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C M Wood

Publications and source records attributed to C M Wood.

At least 19 recordsLinked to original sources
PubMed2006

Dietary Pb accumulation in juvenile freshwater rainbow trout (Oncorhynchus mykiss).

Three different diets amended with lead (Pb) nitrate Pb(NO3)2 (7, 77, and 520 microg Pb/g dry weight) and a Pb-free control diet (0.06 microg Pb/g dry weight) were fed to juvenile freshwater rainbow trout for 21 days. Accounting for measured food consumption, the calculated doses per fish were 0.02, 3.7, 39.6, and 221.5 microg/day, for the control, low, intermediate, and high Pb treatments, respectively. The patterns of Pb accumulation over time were determined in various tissues (gills, liver, kidney, intestine, carcass), red blood cells (RBC), and plasma, as well as feeding, growth, hematological, and ionoregulatory parameters. Pb accumulation occurred in a dose-dependent manner in all tissues except the plasma, where accumulation was minimal. Overall, when fed the highest Pb diet, the intestine exhibited the greatest Pb burden (17.8 microg Pb/g tissue wet weight), with high concentrations also found in the kidney (2.4 microg Pb/g tissue wet weight) and liver (1.9 microg Pb/g) at the highest dietary Pb treatment by day 21. The RBCs accumulated a substantial amount of Pb (1.5 microg Pb/g) when compared to the plasma (0.012 microg Pb/g) in the high treatment group. The percentage of Pb retained in the fish decreased with increasing dietary Pb concentrations. Growth, survival, plasma protein, and hematocrit were not significantly affected by dietary Pb. Plasma Ca2+ levels decreased at the beginning of the experiment, whereas Mg2+ levels decreased during the middle of the experiment in both the intermediate and high dietary treatments. Both the Ca2+ and Mg2+ levels stabilized by day 21. Branchial Ca2+ and Na+ influx rates were not affected by dietary Pb, except on day 8 where Na+ influx rates were significantly elevated. The results of this study show that Pb does accumulate internally from the diet when present at levels within the range reported in contaminated benthic invertebrates in nature. We further identify the intestine as a potential target site of chronic toxicity of Pb via the diet, and RBCs as a reservoir of dietary Pb.

Animals↗
PubMed2006

Bioavailability of sediment-associated Cu and Zn to Daphnia magna.

Exposures to mining-impacted, field-collected sediment (Clear Creek, CO, USA) contaminated with Cu (2.4 mg/g) and Zn (5.2 mg/g) were acutely toxic to juvenile Daphnia magna. Dissolved Cu and Zn in the overlying water (sediment+reference water) were at levels that could cause acute toxicity. To reduce dissolved metals below toxic levels, the sediment was repeatedly rinsed to remove any easily mobilized metals. Washing the sediment reduced dissolved Cu by 60% and Zn by 80%. D. magna exposed to washed sediment experienced higher survival (95%) compared to those exposed to the original sediment (<50%). Cu and Zn that remained associated with suspended sediment after washing were not bioavailable, since survival and tissue metal concentrations in D. magna exposed to both filtered (>0.45 microm) and unfiltered overlying water were statistically similar. Multiple regression analysis indicated that only dissolved Cu significantly contributed to mortality of D. magna whereas particulate Cu, particulate Zn, and dissolved Zn did not. Regression analysis on a combined dataset from all Clear Creek exposures (washed and unwashed), revealed a significant (p < 0.0001, r(2) = 0.76) relationship between the concentration of dissolved copper in the overlying water and the mortality of exposed Daphnia, yielding an estimated LC50 of 26 microg/L dissolved copper (hardness approximately 140 mg/L). The results of this study indicate that if the sediment of Clear Creek was subjected to a resuspension event that there would be a significant efflux of metals from the sediment into the water column, resulting in potentially toxic levels in the water column.

Animals↗
PubMed2006

Interaction between dietary calcium supplementation and chronic waterborne zinc exposure in juvenile rainbow trout, Oncorhynchus mykiss.

