Mechanisms Of Cd Toxicity Research Articles

Cadmium causes spleen toxicity in chickens by regulating mitochondrial unfolded protein response and nuclear receptors response

Cadmium (Cd) is a heavy metal that pollutes the environment and threatens human and animal health via the food chain. The spleen is one of the target organs affected by Cd toxicity. However, the mechanism of Cd toxicity is not fully understood. In this study, 80 chicks were allocated into 4 groups (n = 20) and exposed to different doses of CdCl2 (0 mg/kg, 35 mg/kg, 70 mg/kg and 140 mg/kg) for 90 d. The pathological changes in the spleen, mitochondrial dynamics-related factors, cytochrome P450 (CYP450) enzyme system contents, activities, transcription levels, nuclear receptors (NRs) response molecule levels, and mitochondrial unfolded protein-related factors were detected. The findings indicate that exposure to Cd significantly leads to spleen injury. In Cd groups, the total contents of CYP450 and cytochrome b5 (Cyt b5) increased, and the activities of the CYP450 enzyme system (APND, ERND, AH, and NCR) changed. The NRs response was induced, and the gene levels of AHR/CAR and corresponding CYP450 isoforms (CYP1B1, CYP1A5, CYP1A1, CYP2C18, CYP2D6 and CYP3A4) were found altered. The study found that Cd exposure altered the mRNA expression levels of mitochondrial dynamics-related factors, such as OPA1, Fis1, MFF, Mfn1, and Mfn2, breaking mitochondrial fusion and cleavage and ultimately leading to mitochondrial dysfunction. Changes were detected in the gene levels of several mitochondrial unfolded protein response (mtUPR)-related factors, namely (SIRT1, PGC-1α, NRF1, TFAM, SOD2, and HtrA2). Cd also altered the gene levels of mitochondrial function-related factors (VDAC1, Cyt-C, COA6, PRDX3, RAF and SIRT3). It is showed that Cd can initiate the NRs response, influence the homeostasis of the CPY450 enzyme system, trigger the mtUPR, impair mitochondrial function, and ultimately lead to Cd toxicity in the spleen of chickens.

Study of the Effect of Cadmium Chloride on Some Marker Liver Enzymes of Experimental Animals

Introduction. Cadmium (Cd) is one of the most powerful and dangerous pollutants. Cd exposure is associated with multiple organ damage in both animals and humans. The mechanism of Cd toxicity is the disruption of the body’s antioxidant system (AOS), which leads to transformation of the functional integrity of the liver. The extent of target organ damage can be examined by measuring concentrations of key indicators of hepatocellular injury. The purpose of the work is to evaluate changes in the activity of enzyme markers of hepatotoxicity in the blood serum of laboratory animals after oral exposure to an aqueous solution of cadmium chloride (CdCl2) under the conditions of a subchronic experimental model with a period of remission. Materials and methods. The study was conducted on 40 white outbred rats. Animals of three experimental groups were intragastrically administered a pollutant in various dosages for 3 months. The duration of the remission stage was 1 month. The activity of aspartate aminotransferase (AST), alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and alkaline phosphatase (ALP) was determined in the blood serum of animals. Results. When CdCl2 was administered to animals at a dose of 1 μg/kg, an increase in AST activity was observed by 45.9% relative to the control (p=0.006). An increase in the concentration of ALT and LDH is shown. A dose-dependent decrease in the level of alkaline phosphatase was revealed in three groups of animals by 24.7%, 37.5% and 55.4%, respectively (p=0.002). The noted trends indicate pathological processes occurring in hepatocytes. Conclusion. In the course of this study, it was found that under the conditions of a subchronic model of the experiment with a period of remission, cadmium, having a pronounced hepatoxic effect, induces liver damage in experimental animals.

Cadmium Exposure Affects Serum Metabolites and Proteins in the Male Guizhou Black Goat.

