Cd2+ binds to Atx1 and affects the physical interaction between Atx1 and Ccc2 in Saccharomyces cerevisiae

The ATX1 deletion strain of Saccharomyces cerevisiae is more resistant to Cd²⁺ than the wild-type. To investigate the function of Atx1 in Cd²⁺ toxicity, we used a metal-binding assay to study the interaction between Atx1 and Cd²⁺ in vitro. Using circular dichroism and two-hybrid analyses, we found that Atx1 can bind Cd²⁺ specifically and that Cd²⁺ binding to Atx1 affects the physical interaction between Atx1 and Ccc2. These results imply that Atx1 delivers Cd²⁺ to Ccc2 and that this delivery is, at least in part, responsible for Cd²⁺ toxicity in S. cerevisiae.     

Solid phase speciation of Zn and Cd in zinc smelter effluent-irrigated soils

Solubility of metal in contaminated soils is a key factor which controls the phytoavailability and toxic effects of metals on soil environment. The chemical equilibria of metal ions between soil solution and solid phases govern the solubility of metals in soil. Hence, an attempt was made to identify the probable solid phases (minerals), which govern the solubility of Zn²⁺ and Cd²⁺ in zinc smelter effluent-irrigated soils. Estimation of free ion activities of Zn²⁺ (pZn²⁺) and Cd²⁺ (pCd²⁺) by Baker soil test indicated that metal ion activities were higher in smelter effluent-irrigated soils as compared to that in tubewell water-irrigated soils. Identification of solid phases further reveals that free ion activity of Zn²⁺ and Cd²⁺ in soil highly contaminated with Zn and Cd due to long-term irrigation with zinc smelter effluent is limited by the solubility of willemite (Zn₂SiO₄) in equilibrium with quartz and octavite (CdCO₃), respectively. However, in case of tubewell water-irrigated soil, franklinite (ZnFe₂O₄) in equilibrium with soil-Fe and exchangeable Cd are likely to govern the activity of Zn²⁺ and Cd²⁺ in soil solution, respectively. Formation of highly soluble minerals namely, willemite and octavite indicates the potential ecological risk of Zn and Cd, respectively in smelter effluent irrigated soil.     

Toxicity of Cd to signal grass (Brachiaria decumbens Stapf.) and Rhodes grass (Chloris gayana Kunth.)

Given that Cd accumulates within plant tissues to levels that are toxic to animals, it is necessary to understand the role of plants in highly Cd-contaminated systems and their subsequent impact on the health of animals. A solution culture experiment was conducted to elucidate the effects of increasing Cd²⁺ activity ({Cd²⁺}) on growth of Rhodes grass (Chloris gayana Kunth.) and signal grass (Brachiaria decumbens Stapf.). The shoot and root fresh mass of both Rhodes grass and signal grass was reduced by 50% at ca. 0.5 µM {Cd²⁺}. Elevated {Cd²⁺} resulted in a significant decrease in the tissue Mn concentration for both the shoots and roots, and caused a chlorosis of the veins in the shoots. Root hair growth was prolific even at high {Cd²⁺}, thus root hair growth appeared to be less sensitive to elevated Cd than was root growth per se. The critical shoot tissue concentrations (50% reduction in growth), 230 µg g^?1 for Rhodes grass and 80 µg g^?1 for signal grass, exceeded the maximum level of Cd tolerated in the diet of animals (ca. 5 µg g^?1). When assessing the risk associated with the revegetation of Cd-contaminated sites with Rhodes grass or signal grass, careful consideration must be given, therefore, to the transfer of toxic concentrations of Cd to grazing animals and through the wider food chain.     

A new method for determining the relation between soil- and plant-cadmium

On soils differing in total Cd concentration, organic matter content and pH, but with the same compost treatment, a significant linear relation was found between the calculated Cd²⁺ concentration of the soil solution and the Cd concentration of lettuce grown under field conditions. The Cd²⁺ concentration was calculated with the equation for the exchange reaction between Cd²⁺ and Ca²⁺.     

