in juvenile rainbow trout. Fish were acclimated for 5 days to four different salinity regimes (0.5, 6.3, 11.9, 16.8 deciSiemens (dS/m) per meter. To mimic arid agricultural runoff solutes, the water was reconstituted with ions found in drainage water of the San Joaquin River in California. Following 7 days of dietary exposure to 180 mg/kg SeMe, mortality, as well as hepatic selenium concentrations and reduced:oxidized glutathione ratios were measured. Hypersaline conditions protected fish from dietary SeMe toxicity. Fish exposed to 0.5 dS/m water experienced 100% lethality in 2.5 days, whereas fish acclimated to 16.8 dS/m water-only experienced 16.7% mortality, which took 5-7 days to occur. There were no significant differences in hepatic selenium concentrations, but diminishment of reduced glutathione:oxidized glutathione (GSH:GSSG) ratios was observed in SeMe-treated fish held in 0.5 dS/m water. SeMe inhibited flavin-containing monoxygenase catalyzed trimethylamine oxidase activity, but salinity failed to induce expression in trout, indicating an oxygenation of organoselenides may play a minor role in SeMe toxicity.     

Differential toxicity of trans-permethrin in rainbow trout and mice: I. Role of biotransformation

The trans isomer of [1R,S] permethrin (t-per) was > 110 times more toxic to rainbow trout than to mice by both iv and ip administration. The importance of trans-permethrin biotransformation in this differential toxicity was assessed by measuring rates of t-per biotransformation in trout and mouse tissues in vitro, and the effect of inhibitors of drug metabolism on t-per lethality in both species. A previous study had shown that ester hydrolysis by trout liver, plasma, and kidney is much slower than that seen in these same tissues in mice. The present work further indicates that oxidation of t-per is 35 times slower in trout liver microsomes than mouse microsomes when the tissue suspensions were incubated at the body temperature of trout and mice (12°C for trout and 37°C for mice). Inhibition of esterase activity with tri-o-tolyl phosphate (TOTP) produced no potentiation of t-per lethality in trout while the same compound potentiated t-per lethality at least 1.5-fold in mice. Piperonyl butoxide (PIP) alone produced no potentiation in mice but slightly increased t-per toxicity when administered in conjunction with TOTP. PIP caused a slight increase in t-per lethality in rainbow trout but no increase in t-per lethality from control was observed when trout were pretreated with both TOTP and PIP. When drug metabolism was inhibited, t-per was still 65 times more toxic to trout than to mice. The data indicate that trout, in addition to hydrolyzing t-per slowly, also oxidize the compound considerably slower than mice in vitro. Potentiation of t-per lethality by TOTP suggests ester hydrolysis to be an important t-per detoxification reaction in mice but not in trout. However, since t-per was 65 times more toxic to the trout than mouse when drug metabolism was inhibited, other factors, such as differences in target organ sensitivity may be involved in the differential toxicity of permethrin.     

Effect of pH on the acute toxicity of hexavalent chromium to rainbow trout (Salmo gairdneri)

The acute toxicity of hexavalent chromium, Cr(VI). to rainbow trout (Salmo gairdneri) increased with decreasing pH in the range from 7.8 to 6.5. Morphological changes that could be associated with acute Cr(VI) poisoning at pH 7.8 were found in gills, kidney and stomach, whereas those at pH 6.5 appeared to be restricted to the gills only. At both pH values, however, similar alterations in plasma osmolality and hematocrit values of blood were found in fish surviving an exposure to acute toxic concentrations.To explain the observed effects, hydroehromate (HCrO₄^?) and chromate (CrO^2?₄) were considered as the toxic species of Cr(VI). An attempt was made to calculate the relative toxicities of these ionic species from empirical toxicity relationships for weak acids in fish, as described in the literature.     

Induction of peroxisome proliferation in rainbow trout exposed to ciprofibrate

Rainbow trout (Salmo gairdneri), average body weight of 450 g, were treated with 15, 25, or 35 mg/kg of ciprofibrate via intraperitoneal injection every other day for 2 to 3 weeks. The effects on hepatic peroxisomal acyl-CoA oxidase, polypeptide PPA-80, catalase, and liver weight were measured. The treatment of trout with ciprofibrate showed significant dose-related increases in peroxisomal acyl-CoA activity, polypeptide PPA-80, and catalase after 3 weeks of exposure. Peroxisomal oxidase activity showed a significant (p = 0.0008) increase (78%) at 35 mg/kg and a marginal (p = 0.1) increase (27%) at 25 mg/kg after 3 weeks of exposure. Densitometric analysis of polypeptide PPA-80 and catalase showed increases up to 48 and 236% at 35 mg/kg, respectively. Morphometric analysis on livers of trout administered 35 mg/kg for 3 weeks showed a 2.3-fold increase of peroxisomal volume density, as compared to control. This study demonstrates the induction of peroxisome proliferation in rainbow trout administered ciprofibrate, a known peroxisome proliferator in rodents.     

