Xanthate effects on cadmium intracellular distribution in rainbow trout (Oncorhynchus mykiss) gills

The uptake of ¹⁰⁹cadmium through perfused rainbow trout gills in the presence of xanthates was studied, and the subcellular distribution of cadmium in perfused gill tissue was determined. Pnenol absorption was also studied because xanthates form hydrophobic Cd complexes with a log P_{octanol/water} similar to that of phenol.

1. Xanthate concentrations higher than 10⁻⁵ M increased the rate of cadmium transfer through the gills and cadmium retention in gill tissue. Cadmium was present as a hydrophobic complex at this and higher xanthate concentrations.

2. A redistribution of cadmium from metallothionein to high molecular weight cadmium binding fractions occurred in the presence of 10⁻⁴ M xanthate.

3. The rate of phenol transfer across the gill epithelium was much higher than the rate of cadmium transfer regardless of whether xanthate was present. The rate of phenol transfer stabilized much faster than the rate of cadmium transfer irrespective of whether xanthate was present, indicating that different uptake mechanisms were involved.

We conclude that in the presence of xanthate concentrations higher than 10⁻⁵ M cadmium is taken up as a hydrophobic Cd(xanthate)₂ complex by the epithelial cells. Within the cell the complex dissociates, and the metal ion is bound to intracellular cadmium-binding ligands. The metal is probably translocated through the basolateral membrane as a free ion.     

In vivo and in vitro cadmium accumulation during the moult cycle of the male shore crab Carcinus maenas--interaction with calcium metabolism

The effect of moult stage on cadmium accumulation and distribution was investigated in vivo in male shore crabs Carcinus maenas exposed to 1 mg Cd l(-1) for 7 days. The accumulation of cadmium in all tissues examined was markedly higher in postmoult (A(1-2) and B(1-2)) compared to intermoult (C1, C3 and C4) and premoult (D(0-3)). In addition, elevated levels of cadmium were found in gills of late premoult (D(2-3)) animals. The total amount of cadmium accumulated in the tissues (haemolymph, gills, midgut gland and muscle) increased from 43 microg Cd in early premoult (D(0-1)) to 391 microg Cd in late postmoult (B(1-2)). Gills and midgut gland were the primary cadmium accumulating tissues in C4-intermoult and premoult (D(0-3)); in early postmoult (A(1-2)) haemolymph and midgut gland were the main cadmium containing tissues, while midgut gland dominated in late postmoult (B(1-2)) and early intermoult (C1 and C3). A detailed account of calcium distribution in haemolymph, gills, midgut gland, muscle and exoskeleton during the moult cycle is presented. Mechanistic links between cadmium and calcium uptake in posterior gills of C4-intermoult and early postmoult (A(1-2)) crabs were explored using an in vitro gill perfusion technique. Calcium and cadmium influxes were markedly higher in postmoult compared to intermoult. No differences between intermoult and postmoult effluxes were found for either calcium or cadmium. From intermoult to postmoult net influx increased from 2.4 to 29 micromol Ca2+ g(-1) ww(gill) h(-1) and from 0.24 to 25 nmol Cd2+ g(-1) ww(gill) h(-1). The results indicate that the postmoult increase in cadmium influx is due to increased active transport of cadmium, at least partly, by accidental uptake via calcium transporting proteins. The in vitro net influx rates corresponded accurately to the observed in vivo accumulation of both cadmium and calcium. Although cadmium accumulation and distribution are clearly linked to changes in calcium requirements, cadmium did not interfere with calcium accumulation or distribution at any stage during the moult cycle.     

Cadmium and zinc kinetics in fish: studies on water-borne 109Cd and 65Zn turnover and intracellular distribution in minnows, Phoxinus phoxinus

This study investigates the short- and long-term turnover of zinc and cadmium in fish. Juvenile minnows, Phoxinus phoxinus, were exposed to water-borne 109Cd and 65Zn for 24 hr. Tracer uptake, redistribution, elimination, and intracellular tracer distribution were studied for 60 days in tracer-free water. The influx of 65Zn from the water to the internal organs was more rapid than the influx of 109Cd, and the 65Zn turnover in the liver and kidney was considerably faster than the turnover of 109Cd. Moreover, in the gills and kidney, intracellular 65Zn was more mobile between intracellular compartments than 109Cd. The liver and kidney accumulated the major part of the 109Cd originating from the gills, whereas the head and skin, and muscle and bone-fractions retained the majority of the 65Zn. This indicates that the metals have different pathways in the fish body, after entering the body from the water. The cadmium levels in the gills, liver and kidney increased drastically because of the cadmium exposure, but the zinc levels in the organs were not markedly affected by a fifteen-fold increase in external zinc concentration, indicating a homeostatic control of zinc in the minnow.     