Cadmium Toxicity to Microcystis aeruginosa PCC 7806 and Its Microcystin-Lacking Mutant

The adverse effects of microcystin (MC) produced by cyanobacteria have drawn considerable attention from the public. Yet it remains unclear whether MC confers any benefits to the cyanobacteria themselves. One suggested function of MC is complexation, which may influence the bioaccumulation and toxicity of trace metals. To test this hypothesis, we examined Cd toxicity to wild-type Microcystis aeruginosa PCC 7806 (WT) and its MC-lacking mutant (MT) under nutrient-enriched (+NP), phosphorus-limited (-P), and nitrogen-limited (-N) conditions. The accumulation of Cd and the biochemical parameters associated with its detoxification [total phosphorus (TP), inorganic polyphosphate (Poly-P), and glutathione (GSH) in the cells as well as intra- and extra-cellular carbohydrates] were quantified. Although the –P cyanobacteria accumulated less Cd than their +NP and –N counterparts, the different nutrient-conditioned cyanobacteria were similarly inhibited by similar free ion concentration of Cd in the medium ([Cd²⁺]_F). Such good toxicity predictability of [Cd²⁺]_F was ascribed to the synchronous decrease in the intracellular concentrations of Cd and TP. Nevertheless, Cd toxicity was still determined by the intracellular Cd to phosphorus ratio (Cd/P), in accordance with what has been reported in the literature. On the other hand, the concentrations of TP, Poly-P, and carbohydrates went up, but GSH concentration dropped down with the enhancement of [Cd²⁺]_F, indicating their association with Cd detoxification. Although the inactivation of MC peptide synthetase gene had some nutrient and Cd concentration dependent effects on the parameters above, both cyanobacterial strains showed the same Cd accumulation ability and displayed similar Cd sensitivity. These results suggest that MC cannot affect metal toxicity either by regulating metal accumulation or by altering the detoxification ability of the cyanobacteria. Other possible functions of MC need to be further investigated.     

镉暴露对黑斑蛙精巢ROS的诱导及其蛋白质氧化损伤作用机理

重金属镉对精巢发育、呼吸及神经系统信号转导等途径均有不良影响,被认为是造成两栖动物种群数量急剧下降的重要原因之一。然而,有关镉对精巢损伤的分子机理还不清楚。通过对镉暴露后的黑斑蛙精巢活性氧自由基(ROS)、蛋白质羰基(PCO)以及DNA蛋白质交联(DPC)等指标的系统分析,探讨了镉对精巢毒害的分子作用机理。随镉浓度的增加,黑斑蛙精巢细胞线粒体ROS随镉暴露浓度的增加而升高,0.5、1.0 mg/L镉染毒组与对照组比较有显著性差异(P<0.05);精巢组织PCO和DPC也随镉暴露浓度的增加而逐渐上升,且均呈明显的浓度-效应关系。结果表明:镉诱导机体产生ROS,进而导致蛋白质氧化损伤以及DNA损伤,说明精巢组织ROS的产生是镉致雄性生殖毒效应机制的重要因素之一。     

重金属镉(Cd)在植物体内的转运途径及其调控机制

重金属镉(Cd)的毒害效应与其由土壤向植物地上部分运输有关,揭示Cd~(2+)转运途径及其调控机制可为提高植物抗镉性以及镉污染的植物修复提供依据。对Cd~(2+)在植物体内的转运途径,特别是限制Cd~(2+)移动的细胞结构和分子调控机制研究进展进行了回顾。Cd~(2+)通过共质体和质外体途径穿过根部皮层进入木质部的过程中,大部分在皮层细胞间沉积,少部分抵达中柱后转移到地上部分。为了免受Cd~(2+)的危害,植物体产生了多种限制Cd~(2+)吸收和转移的生理生化机制:1)环绕在内皮层径向壁和横向壁上的凯氏带阻止Cd~(2+)以质外体途径进入木质部;2)螯合剂与进入根的Cd~(2+)螯合形成稳定化合物并区隔在液泡中;3)通过H+/Cd~(2+)离子通道等将Cd~(2+)逆向转运出根部。植物共质体和质外体途径转运重金属镉的能力以及两条途径的串扰尚待进一步明晰和阐明。     

Molecular Features of the Zn2+ Binding Site in the Prion Protein Probed by 113Cd NMR