This study investigated the effects of dietary Ca2+ on branchial Ca2+ and Zn2+ uptake, new and total zinc accumulation in target tissues (gill, liver and kidney), calcium and zinc homeostasis, and acute tolerance to waterborne zinc in fish chronically exposed to waterborne zinc. Juvenile rainbow trout (Oncorhynchus mykiss) were maintained on a calcium-enriched diet [41.2 mg vs. 21.2 mg (control) calcium/g dry wt. of food] and chronic waterborne zinc exposure (2.3 micromol/L), both separately and in combination, for 28 days. Calcium-supplemented diet in the absence of waterborne zinc significantly reduced branchial Ca2+ and Zn2+ influx rates, and new and total zinc accumulations in target tissues relative to control. However it did not protect against the acute zinc challenge. In contrast, waterborne zinc exposure significantly increased branchial Ca2+ and Zn2+ influx rates, new and total zinc concentrations in target tissues, and acute zinc tolerance relative to control. Interestingly, no such changes in any of these parameters were recorded in fish treated simultaneously with elevated dietary Ca2+ and waterborne zinc, except acute zinc tolerance which was highest among all the treatments. Thus, we conclude that the interactions between elevated dietary Ca2+ and waterborne zinc can protect freshwater fish against waterborne zinc toxicity.

Animals↗
PubMed2006

Food selection, growth and physiology in relation to dietary sodium chloride content in rainbow trout (Oncorhynchus mykiss) under chronic waterborne Cu exposure.

Waterborne Cu is toxic to Na(+) and Cl(-) regulation in freshwater fish, and Cu is taken up, at least in part, via the Na(+)-transport pathway in the gills. Therefore, we hypothesized that freshwater fish may mitigate the toxic effects of waterborne Cu by selecting a NaCl-enriched diet over a normal diet. We tested this hypothesis in juvenile rainbow trout (Oncorhynchus mykiss) by offering them the choice between NaCl-enriched (1.9 mmol g(-1)Na(+)) and normal (0.2 mmol g(-1)Na(+)) diets under a chronic waterborne Cu exposure of 55 microg L(-1) for a period of 28 days. Contrary to expectation, trout exhibited a preference for NaCl-enriched diet under control conditions, while exposure to chronic waterborne Cu severely disrupted their normal feeding pattern with an accompanying loss of preference for the NaCl-enriched diet. Waterborne Cu exposure also severely affected appetite and growth. Both appetite and growth gradually recovered with time, but remained significantly impaired relative to Cu-unexposed fish until the end of the exposure. Waterborne Cu exposure also significantly increased Cu accumulations in target organs (gill, liver, and gut), plasma and whole body. However, Cu accumulation decreased substantially towards the end of the exposure in target organs and whole body as well as in plasma in Cu-exposed fish with dietary choice relative to Cu-exposed fish with normal diet. These adjustments were concurrent with the gradual recovery of appetite, which also led to increased ingestion of the NaCl-enriched diet. Interestingly, this elevated dietary uptake of NaCl produced significant stimulation of Na(+) efflux in Cu-exposed fish. Subsequently, it also led to significant elevation of Na(+) levels in target organs and whole body, and restored the decrease of plasma Na(+) and Cl(-) levels in Cu-exposed fish. The NaCl supplemented diet appeared to be beneficial in compensating Na(+) and Cl(-) losses from the body induced by waterborne Cu. Overall, these results demonstrate that a NaCl-enriched diet, although consumed in relatively reduced quantities due to the impairment of food selection and appetite, can help to protect freshwater fish against chronic waterborne Cu toxicity.

Animal Structures↗
PubMed2006

Characterization of a branchial epithelial calcium channel (ECaC) in freshwater rainbow trout (Oncorhynchus mykiss).