Food safety and environmental pollution are the hotspots of general concern globally. Notably, long-term accumulation of trace toxic heavy metals, such as cadmium (Cd), in animals may endanger human health via the food chain. The mechanism of Cd toxicity in the goat, a popular farmed animal, has not been extensively investigated to date. Therefore, in this study, ten male goats (Nubian black goat × native black goat) were exposed to Cd via drinking water containing CdCl2 (20 mg Cd·kg-1·BW) for 30 days (five male goats per group). In this study, we used an integrated approach combining proteomics and metabolomics to profile proteins and metabolites in the serum of Cd-exposed goats. It was found that Cd exposure impacted the levels of 30 serum metabolites and 108 proteins. The combined proteomic and metabolomic analysis revealed that Cd exposure affected arginine and proline metabolism, beta-alanine metabolism, and glutathione metabolism. Further, antioxidant capacity in the serum of goats exposed to Cd was reduced. We identified CKM and spermidine as potential protein and metabolic markers, respectively, of early Cd toxicity in the goat. This study details approaches for the early diagnosis and prevention of Cd-poisoned goats.

An Assessment of Metallothionein-Cadmium Binding in Rat Uterus after Subchronic Exposure Using a Long-Term Observation Model.

Cadmium (Cd) is an environmental pollutant known to pose a public health issue. The mechanism of Cd toxicity on the uterus, including the protective role of metallothionein (MT), is still not fully understood. The aim of the study was to evaluate the degree of MT-Cd binding in the uterus of rats exposed per os to Cd at daily doses of 0.09, 0.9, 1.8 and 4.5 mg Cd/kg b.w. for 90 days. To assess the permanence of the bond, the rats were observed over long observation periods: 90 and 180 days after termination of exposure. Additionally, uterine concentration of Zn, Cu, Ca, Mg was determined. Cd leads immediately after exposure to a max. 30-fold increase in the concentration of Cd in the uterus, with only small amounts being bound to MT. After 90 days following termination of exposure, and especially after 180 days, an increase in MT-Cd concentration was noted for the three highest doses; even so, the degree of Cd binding by MT was still small. Additionally, the accumulation of Cd in the uterus disturbs the homeostasis of determined essential elements, manifested by a significant increase in Cu concentration and a decrease in Zn, Mg and Ca, especially 180 days after termination of exposure. The obtained results indicate that MT has only a slight protective role in the uterus and that Cd ions may have harmful effects not related to MT: directly on the uterine tissue, and indirectly by disturbing the homeostasis of its essential elements.

Physiological and thylakoid proteome analyses of Anabaena sp. PCC 7120 for monitoring the photosynthetic responses under cadmium stress

Photosynthetic organisms are highly susceptible to cadmium (Cd) as it interferes with the structural and functional aspects of the photosynthesis. As a major group of photosynthetic prokaryotes, cyanobacteria are also affected by Cd. The inhibitory effects of Cd on cyanobacterial photosynthesis have been studied from an early stage, but the mechanism of Cd toxicity is still unclear. Therefore, we investigated the photosynthetic responses of Anabaena sp. PCC 7120 under Cd stress (LC50) at physiological and thylakoid proteome levels via chlorophyll a fluorescence measurements and blue native (BN)-SDS PAGE, respectively. The findings revealed that Cd exposure triggered the intracellular ROS production and negatively affected the photosynthetic performance. With Cd exposure, effective photochemical quantum yield of PSII (Y(II)) and photochemical quenching efficiency (qP and qL) were significantly reduced, whereas the non-regulated energy dissipation (Y(NO)) was increased. Fast fluorescence kinetic measurements showed that Cd exposure resulted in the inactivation of PSII reaction centres, which interfered with the transfer of energy from antenna complexes to reaction centre, decreased the ability to convert excitation energy into electron transport, increased thermal dissipation, and thus decreased linear electron flow efficiency. Conversely, the efficiency of electron transfer from intermediate carriers to final PSI acceptors was increased, which might be related to the induction of PSI-based cyclic electron flow. This assumption was confirmed by an enhanced post-illumination fluorescence transient. Consistent with these observations, BN-SDS PAGE showed that Cd exposure significantly decreased PSII subunit proteins accumulation, but slightly increased PSI proteins accumulation. Additionally, only minor reductions in the accumulation of ATP synthase/NDH-1 and Cytochrome b6f subunit proteins were observed. The transcript levels of most of the selected subunit proteins were in accordance with BN-SDS PAGE. Collectively, our experiments show that a shift to PSI-based cyclic electron flow was a protective strategy of Anabaena sp. PCC 7120 against Cd-induced PSII photo-damage.