The cellular prion protein (PrP^C) is a zinc-binding protein that contributes to the regulation of Zn²⁺ and other divalent species of the central nervous system. Zn²⁺ coordinates to the flexible, N-terminal repeat region of PrP^C and drives a tertiary contact between this repeat region and a well-defined cleft of the C-terminal domain. The tertiary structure promoted by Zn²⁺ is thought to regulate inherent PrP^C toxicity. Despite the emerging consensus regarding the interaction between Zn²⁺ and PrP^C, there is little direct spectroscopic confirmation of the metal ion’s coordination details. Here, we address this conceptual gap by using Cd²⁺ as a surrogate for Zn²⁺. NMR finds that Cd²⁺ binds exclusively to the His imidazole side chains of the repeat segment, with a dissociation constant of ～1.2 mM, and promotes an N-terminal-C-terminal cis interaction very similar to that observed with Zn²⁺. Analysis of ¹¹³Cd NMR spectra of PrP^C, along with relevant control proteins and peptides, suggests that coordination of Cd²⁺ in the full-length protein is consistent with a three- or four-His geometry. Examination of the mutation E199K in mouse PrP^C (E200K in humans), responsible for inherited Creutzfeldt-Jakob disease, finds that the mutation lowers metal ion affinity and weakens the cis interaction. These findings not only provide deeper insight into PrP^C metal ion coordination but they also suggest new perspectives on the role of familial mutations in prion disease.     

Rat kidney epithelial cell culture for metal toxicity studies

Summary Evaluation of the potential adverse human health effects of low-level chronic exposure to heavy metals is dependent on the basic knowledge of the cellular and molecular toxicology of these metals. The use of various cell culture systems has greatly facilitated our knowledge of the cellular effects. Inasmuch as most of the acute and chronic toxic effects of metals occur primarily on the renal proximal tubules, the development of a rat kidney epithelial cell culture has provided a unique system to study the uptake and mechanism of toxicity of metals and their intracellular binding ligands. In the presence ofd-valine, fibroblast growth was retarded and a primary epithelial monolayer culture was selectively grown from rat kidney cells. A distinct difference in the uptake of chemically similar divalent metals, such as Pb²⁺, Hg²⁺, Cd²⁺, and Zn²⁺, was observed in these cells. Both Pb²⁺ and Hg²⁺ were more avidly taken up by kidney cells than Cd²⁺ and Zn²⁺ salts and they also showed increased toxicity. On the other hand, the cellular uptake of Cd from cadmium-metallothionein (CdMT) was much less than from CdCl₂, but CdMT was about seven times more toxic than CdCl₂ when added to the renal cell culture. The cytotoxicity of CdCl₂ was decreased significantly with pretreatment of the cells with CdCl₂, although this had no effect on the toxicity of CdMT. The cellular toxicity of CdMT occurred probably during the process of its transport across the plasma membrane whereas that of CdCl₂ occurred after it had entered the cell. Thus rat kidney epithelial cells may be a useful tool to study the mechanism of renal toxicity of environmental chemicals and drugs. This work was funded by grants-in-aid of research from the Kidney Foundation of Canada.     

Cadmium uptake kinetics in intact soybean plants

The absorption characteristics of Cd²⁺ by 10- to 12-day-old soybean plants (Glycine max cv Williams) were investigated with respect to influence of Cd concentration on adsorption to root surfaces, root absorption, transport kinetics and interaction with the nutrient cations Cu²⁺, Fe²⁺, Mn²⁺, and Zn²⁺. The fraction of nonexchangeable Cd bound to roots remained relatively constant at 20 to 25% of the absorbed fraction at solution concentration of 0.0025 to 0.5 micromolar, and increased to 45% at solution concentration in excess of 0.5 micromolar. The exchangeable fraction represented 1.4 to 32% of the absorbed fraction, and was concentration dependent. Using dinitrophenol as a metabolic inhibitor, the `metabolically absorbed' fraction was shown to represent 75 to 80% of the absorbed fraction at concentration less than 0.5 micromolar, and decreased to 55% at 5 micromolar. At comparatively low Cd concentrations, 0.0025 to micromolar 0.3, root absorption exhibited two isotherms with K₂ values of 0.08 and 1.2 micromolar. Root absorption and transfer from root to shoot of Cd²⁺ was inhibited by Cu²⁺, Fe²⁺, Mn²⁺, and Zn²⁺. Analyses of kinetic interaction of these nutrient cations with Cd²⁺ indicated that Cu²⁺, Fe²⁺, Zn²⁺, and possibly Mn²⁺ inhibited Cd absorption competitively suggesting an involvement of a common transport site or process.     