The entry of calcium (Ca2+) through an apical membrane epithelial calcium channel (ECaC) is thought to a key step in piscine branchial Ca2+ uptake. In mammals, ECaC is a member of the transient receptor potential (TRP) gene family of which two sub-families have been identified, TRPV5 and TPRV6. In the present study we have identified a single rainbow trout (Oncorhynchus mykiss) ECaC (rtECaC) that is similar to the mammalian TRPV5 and TRPV6. Phylogenetic analysis of the protein sequence suggests that an ancestral form of the mammalian genes diverged from those in the lower vertebrates prior to the gene duplication event that gave rise to TRPV5 and TRPV6. The putative model for Ca2+ uptake in fish proposes that the mitochondria-rich cell (also termed ionocyte or chloride cell) is the predominant or exclusive site of transcellular Ca2+ movements owing to preferential localisation of ECaC to the apical membrane of these cells. However, the results of real-time PCR performed on enriched gill cell populations as well as immunocytochemistry and in situ hybridisation analysis of enriched cells, cell cultures and whole gill sections strongly suggest that ECaC is not exclusive to mitochondria-rich cells but that it is also found in pavement cells. Not only was ECaC protein localized to areas of the gill normally having few mitochondria-rich cells, but there was also no consistent co-localization of ECaC- and Na+/K+-ATPase-positive (a marker of mitochondria rich cells) cells. Taken together, the results of the present study suggest that although ECaC (mRNA and protein) does exist in trout gill, its cellular distribution is more extensive than previously thought, thus suggesting that Ca2+ uptake may not be restricted to mitochondria-rich cells as was proposed in previous models.

Amino Acid Sequence↗
PubMed2005

Effects of water hardness on the physiological responses to chronic waterborne silver exposure in early life stages of rainbow trout (Oncorhynchus mykiss).

Early life stages of rainbow trout were exposed to 0, 0.1 and 1 microg/L Ag (as AgNO(3)) in very soft water (2mg/L CaCO(3)), moderately hard water (150 mg/L CaCO(3)) and hard water (400mg/L CaCO(3)) of low dissolved organic carbon concentration (0.5mg C/L) from fertilization to swim-up (64 days) under flow-through conditions, and monitored for whole embryo/larval silver accumulation, Na(+) and Cl(-) concentrations, Na(+) uptake and Na(+)K(+)-ATPase activity. The objective of the study was to investigate potential protective effects of water hardness on the physiological responses to chronic silver exposure. In the absence of silver, there was little effect of hardness on the ionoregulatory parameters studied, though higher hardness did improve survival post-hatch. At all three water hardness levels, whole embryo/larval Na(+) uptake was low and relatively constant prior to 50% hatch, but dramatically increased following 50% hatch, whereas Na(+)K(+)-ATPase activity steadily increased over development. Whole embryo/larval Na(+) and Cl(-) concentrations were low and constant prior to 50% hatch, but following 50% hatch Na(+) concentration increased, while Cl(-) concentration decreased. Following 50% hatch, exposure to 0.1 and 1 microg/L Ag resulted in a decrease in whole embryo/larval Na(+) concentration, Cl(-) concentration, Na(+) uptake and Na(+)K(+)-ATPase activity, indicating that the mechanism of chronic silver toxicity involves an ionoregulatory disturbance, and is similar to the mechanism of acute silver toxicity. An increase in water hardness reduced or eliminated the effect of silver on these parameters while enhancing survival, suggesting that the nature of the protective effect of hardness involves effects on the ionoregulatory disturbance associated with silver exposure. An increase in water hardness did not fully protect against the accumulation of silver associated with silver exposure. These results suggest that it may be possible to model chronic silver toxicity using a biotic ligand type model, and that a physiologically based model may be more appropriate because Na(+)K(+)-ATPase activity or Na(+) uptake is an endpoint for prediction rather than whole embryo or larval silver accumulation.

Animals↗
PubMed2005

Tissue-specific cadmium and metallothionein levels in rainbow trout chronically acclimated to waterborne or dietary cadmium.