Cadmium Toxicity on Chondrocytes and the Palliative Effects of 1α, 25-Dihydroxy Vitamin D3 in White Leghorns Chicken's Embryo.

Cadmium (Cd) can causes osteoporosis and joint swelling. However, the mechanism of Cd toxicity in chondrocytes and how to alleviate Cd poisoning to chondrocytes are still unclear. Herein, we evaluated the toxicity of Cd to chicken chondrocytes, and whether vitamin D can relieve the toxicity of Cd to chondrocytes. Primary chondrocytes were collected from knee-joint cartilage of 15-day-old chicken embryos. They were treated with (0, 1, 2, and 4) μM Cd alone, 10−8 M 1α,25-(OH)2D3 alone, or 2 μM Cd combined with 10−8 M 1α,25-(OH)2D3. We found that Cd significantly inhibited Sox9 and ACAN mRNA expression, which are markers for chondrocyte differentiation, downregulated the mitochondrial membrane potential, upregulated the Bax/B-cell lymphoma 2 ratio. Furthermore, Cd significantly promoted matrix metalloproteinase (MMP)-9 expression, thus accelerating the degradation of extracellular matrix. And Cd also inhibited the expression of main macromolecular protein of extracellular matrix, Collagen type IIα1 (COL2A1) and acid mucopolysaccharide. However, 1α,25-(OH)2D3 pretreatment significantly alleviated the toxicity effects of Cd on the differentiation, apoptosis and extracellular matrix gene expression in primary chondrocytes. Conclusively, Cd exposure could inhibited chicken embryo chondrocytes differentiation, extracellular matrix gene expression, and induced chondrocyte apoptosis. However, these toxic effects of Cd are alleviated by the pretreatment of chondrocytes with 1α,25-(OH)2D3.

Nephrotoxicity Profile of Cadmium Revealed by Proteomics in Mouse Kidney.

Cadmium (Cd) is a highly toxic metal and kidney is its main target. However, the molecular effects and associated potential impacts of Cd-accumulated kidney have not been well investigated. In this study, mouse was used as a model to investigate the Cd-induced proteomic profile change in kidney, and a total of 34 differentially expressed proteins were detected by two-dimensional gel electrophoresis (2-DE) and further identified by matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS). Through Gene Ontology analysis and KEGG pathway annotation, it showed that Cd-regulated kidney metabolism and promoted renal damage and cell migration. By validation of Western blotting and RT-qPCR, metastasis-related proteins LIM and SH3 domain protein 1 (LASP1) and phosphoenolpyruvate carboxykinase/cytosolic [GTP] (PEPCK1) were confirmed to be upregulated; Acyl-CoA synthetase medium-chain family member 3 (ACSM3) was downregulated. Furthermore, carcinoma development-related proteins initiation factor 4A (eIF4A) and pyridoxine-5'-phosphate oxidase (PNPO) were upregulated, and pyridoxal kinase (PK) was downregulated. The downregulation of Na(+)/H(+) exchange regulatory cofactor (NHERF3) might promote renal damage which associated with decrease of transferrin (TRF) in kidney. Taken together, our results revealed proteomic profile of Cd-induced nephrotoxicity and provided data for further insights into the mechanisms of Cd toxicity.

The Recovery of Soybean Plants after Short-Term Cadmium Stress.