Association between cadmium and calcium uptake and distribution during the moult cycle of female shore crabs, Carcinus maenas: an in vivo study

Net influxes into the haemolymph and tissue distribution of 45Ca and 109Cd were studied in vivo in female Carcinus maenas at different moult stages. Net influxes of 45Ca and 109Cd from water were higher in postmoult (A and B) C. maenas than in C3- and C4-intermoult crabs and the net influx of calcium was higher in C3-intermoult crabs than in C4-intermoult crabs. The net influxes of 45Ca and 109Cd increased in postmoult C. maenas with decreasing external calcium concentrations at constant salinity. At all external calcium concentrations a significant correlation existed between 45Ca and 109Cd accumulated in the haemolymph of individual animals. In vivo exposure of postmoult C. maenas to external lanthanum decreased the 45Ca and 109Cd uptake rates to 30 and 10%, respectively, of the control values. About 30% of injected 109Cd were found in the midgut gland, 10-20% in the gills and only a few (1-2) percent was lost to the seawater 24 h after injection. No major variations in tissue distribution of 109Cd were observed between moult stages in these tissues. Premoult crabs retained more cadmium in the haemolymph 24 h after injection than other moult stages, and postmoult crabs retained more in muscle. Between 20 and 40% of the injected 45Ca were excreted to the water, while only a few percent of the injected 45Ca were found in the soft tissues 24 h after injection. Large moult stage variations, however, were observed in the tissue distribution of internalised 45Ca. This study demonstrates that cadmium and calcium uptakes are elevated in postmoult C. maenas. The results indicate that cadmium and calcium in this stage are taken up via Ca2+-channels located in the apical membrane of gill epithelium cells. When internalised, however, cadmium and calcium are metabolised in fundamentally different ways, determined by the chemical properties and biological significance of the two metals.     

Morphological and biochemical changes in the gills of Tilapia (Oreochromis mossambicus) to ambient cadmium exposure

Tilapia, Oreochromis mossambicus, were reared in freshwater and exposed to 40, 80 and 160 ppb ambient cadmium for a period of 7 days to investigate the effects of short-term Cd exposure on the cellular function of gill chloride cells. Gills were sampled after 3 and 7 days exposure. The accumulated Cd concentration in gills was analyzed using a graphite furnace atomic absorption spectrophotometer while the morphological changes of pavement and chloride cells were examined using scanning and transmission electron microscopes. Gill Cd concentration was significantly increased in samples (10.03-44.36 ppb) at 3 and 7 days exposure. Accompanying this was an augmentation of microridge in pavement cells, and an increase in the density (1964-3603 /mm(2)) and apical membrane area (11.57-46.32 μm(2)) in chloride cells, indicating an adaptational modification of the cell morphology in assisting gaseous transfer and Ca(2+) uptake, respectively. However, biochemical analyses of the gill tissues enumerated a decrease in both the activities of alkaline and high-affinity Ca(2+)-ATPases. This indicated a reduction in the Ca(2+)-transport capacity per unit chloride cell, suggesting chloride cells being the primary target of Cd which subsequently lead to fish hypocalcemia.     

Effects of long term sublethal Cd exposure in rainbow trout during soft water exposure: implications for biotic ligand modelling