Rainbow trout were exposed to a sublethal concentration of waterborne Cd (0 or 3 microg/L) or dietary Cd (0 or 500 mg/kg dry wt) for 30 days to induce acclimation, and tissue Cd and metallothionein (MT) levels were examined. The greatest Cd concentrations were observed in the kidney followed by the gills and liver of the fish exposed to Cd via water, but in the gut tissues followed by the kidney, liver, and gills for dietary-exposed fish, reflecting a variation depending on the route of Cd exposure. Some MT was found in the nonacclimated naïve fish with no experience of elevated Cd exposure, and these background MT levels were quite high in the posterior intestine (480 microg/g), cecae (257 microg/g), and liver (248 microg/g) relative to other tissues (7-50 microg/g). With exposure to both waterborne and dietary Cd, MT levels rose significantly in all observed tissues. The increases relative to the control levels of MT in naïve fish were in the order: kidney (5.4 times) > gills (4.6) > liver (1.3) for the waterborne exposure group, and in the order kidney (19.3 times) >> cecae and posterior intestine (approximately 6.5 times) > liver and stomach (approximately 5 times) > midintestine (4.3 times) > gills (2.1 times) for the dietary exposure group. At 24 hours after an acute gastrointestinal dose of Cd (276 microg/kg) infused into the stomach of dietary exposure groups, large increases of total Cd but not MT levels were found in the gut tissues of nonacclimated fish; in the Cd-acclimated fish, the posterior intestine was greatly affected with decreases in Cd (71%), Zn (33%), Cu (70%) and MT (46%) levels, suggesting an enhanced sloughing of tissue materials after infusion. Exposure to Cd did not cause any notable decrease of Zn or Cu in any tissue, except that found in the posterior intestine. However, a molar analysis indicated that although Cd levels remained less than MT binding capacity in both waterborne and dietary exposure groups, the total metal levels (Cd + Zn + Cu) greatly exceeded MT binding capacity in all tissues of Cd-exposed fish, suggesting a potential competition of Cd with other metals for binding sites on MT and non-MT proteins in the tissues.

Adaptation, Physiological↗
PubMed2004

Daphnia need to be gut-cleared too: the effect of exposure to and ingestion of metal-contaminated sediment on the gut-clearance patterns of D. magna.

The presence of sediment particles in the gut indicated that Daphnia magna used in whole-sediment bioassays ingest sediment. If gut contents are not removed prior to whole-body tissue-burden analysis, then the bioavailability of any sediment-associated contaminants (e.g. metals) can be overestimated. Gut clearing patterns were determined for D. magna after exposure to both clean and metal-contaminated (Cu and Zn) field-collected sediments. D. magna exposed to reference sediment had fuller guts than those exposed to metal-contaminated sediment (95% versus 60% full). Neither reference- nor metal-exposed D. magna could clear their gut completely of sediment particles when held in clean water for 24 h. When Daphnia were transferred to clean water after exposure to metal-contaminated sediment, there was no significant decrease in gut-fullness (P>0.05) even after 48 h of purging. By comparison, animals transferred to water containing 5 x 10(5) cells of algae (Pseudokircheriella subcapita) after exposure to contaminated sediment showed a significant drop in gut fullness from 56% immediately after exposure to 17% after 4 h of gut-clearance. Although gut fullness did not change significantly beyond 2 h of purging, data were much less variable after 8 h of gut-clearance than after 2 h or 4 h. The depuration of Cu was well described with a two-compartment first-order kinetic model (r2=0.78, P<0.0001) indicating that D. magna exposed to metal-contaminated sediment have one pool of Cu that is quickly depurated (0.2 h(-1)), and one that has been incorporated into the tissues (<<0.00001 h(-1)). Assuming tissue background of 48 microg/g, an exposed animal which has not been depurated or which has been purged with water alone would yield whole-body tissue Cu concentrations that are 5.6- and 4-fold higher, respectively, than that purged with algae + water (8 h). We recommend that D. magna used to estimate metal bioavailability from sediment be gut-cleared in the presence of algae for 8 h prior to determination of whole-body metal concentrations.

Animals↗
PubMed2004

Bicarbonate secretion plays a role in chloride and water absorption of the European flounder intestine.