Background: Cadmium is a non-essential heavy metal, which is toxic even in relatively low concentrations. Although the mechanisms of Cd toxicity are well documented, there is limited information concerning the recovery of plants after exposure to this metal. Methods: The present study describes the recovery of soybean plants treated for 48 h with Cd at two concentrations: 10 and 25 mg/L. In the frame of the study the growth, cell viability, level of membrane damage makers, mineral content, photosynthesis parameters, and global methylation level have been assessed directly after Cd treatment and/or after 7 days of growth in optimal conditions. Results: The results show that exposure to Cd leads to the development of toxicity symptoms such as growth inhibition, increased cell mortality, and membrane damage. After a recovery period of 7 days, the exposed plants showed no differences in relation to the control in all analyzed parameters, with an exception of a slight reduction in root length and changed content of potassium, magnesium, and manganese. Conclusions: The results indicate that soybean plants are able to efficiently recover even after relatively severe Cd stress. On the other hand, previous exposure to Cd stress modulated their mineral uptake.

NIX compensates lost role of parkin in cd-induced mitophagy in HeLa cells through phosphorylation

Our previous study demonstrated that cadmium (Cd) is an effective inducer of mitophagy, which is mainly mediated by PINK1/Parkin pathway. However, the role of other mitophagy pathways in Cd-induced mitophagy remains elusive. The present study employed HeLa cells, lacking fully functional Parkin, as a cell model to study Parkin-independent mitophagy pathway induced by Cd. Our results showed that BCL2/adenovirus E1B 19 kDa protein-interacting protein 3-like (Bnip3L/NIX), an outer mitochondrial membrane mitophagy receptor, could provide an alternate pathway for Cd-induced mitophagy in HeLa cells. Specifically, 10 μM Cd for 12 h induced mitophagy in GM00637 and HeLa cells which was assessed by mitochondrial fusion to lysosomes and decreased expression of mitochondrial markers such as COX-IV and HSP60. Notably, in GM00637 cells, Cd-induced mitophagy was predominantly mediated by PINK1/Parkin pathway as evinced by translocation of Parkin to mitochondria. Interestingly, in HeLa cells, significant increase in NIX expression was occurred and mitophagy was induced under Cd exposure, suggesting NIX compensates lost role of Parkin in Cd-induced mitophagy in HeLa cells. These results were verified by knocking down NIX using siRNA in HeLa cells, which lead to abolished mitophagy process. Moreover, NIX phosphorylation at serine-81 significantly increased in cells treated with Cd implying that phosphorylation of NIX plays an important role in NIX-mediated mitophagy. These findings reveal a novel mechanism of Cd toxicity and suggest a compensatory role of NIX in Cd-induced mitophagy.

High-throughput gene expression in soil invertebrate embryos – Mechanisms of Cd toxicity in Enchytraeus crypticus

Gene expression can vary with the organisms' life stage. It is known that embryos can be more sensitive to toxicant exposure, as previously demonstrated for Enchytraeus crypticus (Oligochaeta) exposed to cadmium (Cd), known to cause embryotoxicity and hatching delay. It was shown that Ca enters embryos via the L-type Ca channels in the cocoon membrane, this being affected in Cd exposed embryos (Cd-Ca competition is well-known). In the present study, the embryotoxic mechanisms of Cd were studied via high-throughput gene expression for E. crypticus. Cocoons (1–2 days old), instead of the adult organism, were exposed in Cd spiked LUFA 2.2 soil during 1 day. Results showed that Cd affected Ca homeostasis which is implicated in several other molecular processes. Several of the major modulators of Cd toxicity (e.g., impaired gene expression, cell cycle arrest, DNA and mitochondrial damage) were identified in the embryos showing its relevancy as a model in ecotoxicogenomics. The draft Adverse Outcome Pathway was improved. Previously was hypothesized that gene regulation mechanisms were activated to synthesize more Ca channel proteins – this was confirmed here. Further, novel evidences were that, besides the extracellular competition, Cd competes intracellularly which causes a reduction in Ca efflux, and potentiates Cd embryotoxicity.