The objectives of the study were to determine the physiological and toxicological effects of chronic cadmium exposure on juvenile rainbow trout in soft water. Particular attention focused on acclimation, on comparison to an earlier hard water study, and on whether a gill surface binding model, originally developed in dilute soft water, could be applied in this water quality to fish chronically exposed to Cd. Juvenile rainbow trout, on 3% of body weight daily ration, were exposed to 0 (control), 0.07, and 0.11 microg l(-1) Cd [as Cd(NO(3))(2).4H(2)O] in synthetic soft water (hardness=20 mg l(-1) as CaCO(3), alkalinity=15 mg l(-1) as CaCO(3), pH 7.2) for 30 days. Mortality was minimal for all treatments (up to 14% for 0.11 microg l(-1) Cd). No significant effects of chronic Cd exposure were seen in growth rate, swimming performance (stamina), routine O(2) consumption, or whole body/plasma ion levels. In contrast to the hard water study, no acclimation occurred in either exposure group in soft water, with no significant increases in 96-h LC(50) values. Cadmium accumulated in a time-dependent fashion to twice the control levels in the gills and only marginally in the liver by 30 days. No significant Cd accumulation occurred in the gall bladder or whole body. Cadmium uptake/turnover tests were run using radioactive 109Cd for acute (3 h) exposures. Saturation of the gills occurred for control fish but not for Cd-exposed fish when exposed to up to 36 microg l(-1) Cd for 3 h. Cd-exposed trout accumulated less 'new' Cd in their gills compared to controls and they internalized less 109Cd than control fish. This effect of lowered Cd uptake by the gills of acclimated trout was earlier seen for the fish acclimated to 10 microg l(-1) Cd in hard water. The affinity of the gill for Cd was greater in hard water (logK(Cd-gill)=7.6) than in soft water (logK(Cd-gill)=7.3) but the number of binding sites (B(max)=0.20 microg g(-1) gill) was similar in both media. In addition, there was a shift in affinity of the gill for Cd (i.e. lowered logK(Cd-gill)) and increased B(max) with chronic Cd exposure in both soft water and hard water. We conclude that the present gill modelling approach (i.e. acute gill surface binding model or Biotic Ligand Model) does work for soft and hard water exposures but there are complications when applying the model to fish chronically exposed to cadmium.     

Exocytotic secretion of catecholamines from the cat adrenal medulla by sodium deprivation: involvement of calcium influx mechanism

1 Cat adrenal glands were perfused with Ca-deficient medium and secretion of catecholamines (CA) was induced by perfusion with Na-free medium in which NaCl was replaced by an osmotically equivalent amount of sucrose. 2 Release of CA and dopamine-beta-hydroxylase (DBH), but not that of phenylethanolamine-N-methyltransferase, was concomitantly found in the effluents when the adrenals were stimulated, indicating that secretion was due to exocytosis. 3 Secretion of CA induced by Na-free (sucrose) medium was dependent on the concentration of Ca and was saturated at 0.5 mM of Ca. 4 Sr or Ba substituted for Ca in maintaining secretion by Na-free (sucrose) medium. 5 The addition of Na, Li or alkali metal ions to Na-free (sucrose) medium containing Ca reduced the response to a variable extent but this inhibition was reversed by raising the concentration of Ca in the Na-free medium. 6 All of the Na substitutes used induced secretion only when this medium contained Ca. However, different Na substitutes released different amounts of CA; sucrose was most effective, K, Tris and choline were moderately and Li least effective. 7 Secretion of CA by Na-free (sucrose) medium was strongly inhibited by D-600, tetracaine or divalent cations such as Co, Ni, Zn and Mg. The inhibition by Co was partially reversed by raising the concentration of Ca in the Na-free medium. 8 Secretion of CA from bovine isolated chromaffin cells was induced by Na-deficient (sucrose) medium and was dependent on the concentrations of ionized Ca involved. 9 All the Na substitutes tested increased secretion of CA and 45Ca uptake, in a parallel fashion. 10 A correlation between secretion and 45Ca uptake was found under various experimental manipulations which reduced secretion of CA. 11 These results demonstrated that unlike the perfused bovine adrenals, the Ca influx mechanism is essential for secretion by Na deprivation in the perfused cat adrenals as it is in bovine isolated chromaffin cells. 12 It is suggested that Na deprivation increases Ca entry through the Ca channels by eliminating the competition between Na and Ca, and possibly by activating Ca influx linked with Na efflux.     