COMPARATIVE pH DEPENDENT METAL INHIBITION OF NUTRIENT UPTAKE BY SCENEDESMUS QUADRICAUDA(CHLOROPHYCEAE)1,2

Cadmium and copper inhibition of nutrient uptake by the green alga Scenedesmus quadricauda is highly pH dependent in an inorganic medium; both metals are less toxic at low pH. The alga was grown in chemostats with both N and P approaching limiting levels; it was then possible to study metal toxicity to the nitrate, ammonium, and phosphate uptake systems of algae in an identical physiological state. When the logarithm of the Cd concentration causing 25% inhibition of nitrate, ammonium, and phosphate uptake was regressed against pH almost perfect linear relationships were obtained. This was also true at the 50% inhibition level, except for a smaller than predicted increase in Cd toxicity to ammonium uptake at pH 8, which may be due to the beginning of Cd precipitation at this pH. Cu²⁺ toxicity was linearly related to pH for ammonium and phosphate uptake and although, its toxicity for nitrate uptake also increased with pH, the increase was not perfectly linear. The toxicity of total Cu showed no linear relationship to pH. Cd²⁺ and Cu²⁺ toxicity increased by up to four orders of magnitude from pH 5 to 8. Competition between free metal and hydrogen ions for uptake sites on the cell surface is suggested as a mechanism increasing the toxicity of free metal, ions as the hydrogen ion content decreases (i.e. at higher pH).     

Cadmium effects on transcriptional expression of rhlB/rhlC genes and congener distribution of monorhamnolipid and dirhamnolipid in Pseudomonas aeruginosa IGB83

While variable production of the biosurfactant, rhamnolipid, by Pseudomonas aeruginosa has been shown to be dependent on growth conditions, no research has evaluated potential relationships between rhamnolipid production and the presence of heavy metals. The current investigation evaluates the influence of Cd²⁺ on rhamnolipid synthesis. Cultures grown in the presence of 0.45 and 0.89 mM Cd²⁺ were monitored for rhlB/rhlC expression, rhamnolipid yield, and the ratio of monorhamnolipid (RL1) and dirhamnolipid (RL2) produced. Results show a Cd-induced enhancement of rhlB expression in mid-stationary phase (53 h). In addition, sustained production of rhamnolipid through late stationary growth phase (96 h) was observed for Cd-amended cultures, unlike Cd-free control cultures that ceased rhamnolipid production by mid-stationary growth phase. Most significant was an observed increase in the ratio of RL2 to RL1 congeners produced by cultures grown in the presence of Cd²⁺. Previous results have shown that the complexation constant for RL2–Cd is several orders of magnitude larger than that of RL1–Cd thus the preferential production of RL2 in the presence of Cd²⁺ impacts its bioavailability and toxicity both for the cell and in the surrounding environment.     

Impact of chelator-induced phytoextraction of cadmium on yield and ionic uptake of maize

Enhanced phytoextraction uses soil chelators to increase the bioavailability of heavy metals. This study tested the effectiveness of ethylenediaminetetraacetic acid (EDTA) and citric acid in enhancing cadmium (Cd) phytoextraction and their effects on the growth, yield, and ionic uptake of maize (Zea mays). Maize seeds of two cultivars were sown in pots treated with 15 (Cd₁₅) or 30 mg Cd kg^?1 soil (Cd₃₀). EDTA and citric acid at 0.5 g kg^?1 each were applied 2 weeks after germination. Results demonstrated that the growth, yield per plant, and total grain weight were reduced by exposure to Cd. EDTA increased the uptake of Cd in shoots, roots, and grains of both maize varieties. Citric acid did not enhance the uptake of Cd, rather it ameliorated the toxicity of Cd, as shown by increased shoot and root length and biomass. Cadmium toxicity reduced the number of grains, rather than the grain size. The maize cultivar Sahiwal-2002 extracted 1.6% and 3.6% of Cd from soil in both Cd+ EDTA treatments. Hence, our study implies that maize can be used to successfully phytoremediate Cd from soil using EDTA, without reducing plant biomass or yield.     