Response of antioxidant enzymes to cadmium-induced cytotoxicity in rat cerebellar granule neurons

AbstractCadmium (Cd) accumulates in the brain and can damage neurons via complex processes involving oxidative stress induction. In this study we used a homogenous population of neurons which are cerebellar granule neurons (CGNs) to investigate damage induced by Cd and its effects on antioxidant enzyme activity. The exposure of CGNs to increasing concentrations of Cd (2.5 μM-100 μM) during 24 h, 48 h, or 72 h led to the induction of neuronal death in a dose- and exposure time-dependent manner. The necrotic and/or apoptotic pathway involved in the cell death trigged by Cd seems to depend on the concentration of Cd and the exposure time. In addition to its cell damage, Cd was shown to affect the activity of superoxide dismutase (SOD) and catalase (CAT) depending on the concentration of Cd and the exposure time. We also found that the exposure to Cd induces a bigger change in SOD activity than in CAT activity. Taken together, our findings explain, in part, the mechanism of Cd toxicity in a specific type of neuron which can provide information related to neurological pathologies ascribed to Cd toxicity.

Alteration of Heart Tissue Protein Profiles in Acute Cadmium-Treated Scallops Patinopecten yessoensis

Cadmium (Cd) is an extremely toxic metal that induces a wide spectrum of toxic responses in organisms in the environment. In the present study, scallops (Patinopecten yessoensis), after acclimation for 1 week in the laboratory, were subjected to acute Cd chloride (CdCl₂) toxicity, and ultramorphological and proteomic changes in their heart tissues were analyzed and compared with those of the nonexposed control group. Electron microscopy showed that ultrastructures of the cytoplasm and mitochondria in scallop hearts were badly damaged, and two-dimensional gel electrophoresis showed 32 protein spots that were differentially expressed after exposure to 10 mg/l CdCl₂ for 24 h. Of these spots, 8 were upregulated, 16 were downregulated, and 8 showed low expression. Proteins from these spots were identified using matrix-assisted laser desorption/ionization-time of flight mass spectrometry and database searching. The results indicated that these proteins are involved in the regulation of cell structure, transport, signal transduction, and metabolism. Among other things, four proteins-identified as amino acid adenosine triphosphate (ATP)-binding cassette transporter, glycerol-3-phosphate dehydrogenase (nicotinamide adenine dinucleotide phosphate), nicotinamide adenine dinucleotide oxidase, and ATPase-were demonstrated to be especially associated with Cd toxicity. Some of the other proteins observed in this work are of particular interest in terms of their responses to Cd, which have not been reported previously. These data may provide novel biomarkers for monitoring the Cd contamination level of flowing seawater as well as provide useful insights into the mechanisms of Cd toxicity.

Effects of acute cadmium toxicity on oxidative damage in nervous tissue

Cadmium is a wide-spread environmental pollutant, redox-active metal that mainly accumulates in the liver and kidney, bones, pancreas and adrenals, rarely in the brain. The mechanisms of Cd toxicity are poorly understood, although some studies indicate that cellular damage results from an increase in production of reactive oxygen species and inhibition of antioxidant enzymes. We tested the hypothesis that acute Cd exposure would lead to increased oxidative damage in various brain regions (prefrontal cortex, hippocampus, nc.caudatus). Adult male rats were treated either with a single dose of 50 ppm of CdCl2 (LD50), or a single dose of 100 ppm CdCl2 (LD50), against control group not exposed to Cd. The enzymatic activity of total and mitochondrial SOD, as well as GR was significantly and dose depending decreased, but MDA content has shown only a moderate increase. Results demonstrated the harmful effects of acute Cd exposure, in the nervous tissue, through mechanisms of oxidative damage.