Experiments performed on isolated intestinal segments from the marine teleost fish, the European flounder (Platichthys flesus), revealed that the intestinal epithelium is capable of secondary active HCO3(-) secretion in the order of 0.2-0.3 micromol x cm(-2) x h(-1) against apparent electrochemical gradient. The HCO3(-) secretion occurs via anion exchange, is dependent on mucosal Cl(-), results in very high mucosal HCO3(-) concentrations, and contributes significantly to Cl(-) and fluid absorption. This present study was conducted under in vivo-like conditions, with mucosal saline resembling intestinal fluids in vivo. These conditions result in a transepithelial potential of -16.2 mV (serosal side negative), which is very different from the -2.2 mV observed under symmetrical conditions. Under these conditions, we found a significant part of the HCO3(-) secretion is fueled by endogenous epithelial CO2 hydration mediated by carbonic anhydrase because acetazolamide (10(-4) M) was found to inhibit HCO3(-) secretion and removal of serosal CO(2) was found not to influence HCO3(-) secretion. Reversal of the epithelial electrochemical gradient for Cl(-) (removal of serosal Cl(-)) and elevation of serosal HCO3(-) resulted in enhanced HCO3(-) secretion and enhanced Cl(-) and fluid absorption. Cl(-) absorption via an anion exchange system appears to partly drive fluid absorption across the intestine in the absence of net Na(+) absorption.

Acetazolamide↗
PubMed2004

Glucocorticoid receptors are involved in the regulation of pulsatile urea excretion in toadfish.

The objectives of this study were to characterize the pattern of pulsatile urea excretion in the gulf toadfish in the wake of exogenous cortisol loading and to determine the receptors involved in the regulation of this mechanism. Toadfish were fitted with indwelling arterial catheters and were infused with isosmotic NaCl for 48 h after which fish were treated with cortisol alone, cortisol + peanut oil, cortisol + RU486 (a glucocorticoid receptor antagonist) or cortisol + spironolactone (a mineralocorticoid receptor antagonist). Upon cortisol loading, fish treated with cortisol alone, cortisol + oil or cortisol + spironolactone experienced a two- to threefold reduction in pulsatile urea excretion. This reduction was due to a decrease in urea pulse size with no effect on pulse frequency compared to values measured during the control NaCl infusion period. In addition, these fish showed an increase in plasma urea concentrations upon treatment. These apparent effects of cortisol treatment were abolished in fish treated with cortisol + RU486. In contrast, these fish showed an increase in pulsatile urea excretion mediated by a twofold increase in pulse size with no change in frequency. Likewise, fish treated with cortisol + RU486 showed a significant decrease in plasma urea concentrations over the course of the experiment. The findings of this study indicate that high levels of cortisol reduce pulsatile urea excretion by decreasing pulse size. In addition, it appears that glucocorticoid receptors and not mineralocorticoid receptors are involved in the regulation of the toadfish pulsatile urea excretion mechanism.

Analysis of Variance↗
PubMed2004

Gastrointestinal uptake and fate of cadmium in rainbow trout acclimated to sublethal dietary cadmium.

Adult rainbow trout were pre-exposed to a sublethal concentration of dietary Cd (500 mg/kg dry wt.) for 30 days to induce acclimation. A gastrointestinal dose of radiolabeled Cd (276 microg/kg wet wt.) was infused into the stomach of non-acclimated and Cd-acclimated trout through a stomach catheter. Repetitive blood samples over 24 h and terminal tissue samples were taken to investigate the gastrointestinal uptake, plasma clearance kinetics, and tissue distribution of Cd. Only a small fraction of the infused dose (non-acclimated: 2.4%; Cd-acclimated: 6.6%) was internalized across the gut wall, while most was bound in the gut tissues (10-24%) or remained in the lumen (16-33%) or lost from the fish (approximately 50%) over 24 h. Cadmium loading during pre-exposure produced a profound increase of total Cd in the blood plasma (approximately 28-fold) and red blood cells (RBC; approximately 20-fold). The plasma Cd-time profiles consisted of an apparent rising (uptake) phase and a declining (clearance) phase with a maximum value of uptake in 4 h, suggesting that uptake of gastrointestinally infused Cd was very rapid. Acclimation to dietary Cd did not affect plasma Cd clearance (approximately 0.5 ml/min), but enhanced new Cd levels in the plasma (but not in the RBC), and resulted in a longer half-life for plasma Cd. Tissue total and new Cd levels varied in different regions of the gastrointestinal tract, and overall levels in gut tissues were much greater than in non-gut tissues, reflecting the Cd exposure route. Dietary Cd, but not the infused Cd, greatly increased total Cd levels of all gut tissues in the order posterior-intestine (640-fold) > cecae (180-fold) > mid-intestine (94-fold) > stomach (53-fold) in Cd-acclimated fish relative to naïve fish. Among non-gut tissues in the Cd-acclimated fish, the great increases of total Cd levels were observed in the liver (73-fold), kidney (39-fold), carcass (35-fold), and gills (30-fold). The results provide some clear conclusions that may be useful for environmental risk assessment of dietary Cd exposure in fish.