Cytotoxicity of aged cadmium-telluride quantum dots to rainbow trout hepatocytes

The purpose of this study was to examine the lethal and sublethal toxicity of cadmium telluride (CdTe) quantum dots (Q-dots) in primary cultures of rainbow trout hepatocytes. Hepatocytes were exposed to concentrations of positively coated and aged (2 months and 2 years) Q-dots for 48 h at 15°C. Post treatment, cellular analysis was done of cell viability, lipid peroxidation (LPO), DNA damage, metallothioneins (MT), labile zinc/cadmium and heat shock proteins (chaperones). Q-dots were found to be toxic to fish hepatocytes at a threshold concentration of 0.1 mg/l. These nanoparticles increased the levels of MT, labile zinc, DNA strand breaks and heat shock proteins of the 70 kDa family. The strongest response was observed with the molecular chaperone of the 70 kDa family, reaching a 7-fold induction in exposed cells. Overall, the assessment of multiple biomarkers in trout hepatocytes exposed to differently ‘aged’ Q-dots suggests that the cytotoxic responses to two-year-old positively coated CdTe Q-dots were largely due to the liberation of Cd²⁺.     

Features of cadmium and calcium uptake and toxicity in rainbow trout (Oncorhynchus mykiss) mitochondria

Molecular features of cadmium (Cd) and calcium (Ca) uptake and toxicity in rainbow trout liver mitochondria were studied using modulators of mitochondrial permeability transition pore (MPTP), mitochondrial calcium uniporter (MCU) and rapid uptake mode (RaM). Malate-glutamate energized mitochondria were exposed to 20μM Cd and 50μM Ca, singly and in combination, with and without addition of ruthenium red (RR), cyclosporin A (CsA), bongkrekic acid (BKA) or dithiothreitol (DTT). State 3 mitochondrial respiration was inhibited by 50% by either Cd or Ca, and by 70% when the two cations were added simultaneously. All the modulators tested reduced the inhibition of state 3 respiration with DTT completely reversing the Cd effect. While state 4 respiration was unaffected by Ca and/or Cd, 1.5-3 fold stimulation was observed on addition of the modulators. Uncoupler-stimulated respiration was inhibited by Cd, Ca and Cd+Ca with complete (DTT) and partial (RR, CsA, BKA) protection of the Cd and Cd+Ca effects. All the modulators completely reversed the Ca-induced inhibition. Swelling, the hallmark of MPTP, measured following incubation of mitochondria with 0-100μM of the two cations, singly and in combination, was abolished by all the modulators. Overall these data show the existence of membrane channels in rainbow trout liver mitochondria with some characteristics similar to mammalian MPTP, MCU and RaM. Moreover, entry of Ca and Cd into mitochondria is important in the toxicity of these cations.     

Preliminary investigations on the comparative chronic toxicity of four dietary arsenicals to juvenile rainbow trout (Salmo gairdneri R.)

Juvenile rainbow trout were fed semi-purified diets in eight-week growth trials to compare the toxicity of four dietary arsenicals: arsenic trioxide (AT); disodium arsenate heptahydrate (DSA); dimethylarsinic acid (DMA); and arsanilic acid (AA). Toxicity responses of reduced growth and feed consumption, and altered feeding behaviour, were noted at all levels of supplementation of AT and DSA (137–1477 μg As/g diet). In contrast, even at the highest levels of supplementation (1497 μg As/g diet as DMA, and 1503 μg As/g diet as AA) the organic arsenicals did not result in these toxicity signs.Carcass arsenic concentration showed a dose-response relationship to dietary arsenic concentration and exposure rate, for each of the arsenicals investigated. At lower levels of exposure, dietary DSA yielded the highest carcass arsenic concentrations, while at higher levels, dietary AT yielded the highest residues.The ‘no observed effect concentration’ (NOEC) for dietary arsenic lies between 1 and 137 μg As/g diet for DSA, between 1 and 180 μg As/g diet for AT, and is at least 1497 μg As/g diet for DMA and AA. It was concluded that disodium arsenate was the most toxic to juvenile rainbow trout of the four dietary arsenicals studied.     

Absence of overt toxicity from feeding the flavonol, quercetin, to rainbow trout (Salmo gairdneri)

The toxicity of the plant flavonol, quercetin, to rainbow trout (Salmo gairdneri) was investigated. Quercetin, which had been confirmed to be mutagenic in the Ames Salmonella/mammalian microsome test, was fed to trout at levels of 1 or 5% in the diet for 8 months. Survival, growth and feed conversion efficiency, selected haematological parameters and the relative weights of heart, liver and spleen were unaffected by the ingestion of quercetin, and there were no histopathological changes in any of the tissues examined.