Cadmium causes the oxidative modification of proteins in pea plants

AbstractIn pea (Pisum sativum L.) leaves from plants grown in the presence of 50 µm CdCl2 the oxidative production of carbonyl groups in proteins, the rate of protein degradation and the proteolytic activity were investigated. In leaf extracts the content of carbonyl groups measured by derivatization with 2,4‐dinitrophenylhydrazine (DNPH), was two‐fold higher in plants treated with Cd than in control plants. The identification of oxidized proteins was carried out by sodium dodecyl sulphate‐polyacrylamide gel electrophoresis of proteins derivatized with DNPH and immunochemical detection with an antibody against DNPH. The intensity of the reactive bands was higher in plants exposed to Cd than in controls. By using different antibodies some of the oxidized proteins were identified as Rubisco, glutathione reductase, manganese superoxide dismutase, and catalase. The incubation of leaf crude extracts with increasing H2O2 concentrations showed a progressive enhancement in carbonyl content and the pattern of oxidized proteins was similar to that found in Cd‐treated plants. Oxidized proteins were more efficiently degraded, and the proteolytic activity increased 20% due to the metal treatment. In peroxisomes purified from pea leaves a rise in the carbonyl content similar to that obtained in crude extracts from Cd‐treated plants was observed, but the functionality of the peroxisomal membrane was not apparently affected by Cd. Results obtained demonstrate the participation of both oxidative stress, probably mediated by H2O2, and proteolytic degradation in the mechanism of Cd toxicity in leaves of pea plants, and they appear to be involved in the Cd‐induced senescence previously reported in these plants.

In vitro andin vivo responses of rat tissues to cadmium-induced lipid peroxidation

Oxidative destruction of polyunsaturated fatty acids of membrane phospholipids, a phenomenon generally termed lipid peroxidation (LPO), is considered to be an important mechanism of toxicity for a wide variety of chemicals. Among these, cadmium (Cd), a pollutant of industrial and environmental importance, induces LPO in various tissues despite its apparent inability to directly generate free radicals under physiological conditions. Consequently, although LPO is not the primary mechanism of Cd toxicity, it represents an early intracellular response of tissues following exposure to Cd compounds. Recently, the authors reported the in vitro specific response to LPO of liver, lung, heart, kidney, testes and brain tissues incubated with various concentrations of CdCl{sub 2}. LPO was assessed by the measurement of thiobarbituric acid reactive substances (TBARS) which include malondialdehyde and lipid hydroperoxydes, and by gaz chromatographic analysis of evolved hydrocarbons, namely ethane and pentane. To compare the results obtained by both methods, they standardized TEP and TBARS values against incubated controls after subtracting endogenous levels of TBARS (time 0 values) because the measurement of endogenous levels of TEP in tissue incubates is not practicable. The objective of the present report is to clarify this concept in order to adequately compare the data obtained frommore » in vitro and in vivo studies. This should permit a better assessment of the relative importance of tissue responses to LPO following exposure to Cd.« less

Glutathione peroxidase and catalase in liver, kidney, testis and brain regions of rats following cadmium exposure and subsequent withdrawal.

Intraperitoneal administration of 0.4 mg/kg Cadmium (Cd) daily for 45 days was found to inhibit the activities of glutathione peroxidase and catalase in liver, kidney, testis and various brain regions at different time intervals. The magnitude of inhibition was increased with the period of exposure. Cd produced significant inhibition of glutathione peroxidase at 15 days in liver, kidney and cerebellum only; however, the enzyme activity was found to be decreased in all the tissues, except corpus striatum, at 30 and 45 days of exposure. Hippocampal glutathione peroxidase remained unaltered throughout the experiment. Catalase was found to be inhibited in all the tissues at different time intervals. The withdrawal of Cd treatment for 15 days after 45 days of exposure did not show significant recovery in the activity of both enzymes of different organs, except kidney and testis where partial and full recoveries respectively were observed. Since these two enzymes constitute an important part of cellular defence mechanism against oxidation, their widespread persistent inhibition may be of great significance in view of the recent reports showing the possible involvement of oxidative stress in the mechanism of Cd toxicity.