Acclimatization↗
PubMed2004

Effects of prolonged copper exposure in the marine gulf toadfish (Opsanus beta). I. Hydromineral balance and plasma nitrogenous waste products.

Acute (96 h) and prolonged (30 days) copper exposure induced osmoregulatory disturbance and impaired nitrogenous waste excretion in the marine teleost, the gulf toadfish (Opsanus beta), which was found to be extremely tolerant to acute copper exposure with a 96 h LC50 exceeding 340 microM but exhibited disturbed mineral balance in response to both acute and prolonged exposure to approximately 12 microM copper. The main cause of copper toxicity was found to be Na+ and Cl- regulatory failure leading to elevated plasma [Na+] and [Cl-] and osmolality which in turn led to fluid loss from muscle tissue. Analysis of intestinal fluid composition revealed a complicated pattern of effects of copper exposure. Intestinal transport physiology was directly influenced by copper exposure with Cl- absorption being the most sensitive parameter. Evidence for increased Na+ and fluid absorption when the fish exhibited elevated plasma osmolality indicates that the intestine may also exhibit a compensatory response to impairment of branchial transport processes, suggesting at least two target organs (gill and intestine) for copper toxicity in marine fish. Plasma Mg2+ was elevated from approximately 1.5 mM to as much as 4.0 mM, likely as a result of increased branchial permeability. While plasma [ammonia] clearly responded to copper exposure, plasma [urea] exhibited a much more sensitive and pronounced response to both acute and prolonged copper exposure, resulting in as much as a three-fold increase in circulating urea levels. This response is most likely the result of the unique ability of this teleost to convert ammonia to urea.

Animals↗
PubMed2004

Effects of prolonged copper exposure in the marine gulf toadfish (Opsanus beta) II: copper accumulation, drinking rate and Na+/K+ -ATPase activity in osmoregulatory tissues.

Gulf toadfish were exposed to sublethal levels of copper (12.8 or 55.2 microM) for 30 days. Drinking in control fish averaged 1 ml kg(-1)h(-1) but exposure to 55.2 microM copper resulted in a complex biophasic pattern with initial (3 h and 1 day) inhibition of drinking rate, followed by an elevation of drinking rate from day 3 onwards. Drinking led to copper accumulation in the intestinal fluids at levels three to five times higher than the ambient copper concentrations, which in turn resulted in intestinal copper accumulation. The gill exhibited more rapid accumulation of copper than the intestine and contributed to early copper uptake leading to accumulation in internal organs. Muscle, spleen and plasma exhibited little if any disturbance of copper homeostasis while renal copper accumulation was evident at both ambient copper concentrations. The liver exhibited the highest copper concentrations and the greatest copper accumulation of all examined internal organs during exposure to 55.2 microM. Elevated biliary copper excretion was evident from measurements of gall bladder bile copper concentrations and appeared to protect partially against internal accumulation in fish exposed to 12.8 microM copper. No inhibition of Na+/K+ -ATPase activity in either gills or intestine was seen despite copper accumulation in these organs. Calculations of inorganic copper speciation suggest that Cu(CO3)(2)2- complexes which dominate in seawater and intestinal fluids are of limited availability for uptake while the low levels of ionic Cu2+, CuOH+ and CuCO3 may be the forms taken up by the gill and the intestinal epithelium.