Binding of cadmium (Cd2+) to E-CAD1, a calcium-binding polypeptide analog of E-cadherin

Recent studies have shown that Cd²⁺ can damage the Ca²⁺-dependent junctions between renal epithelial cells in culture, and preliminary evidence suggests that this effect may involve the interaction of Cd²⁺ with E-cadherin, a Ca²⁺-dependent cell adhesion molecule that is localized at the adhering junctions of epithelial cells. To determine whether or not Cd²⁺ might bind directly to the E-cadherin molecule, we studied the binding of Cd²⁺ to E-CAD1, a recombinant, 145-residue polypeptide that corresponds to one of the extracellular Ca²⁺-binding regions of mouse E-cadherin. By using an equilibrium microdialysis technique, we were able to show that Cd²⁺ could, in fact, bind to E-CAD1. The binding was saturable, with a maximum of one Cd²⁺ binding site per E-CAD1 molecule. The apparent dissociation constant (K_D) for the binding was about 20 μM, a concentration similar to that which has been shown to disrupt the junctions between epithelial cells. Other results showed that the binding of Cd²⁺ was greatly reduced when excess Ca²⁺ was included in the dialysis solution. These results suggest that Cd²⁺ can interact with the Ca²⁺ binding regions on the E-CAD1 molecule, and they provide additional support for the hypothesis that E-cadherin might be a molecular target for Cd²⁺ toxicity.     

Cadmium Uptake by Pinus resinosa Ait. Pollen and the Effect on Cation Release and Membrane Permeability

Cadmium uptake by red pine (Pinus resinosa Ait.) pollen from a graded series of Cd²⁺ solutions (0 to 2.88 microequivalents per 50 milligrams pollen) and its effect on membrane integrity were examined by atomic absorption spectroscopy. Uptake was strongly dependent on Cd²⁺ concentration and was limited to adsorption and cation exchange in pollen walls during a 3-hour measurement period. Good correlation between measured Cd²⁺ uptake and that predicted by the Langmuir and Freundlich isotherm equations indicated the adsorptive nature of Cd²⁺ uptake. While substantial quantities of Ca²⁺ and Mg²⁺ were released by exchange mechanisms concurrent with Cd²⁺ uptake, there was no evidence for leakage of cations due to membrane impairment as indicated by a poor correlation between Cd²⁺ uptake and K⁺ efflux. Virtually all Cd²⁺ removed from solution was freely exchangeable with 0.5 millimolar CaCl₂ and demonstrated that Cd²⁺ did not readily enter pine pollen but was adsorbed on the pollen wall. Ultraviolet transmission spectra of treatment solutions and analyses of phosphate and reducing sugar efflux also indicated that the potent toxicity of Cd²⁺ to pollen germination and germ tube elongation was not the result of membrane damage.     

Submitochondrial particles asin vitro biosensors of heavy metal toxicity

The effects on mitochondrial respiratory parameters of heavy metals, such as Cu, Ni, Pb, Cd, Zn, Ag, Hg, were recorded by using thein vitro response of submitochondrial particles (SMP) from beef heart mitochondria.The toxicity of these elements was estimated by determining their effects on the energy-coupled reverse electron transfer (RET), which is induced by ATP and succinate at first site level of the respiratory chain in SMP.The RET rate was easily monitored by recording spectrophotometrically at 340 nm the production of NADH, arising from the reduction of exogenous NAD⁺ by RET.The toxicity values were expressed as the toxicant molar concentration which decreases the rate of reduction of NAD⁺ to an extent of 50 percent (EC50). The toxicity increased in the following order: Ni²⁺2+2+< Cd²⁺2+2++.The SMP data were compared with the toxicity values obtained from a variety of biological systems currently used for toxicity testing. The results obtained demonstrate that the SMP test generally provides a good estimate of metal toxicity for several fish and invertebrate species. This is demonstrated by the statistical parameters obtained in the regression analysis. The broadened 95% confidence intervals and, in particular, the poor correlations obtained for some aquatic organisms can be ascribed to the more complex metabolic interactions and competing toxic pathways in aquatic organisms, when compared to SMP.     