Cadmium transport, resistance, and toxicity in bacteria, algae, and fungi.

Cadmium is an important environmental pollutant and a potent toxicant to bacteria, algae, and fungi. Mechanisms of Cd toxicity and resistance are variable, depending on the organism. It is very clear that the form of the metal and the environment it is studied in, play an important role in how Cd exerts its effect and how the organism(s) responds. A wide range of Cd concentrations have been used to designate resistance in organisms. To date, no concentration has been specified that is applicable to all species studied under standardized conditions. Cadmium exerts its toxic effect(s) over a wide range of concentrations. In most cases, algae and cyanobacteria are the most sensitive organisms, whereas bacteria and fungi appear to be more resistant. In some bacteria, plasmid-encoded resistance can lead to reduced Cd2+ uptake. However, some Gram-negative bacteria without plasmids are just as resistant to Cd as are bacteria containing plasmids encoding for Cd resistance. According to Silver and Misra (1984), there is no evidence for enzymatic or chemical transformations associated with Cd resistance. Insufficient information is available on the genetics of Cd uptake and resistance in cyanobacteria and algae. Mechanisms remain largely unknown at this point in time. Cadmium is toxic to these organisms, causing severe inhibition of such physiological processes as growth, photosynthesis, and nitrogen fixation at concentrations less than 2 ppm, and often in the ppb range (Tables 2 and 3). Cadmium also causes pronounced morphological aberrations in these organisms, which are probably related to deleterious effects on cell division. This may be direct or indirect, as a result of Cd effects on protein synthesis and cellular organelles such as mitochondria and chloroplasts. Cadmium is accumulated internally in algae (Table 4) as a result of a two-phase uptake process. The first phase involves a rapid physicochemical adsorption of Cd onto cell wall binding sites, which are probably proteins and (or) polysaccharides. This is followed by a lag period and then a slow, steady intracellular uptake. This latter phase is energy dependent and may involve transport systems used to accumulate other divalent cations, such as Mn2+ and Ca2+. Some data indicate that Cd resistance, and possibly uptake, in algae and cyanobacteria is controlled by a plasmid-encoded gene(s). Although considerable information is available on Cd toxicity to, and uptake in fungi, further work is clearly needed in several areas. There is little information about Cd uptake by filamentous fungi, and even in yeasts, information on the specificity, kinetics, and mechanisms of Cd uptake is limited.(ABSTRACT TRUNCATED AT 400 WORDS)

A qualitative and quantitative study of few enzymes in the liver of cadmium fed rats.

Cadmium when administered to animals is known to accumulate in the liver and kidney, causing identifiable toxic effects. These effects on enzyme systems have been described in the present investigation selecting few of them viz. alkaline phosphatase, acid phosphatase, glucse-6-phosphatase and cholinesterase in the liver of rat, Rattus rattus albino. Topographical study on dysenzymia thus made have been found helpful in manifesting further the mechanism of Cd toxicity. Variations in the level of enzyme protein, state of cellular organelle together with processes of phosphorylation, adenylation and oxidative phosphorylation have been discussed explaining the cause and significance of these changes in enzyme activity.

Tomato Root: Site of Initial Alteration in Minor Elements in Cadmium Treated Plants

Tomato plants treated with 0.25 and 0.75 ppm Cd for one month exhibited no visual symptoms of toxicity, nor was the percent dry weight of leaf, stem, or root tissue altered. Cadmium concentrations in treated plants generally followed the trend: roots > leaves > stems. At such concentrations too low to cause phytotoxicity, cadmium altered the minor element concentration in tomato plants. The first changes occurred in the Mn and Fe concentrations of the roots. The reduction of these elements in the root may signal an early event in the mechanisms of Cd toxicity. To test the hypothesis that the root represents the primary site of injury from Cd, a kinetic study should be conducted in which root and shoot tissues are analyzed for Cd and the minor elements as the plants progress from an asymptomatic condition to one of severe Cd toxicity. (JMT)