Cadmium tolerance in the Nile tilapia (Oreochromis niloticus) following acute exposure: assessment of some ionoregulatory parameters

The Nile tilapia (Oreochromis niloticus) can tolerate very high levels of waterborne cadmium. It has one of the highest 96 h LC50 recorded for a freshwater teleost fish (14.8 mg/L Cd; hardness 50 mg/L CaCO(3)). Cadmium is known to perturb ion balance in teleost fishes. However, in an acute time course experiment, plasma Na(+) concentrations were unaffected, and plasma Ca(2+) values only decreased after 96 h exposure in a dose-independent manner. Branchial Na(+)/K(+)-ATPase activity and alpha-subunit protein level expression in crude gill homogenates were not affected by Cd exposure during this period. Branchial chloride cell numbers, identified as Na(+)/K(+)-ATPase immunoreactive cells using immunohistochemistry, decreased 24 h after exposure but recovered thereafter. Histopathological changes did not follow a consistent pattern of variation with exposure time, and the alterations noted in gill epithelium were basically nonspecific to cadmium. Because of its tolerance, it can be concluded that the tilapia O. niloticus would not be a suitable test organism to evaluate sublethal toxicity of cadmium and the realistic impact of this pollutant in the environment. However, it certainly could contribute significantly to our understanding of the toxic mechanism of cadmium exposure in aquatic organisms. This is the first work to investigate the effect of waterborne pollutants on Na(+)/K(+)-ATPase alpha-subunit protein expression in fish gills.     

Dynamics of (Cd,Zn)-metallothioneins in gills, liver and kidney of common carp Cyprinus carpio during cadmium exposure

Cadmium concentrations, (Cd,Zn)-metallothionein (MT) concentrations, MT synthesis and the relative amounts of cadmium bound to (Cd,Zn)-MTs were determined in gills, liver and kidney of common carp Cyprinus carpio exposed to 0, 0.5 microM (0.06 mg.l(-1)), 2.5 microM (0.28 mg.l(-1)) and 7 microM (0.79 mg.l(-1)) Cd for up to 29 days. Cadmium accumulation was in the order kidney > liver > gills. Control levels of hepatic (Cd,Zn)-MT were four times higher compared to those of gills and kidney. No increases in (Cd,Zn)-MT concentrations were observed in liver during the exposure period. In comparison with control carp, (Cd,Zn)-MT concentrations increased up to 4.5 times in kidney and two times in gills. In both these organs, (Cd,Zn)-MT concentrations were linearly related with cadmium tissue levels and with the de novo synthesis of MTs. Hepatic cadmium was almost completely bound to (Cd,Zn)-MT, while percentages of non-MT-bound cadmium were at least 40% in gills and 25% in kidney. This corresponded with a total saturation of (Cd,Zn)-MT by cadmium in kidney and a saturation of approximately 50 and 60% in gills and liver, respectively. The final order of non-MT-bound cadmium was kidney > gills > liver. Our results indicate that cadmium exposure causes toxic effects, which cannot be correlated with the accumulated levels of the metal in tissues. Although cadmium clearly leads to the de novo synthesis of MT and higher (Cd,Zn)-MT concentrations, the role of this protein in the detoxification process is clearly organ-specific and its synthesis does not keep track with cadmium accumulation.     

The effects of K+-depolarization medium, chelating agents and thiol groups on cadmium uptake and efflux in the guinea-pig taenia coli

Cadmium uptake by taenia coli was dose-dependent, achieving equilibrium after approximately 60 min of incubation. The SH-blocker, N-ethylmaleimide inhibited cadmium uptake. When muscles were washed with normal medium or that containing 0.5 mM EDTA following 0.5 mM Cd2+ treatment for 60 min, the tissue cadmium concentration reached equilibrium levels after 60 min and approximately 43 or 27% of the initial tissue cadmium concentration was retained, respectively. Both glutathione and dithiothreitol also increased cadmium efflux. However the contractions of glycerinated taenia coli caused by Ca2+ and Mg-ATP, completely returned to control values after washing with 0.5 mM EDTA medium following 0.5 mM Cd2+ treatment for 60 min, suggesting that EDTA seems to exert intracellular effects in glycerinated taenia coli. These results suggest that SH-dependent mechanisms in cadmium uptake play a role in intact taenia coli. In addition, in intact taenia coli, Cd2+ are accumulated in intracellular compartments which EDTA cannot reach and may exert an inhibitory action on internal sites in the cells.     