Analysis of Variance↗
PubMed2004

A protective effect of dietary calcium against acute waterborne cadmium uptake in rainbow trout.

The present study examined the interactions between elevated dietary calcium (as ionic Ca2+ in the form of CaCl2 x 2H2O) and acute waterborne Cd exposure (50 microg/l as CdNO3 for 3 h) on whole body uptake and internal distribution of newly accumulated Cd, Ca2+, and Na+ in juvenile rainbow trout (Oncorhynchus mykiss). Fish were fed with three diets 20 (control), 30 and 60 mg Ca2+/g food: for 7 days before fluxes were measured with radiotracers over a 3h period. The two elevated Ca2+ diets reduced the whole body uptake of both Ca2+ and Cd by >50% and similarly reduced the internalization of both newly accumulated metals in most tissues, effects which reflect the shared branchial uptake route for Ca2+ and Cd. As the Ca2+ concentrations of the fluid phases of the stomach and intestinal contents were greatly elevated by the experimental diets, increased gastrointestinal Ca2+ uptake likely caused the down-regulation of the branchial Ca2+ (and Cd) uptake pathway. Waterborne Na+ uptake and internal distribution were not affected. While plasma Ca2+ surged after the first two feedings of the 60 mg Ca2+/g diet, internal homeostasis was quickly restored. Total Ca2+, Na+, and Cl- levels in tissues were not affected by diets. While dietary Ca2+ protected against waterborne Cd uptake, it did not protect against the relative inhibition of waterborne Ca2+ uptake caused by waterborne Cd. Acute exposure to 50 microg/l Cd reduced the uptake and internalization of newly accumulated Ca2+ (but not Na+) by 70% or more, regardless of diet. Since elevated dietary Ca2+ reduces waterborne Cd uptake, fish eating a Ca(2+)-rich invertebrate diet may be more protected against waterborne Cd toxicity in a field situation.

Analysis of Variance↗
PubMed2004

Kinetic analyses of waterborne Ca and Cd transport and their interactions in the gills of rainbow trout (Oncorhynchus mykiss) and yellow perch (Perca flavescens), two species differing greatly in acute waterborne Cd sensitivity.

We evaluated the differential nature of interactions between waterborne Ca and Cd transport in the gills of yellow perch (Perca flavescens) and rainbow trout (Oncorhynchus mykiss), two species with a more than 400-fold difference in acute waterborne Cd tolerance. The Jmax (maximum rate of uptake) and K(m) (inverse of affinity) for Ca uptake, in the absence of Cd, were significantly lower in yellow perch (120.48 nM g(-1) wet wt h(-1) and 92.17 microM, respectively) relative to rainbow trout (188.68 nM g(-1) wet wt h(-1) and 243.90 microM, respectively). Similarly, the Jmax for Cd uptake, at the lowest waterborne Ca level (100 microM) tested, was significantly lower in yellow perch (0.27 nM g(-1) wet wt h(-1)) relative to rainbow trout (0.40 nM g(-1) wet wt h(-1), but no significant difference was observed in the K(m) values between the two species (yellow perch: 32.47 nM; rainbow trout: 31.27 nM). Waterborne Cd (0-890 nM) as well as waterborne Ca (100-1,000 microM) competitively inhibited branchial uptake of each other in both species. However, analyses of inhibitor constants for branchial Ca uptake by waterborne Cd (Ki[Cd2+]) revealed that the inhibition was about 1.8 times more potent in rainbow trout compared to yellow perch. In contrast, analyses of inhibitor constants for branchial Cd uptake by waterborne Ca (Ki[Cd2+]) indicated that the inhibition was more than three fold more potent in yellow perch than in rainbow trout. Higher branchial Ca uptake and more potent inhibition by Cd as well as higher branchial Cd uptake and less potent inhibition by Ca were also reflected in whole-body measurements of Ca and Cd influx in trout relative to perch. Overall, whole-body effects were in accord with the branchial kinetic analyses. These results further strengthen the conclusion that branchial influxes of Ca and Cd occur through common pathways. Moreover, interspecific differences in acute waterborne Cd sensitivity can be explained, at least in part, by the differential nature of interactions between waterborne Ca and Cd transport in fish gills.