Tissue-specific accumulation of cadmium in subcellular compartments of eastern oysters Crassostrea virginica Gmelin (Bivalvia: Ostreidae)

Cadmium distribution was studied in different subcellular fractions of gill and hepatopancreas tissues of eastern oysters Crassostrea virginica. Oysters were exposed for up to 21 days to low sublethal Cd concentrations (25 microg L(-1)). Gill and hepatopancreas tissues were sampled and divided into organelle fractions and cytosol by differential centrifugation. Organelle content of different fractions was verified by activities of marker enzymes, citrate synthase and acid phosphatase for mitochondria and lysosomes, respectively. In both tissue types, there was a significant accumulation of cadmium in cytosol reaching 230-350 ng mg(-1) protein. Among organelles, mitochondria were the main target for Cd bioaccumulation in gills (250-300 ng mg(-1) protein), whereas in hepatopancreas tissues, the highest cadmium accumulation occurred in lysosomes (90-94 ng mg(-1) protein). Although 75-83% of total cadmium burden was associated with the cytosol reflecting high volume fraction of this compartment, Cd concentrations in organelle fractions reached levels that could cause dysfunction of mitochondria and lysosomes. Organ- and organelle-specific patterns of cadmium bioaccumulation support our previous in vivo studies, which showed adverse effects of cadmium exposures on mitochondrial oxidation in gills and on the lysosomal system of hepatopancreas. This may have important implications for the development of biomarkers of effect for heavy metals and for understanding the mechanisms of toxic effects of metals.     

Estimation of increased concentration of intracellular Cd(2+) by fluo-3 in rat thymocytes exposed to CdCl(2)

Cadmium, an environmental pollutant, has been reported to induce apoptosis in murine lymphocytes. To reveal the mechanism of cadmium-induced apoptosis, one of important questions is whether cadmium increases intracellular concentration of Ca(2+) ([Ca(2+)](i)), Cd(2+) ([Cd(2+)](i)) or both. It is difficult to detect the increase in [Ca(2+)](i) using Ca(2+)-chelator-based fluorescent Ca(2+) indicators in the presence of Cd(2+) because of their sensitivity to Cd(2+). Therefore, the study on membrane response such as Ca(2+)-dependent hyperpolarization gives a clue to reveal whether the [Ca(2+)](i) or [Cd(2+)](i) is increased. Cadmium at concentrations of 3 μM or more dose-dependently augmented fluo-3 fluorescence in rat thymocytes, presumably suggesting an increased [Ca(2+)](i). However, the membranes were not hyperpolarized although the cells possess Ca(2+)-dependent K(+) channels. One may argue that cadmium inhibits Ca(2+)-dependent K(+) channels so that cadmium fails to hyperpolarize the membranes. It is unlikely because the [Ca(2+)](i) increased by A23187, a calcium ionophore, elicited the hyperpolarization in the presence of Cd(2+). Furthermore, the profile of cytotoxicity induced by cadmium, examined by ethidium bromide and annexin V-FITC, was different from that induced by A23187. Taken together, it is concluded that the application of cadmium increases the [Cd(2+)](i) rather than the [Ca(2+)](i) in rat thymocytes, resulting in the induction of cytotoxicity.     

Effect of selenium on the uptake of methyl mercury across perfused gills of rainbow trout Oncorhynchus mykiss

The uptake of methyl mercury was measured across the perfused gills of rainbow trout Oncorhynchus mykiss. The effect of selenium, either in the blood (perfusion medium), or in the water was investigated. Methyl mercury was effectively taken up from the water across the gills into the perfusate. The uptake rate reached a stable level after 30 min perfusion. When the gills were placed in mercury free water after exposure to mercury in the water for 1 h, they continued to liberate significant amounts of accumulated mercury into the perfusate. Exposure to selenite (SeIV) or selenate (VI) (0.075–0.75 μM) in the external medium did not affect the uptake of methyl mercury across the gills or the liberation of the metal from the gills. Internal selenite or selenate (7.5 μM) augmented the uptake of methyl mercury across the gills and internal selenite also increased the amounts of liberated methyl mercury from the gills in the unload period. Internal selenium, increased the mercury accumulation in the gills, whereas, external selenium did not alter the mercury accumulation in the gills. Uptake of selenium from the water across the gills occurred very slowly.     

Cadmium, zinc and the uptake of calcium by two crabs, Carcinus maenas and Eriocheir sinensis

The uptake of dissolved cadmium and zinc by crustaceans can usually be explained by the passive process of facilitated diffusion involving a transport protein in the membranes of permeable surfaces. Cadmium ions will also enter via uptake routes for calcium, given the similar size of the two free ions. This study has investigated the interaction of cadmium (and comparatively zinc) and calcium uptake in two crabs that show different permeability responses to changes in salinity, with consequently different effects on the uptake of cadmium and zinc with salinity change. Ca uptake rates in Carcinus maenas decreased in reduced salinity (33-15) with the decreased Ca concentration of the medium and increased if the Ca concentration was increased at salinity 20. It is concluded that Ca uptake over the salinity range 33-15 is via apical Ca channels in gill ionocytes, passively down an electrochemical gradient. The Ca uptake rate of Eriocheir sinensis showed no significant decrease over the salinity range 33-10 (probably because of the small differences in an already low Ca uptake rate in this crab against a background of inter-individual variability), but decreased significantly at salinity 5. Added calcium increased the Ca uptake rate of E. sinensis at salinities 15 and 5, supporting the interpretation that Ca uptake in gills is typically passive via apical Ca channels. Cadmium (but not zinc) inhibited calcium uptake in both crabs at 15 salinity, indicating sharing of Ca channels by Cd, but not at salinity 5 (E. sinensis only) when Ca may be taken up into gill ionocytes by another (active?) physiological process.     

Ultrastructural changes in various organs of the fish Puntius gonionotus fed cadmium-enriched cyanobacteria

The accumulation and toxicity of cadmium in Puntius gonionotus fish that consumed the cyanobacterium Spirulina platensis contaminated with cadmium were studied. Fish were fed cadmium-contaminated cells for 4 weeks, after which cadmium accumulation in various organs was determined. The highest cadmium content was found in the kidney (56.0 microg Cd/g wet weight). Cadmium was not detected in the gill during the entire 4 weeks of cadmium feeding. Histopathological alteration of cells was observed in the gill, kidney, and liver. The results showed that dietary cadmium caused hypertrophy and edema of gill filaments. Coagulative necrosis and karyolysis of the nucleus were observed in the kidney. Vacuoles and hyaline droplets had accumulated in the epithelial cells of the proximal tubule. In the liver vacuolation of the cytoplasm, infiltration of macrophages, and focal necrosis were found. The ultrastructural changes that occurred in the cells of different organs were similar. These included a proliferation of vacuoles and lysosomes, formation of myelin bodies, degranulation, vesiculation, and dilation of rough endoplasmic reticulum, as well as swelling of mitochondria with loss of cristae.     

Effect of Excess Zinc on Cadmium Disappearance From Rat Plasma Following Intravenous Injection

Effect of Excess Zinc on Cadmium Disappearance From Rat PlasmaFollowing Intravenous Injection. Frazier, John M.(19Sl).Fundam.Appl.Toxicol. 1:452–456. Studies of the interaction of zincand cadmium in the isolated perfused rat liver indicate thatexcess zinc in the perfusion medium inhibits cadmium uptakeby the liver. In order to verify these observations in vivo,the effect of excess zinc on cadmium clearance from plasma inthe intact rat was investigated at two cadmium dose levels,0.15 and 0.30 mg Cd/kg of body weight. Cadmium disappearancefrom plasma was inhibited by excess zinc in a dose related mannerat both cadmium dose levels. Greatest inhibition (55%) of cadmiumclearance was attained at a Zn:Cd molar ratio of 17, the highestratio investigated. Excess zinc in plasma (concentrations inplasma greater than 200 µmole/L) resulted in an increasein the volume of distribution of cadmium. A suggested explanationfor this effect was displacement of albumin bound cadmium byexcess zinc.     