Analysis of Variance↗
PubMed2004

Acute waterborne cadmium uptake in rainbow trout is reduced by dietary calcium carbonate.

The effects of elevated dietary calcium (as CaCO3) and acute waterborne Cd exposure (50 microg/l) on whole body uptake, tissue uptake, and internal distribution of newly accumulated Cd, Ca2+, and Na+ in juvenile rainbow trout were examined. Fish were fed with three diets (mg Ca2+/g food): 20 (control), 30 and 60 for 7 days before fluxes were measured with radiotracers. The highest dietary Ca2+ elevation reduced waterborne whole body Ca2+ uptake, but did not protect against inhibition of waterborne Ca2+ uptake by waterborne Cd. Both Ca2+-supplemented diets reduced newly accumulated Ca2+ in the gills in relation to the control treatment, but did not prevent the Cd-inhibiting effect against accumulation of new Ca2+ in most compartments. Fish fed with Ca2+-supplemented diets showed markedly lower rates of whole body uptake and internalization (in some tissues) of waterborne Cd, illustrating that, while dietary Ca2+ supplementation did not protect against the impact of waterborne Cd on waterborne Ca2+ uptake, it did protect against the uptake of Cd. Waterborne Cd had no effect on Na+ fluxes, total Cl-, and in most body compartments, newly accumulated Na+ and total Na+ were also not affected. Dietary supplementation with CaCO3 had the same protective effect as demonstrated by dietary supplementation with CaCl2 in an earlier study. Thus, the reduction of waterborne Cd uptake and internalization by dietary Ca2+ was specifically due to Ca2+ and not to the anion.

Animals↗
PubMed2004

Physiological effects of dietary cadmium acclimation and waterborne cadmium challenge in rainbow trout: respiratory, ionoregulatory, and stress parameters.

A suite of respiratory, acid-base, ionoregulatory, hematological, and stress parameters were examined in adult rainbow trout (Oncorhynchus mykiss) after chronic exposure to a sublethal level of dietary Cd (500 mg/kg diet) for 45 days and during a subsequent challenge to waterborne Cd (10 microg/L) for 72 h. Blood sampling via an indwelling arterial catheter revealed that dietary Cd had no major effects on blood gases, acid-base balance, and plasma ions (Ca(2+), Mg(2+), K(+), Na(+), and Cl(-)) in trout. The most notable effects were an increase in hematocrit (49%) and hemoglobin (74%), and a decrease in the plasma total ammonia (43%) and glucose (49%) of the dietary Cd-exposed fish relative to the nonexposed controls. Dietary Cd resulted in a 26-fold increase of plasma Cd level over 45 days (approximately 24 ng/mL). The fish exposed to dietary Cd showed acclimation with increased protection against the effects of waterborne Cd on arterial blood P(aCO2) and pH, plasma ions, and stress indices. After waterborne Cd challenge, nonacclimated fish, but not Cd-acclimated fish, exhibited respiratory acidosis. Plasma Ca(2+) levels declined from the prechallenge level, but the effect was more pronounced in nonacclimated fish (44%) than in Cd-acclimated fish (14%) by 72 h. Plasma K(+) was elevated only in the nonacclimated fish. Similarly, waterborne Cd caused an elevation of all four traditional stress parameters (plasma total ammonia, cortisol, glucose, and lactate) only in the nonacclimated fish. Thus, chronic exposure to dietary Cd protects rainbow trout against physiological stress caused by waterborne Cd and both dietary and waterborne Cd should be considered in determining the extent of Cd toxicity to fish.

Acclimatization↗