Toxicity and accumulation of cadmium with respect to algae and cyanobacteria: A review

Cadmium is always found in association with zinc. However, zinc is an essential micronutrient in living cells, whereas cadmium has no known useful biological function. In fact, cadmium is ranked among the most hazardous trace elements in the environment and is highly toxic to all components of aquatic communities. Cadmium in soils seems tightly held and is not readily removed by leaching, and consequently, cadmium in freshwaters is mostly connected with human activities. The concentration of Cd in natural waters is usually less than 1 μg. L^?1 but the values vary greatly among localities; the highest concentrations of cadmium have been observed in areas with acid mine drainage. The important mechanism of toxic action of Cd on algae and cyanobacteria is thought to be the ?poisoning”? of enzymes, but many other toxic actions are known. A variety of environmental factors are known to modify the toxicity of cadmium. It is very difficult to allow for all of these factors simultaneously to predict the effect that a given amount of a metal will have on a given algal population. Uptake of Cd and other heavy metals to produce an internal concentration than in the external environment appears widespread in algae and cyanobacteria.     

Increased availability of cadmium to perfused rainbow trout (Salmo gairdneri,Rich.) gills in the presence of the complexing agents diethyl dithiocarbamate,ethyl xanthate and isopropyl xanthate

A study was made of the cadmium transfer through and retention of metal in perfused gill tissue from rainbow trout (Salmo gairdneri) in the presence of three cadmium complexing agents; DDC (diethyl dithiocarbamate), ethyl xanthate and isopropyl xanthate. The complexes formed are non-polar.The transfer of complexed cadmium was greater than the transfer of free cadmium ion.The retention of cadmium in gill tissue was increased about ten times in the presence of each of the two xanthates. However, the retention in gill tissue was not altered by DDC.It is concluded that cadmium uptake in fish gills in the presence of complexing agents is not simply a function of complexed versus free metal. It is also heavily dependent on the type of complexing agent present.     

Influence of Certain Chelating Agents on Egress of Cadmium from Cultured Epithelial Cells Containing High Amounts of Metallothionein: A Screening of Cd-Releasing and Toxic Effects

Abstract: Cell cultures have been used to study the effect of 6 different metal chelating compounds on the efflux of Cadmium (Cd) from the cells and on cell growth. The cells had previously been made resistant to high levels of Cd (100 μmol/1) in the medium. They contain large amounts of intracellular Cd (40–50 nmol Cd/mg cell protein), the main part of which is bound to cytoplasmic metallothionein. Among the different monothiol and dithiol compounds tested are some old, well-known and to some extent therapeutically tried substances, i.e. 2,3-dimercapto-1-propanol (BAL), D-penicillamine (PA), N-acetyl-DL-penicillamine (NAPA) and some newer metal chelators, i.e. 2,3-dimercaptopropane-1-sulphonate (BAL-Sulph), mercaptosuccinic acid (MSA) and meso-2,3-dimercaptosuccinic acid (DMSA). The three latter ones all showed better effect on the egress of Cd than PA and NAPA and less toxic effect than BAL on an equimolar basis. All the agents tested increased the efflux of Cd from metallothionein-containing cell cultures which seem to be justified as a test system for primary screening of effect and toxicity of new chelators.     

A putative lectin-binding receptor mediates cadmium-evoked calcium release.

Nanomolar concentrations of cadmium (Cd2+) produce an immediate rise in free Ca2+ in human dermal fibroblasts, which is mostly caused by the release of stored Ca2+ via inositol trisphosphate. Here we have used lectins to evaluate the hypothesis that a cell surface glycoprotein mediates the response to Cd2+. A prior incubation with wheat germ agglutinin (WGA) or certain other lectins inhibited calcium release evoked by Cd2+. WGA reversibly inhibited Cd(2+)-evoked calcium release as indicated by measurements of cytosolic free Ca2+ and 45Ca2+ efflux. WGA half-maximally inhibited Ca2+ release at 1.2 x 10(-7) M. The Kd for the binding of fluoresceinylated WGA was 2.8 x 10(-7) M. Chitotriose dissociated fluoresceinylated WGA from the cells and restored cadmium responsiveness. WGA inhibited Cd(2+)-evoked 45Ca2+ efflux similarly at 18 and 37 degrees C. A brief incubation with chitotriose at 18 or 10 degrees C reversed the inhibition by WGA. WGA neither bound 109Cd2+ nor affected 109Cd2+ uptake by the cells. Succinylated WGA, which binds N-acetylglucosamine but not N-acetylneuraminic acid, failed to inhibit Ca2+ release evoked by Cd2+. WGA probably inhibits Ca2+ release produced by Cd2+ by binding to N-acetylneuraminic acid in the external domain of a plasma membrane receptor.