Catch me if you can! Novel aspects of cadmium transport in mammalian cells

Cadmium (Cd²⁺) is a nonessential divalent metal ion that causes toxicity in multiple organs in humans. In order for toxicity to occur Cd²⁺ must first enter cells by utilizing transport pathways for essential metals. This review focuses on studies in which Cd²⁺ transport was directly demonstrated by electrophysiological, radiotracer or Cd²⁺-sensitive fluorescent dye techniques. The chemistry of Cd²⁺ and metal ions in general is addressed in the context of properties relevant for transport through membrane proteins, such as hydration energy. Apart from transport by the ZIP transporters SLC39A8 and SLC39A14, which is not topic of the review, uptake of free Cd²⁺ has been demonstrated for the Fe²⁺/H⁺ cotransporter divalent metal transporter 1. Moreover, the multiligand endocytic receptors megalin and cubilin take up cadmium-metallothionein complexes via receptor-mediated endocytosis. The role of ATP binding cassette transporters in Cd²⁺ efflux from cells is also discussed. Both the multidrug resistance-associated protein 1 and cystic fibrosis transmembrane conductance regulator are likely to transport cadmium–glutathione complexes out of cells, whereas transport of free Cd²⁺ by the multidrug resistance P-glycoprotein remains controversial. Finally, arguments for and against Cd²⁺ transport by Ca²⁺ channels are presented. Most N- and L-type Ca²⁺ channels are closed at resting membrane potential (with the exception of CaV1.3 channels) and therefore unlikely to allow significant Cd²⁺ influx under physiological conditions. CaV3.1 and CaV3.2 T-type calcium channels are permeated by divalent metal ions, such as Fe²⁺ and Mn²⁺ because of considerable “window” currents close to resting membrane potential and could be responsible for tonic Cd²⁺ entry. TRPM7 and the mitochondrial Ca²⁺ uniporter are other likely candidates for Cd²⁺ transporters, whereas the role of Orai proteins, the store-operated calcium channels carrying Ca²⁺ release-activated Ca²⁺ current, in Cd²⁺ influx remains to be investigated.     

Involvement of Ca2+-calmodulin in Cd2+ toxicity during the early phases of radish (Raphanus sativus L.) seed germination

The toxicity of Cd²⁺in vivo during the early phases of radish (Raphanus sativus L.) seed germination and the in vitro Cd²⁺ effect on radish calmodulin (CaM) were studied. Cd²⁺ was taken up in the embryo axes of radish seeds; the increase in fresh weight of embryo axes after 24 h of incubation was inhibited significantly in the presence of 10 mmol m^?3 Cd²⁺ in the external medium, when the Cd²⁺ content in the embryo axes was c. 1.1 μmol g^?1 FW. The reabsorption of K⁺, which characterizes germination, was inhibited by Cd²⁺, suggesting that Cd²⁺ affected metabolic reactivation. The slight effect of Cd²⁺ on the transmembrane electric potential of the cortical cells of the embryo axes excluded a generalized toxicity of Cd²⁺ at the plasma membrane level. After 24 h of incubation, Cd²⁺ induced no increase in total acid-soluble thiols and Cd²⁺-binding peptides able to reduce Cd²⁺ toxicity. Ca²⁺ added to the incubation medium partially reversed the Cd²⁺-induced inhibition of the increase in fresh weight of embryo axes and concomitantly reduced Cd²⁺ uptake. Equilibrium dialysis experiments indicated that Cd²⁺ bound to CaM and competed with Ca²⁺ in this binding. Cd²⁺ inhibited the activation of Ca²⁺-CaM-dependent calf-brain phosphodiesterase, inhibiting the Ca²⁺-CaM active complex. Cd²⁺ reduced the binding of CaM to the Ca²⁺-CaM binding enzymes present in the soluble fraction of the embryo axes of radish seeds. The possibility that Cd²⁺ toxicity in radish seed germination is mediated by the action of Cd²⁺ on Ca²⁺-CaM is discussed in relation to the in vivo and in vitro effects of Cd²⁺.     

Effect of Cadmium Ion on alpha-Glucosidase: An Inhibition Kinetics and Molecular Dynamics Simulation Integration Study

α-Glucosidase is a critical metabolic enzyme that produces glucose molecules by catalyzing carbohydrates. The aim of this study is to elucidate biological toxicity of Cd²⁺ based on α-glucosidase activity and conformational changes. We studied Cd²⁺-mediated inactivation as well as conformational modulation of α-glucosidase by using kinetics coupled with simulation of molecular dynamics. The enzyme was significantly inactivated by Cd²⁺ in a reversibly binding behavior, and Cd²⁺ binding induced a non-competitive type of inhibition reaction (the K _i was calculated as 0.3863 ± 0.033 mM). Cd²⁺ also modulated regional denaturation of the active site pocket as well as overall partial tertiary structural change. In computational simulations using molecular dynamics, simulated introduction of Cd²⁺ induced in a depletion of secondary structure by docking Cd²⁺ near the saccharides degradation at the active site, suggesting that Cd²⁺ modulating enzyme denaturation. The present study elucidated that the binding of Cd²⁺ triggers conformational changes of α-glucosidase as well as inactivates catalytic function, and thus suggests an explanation of the deleterious effects of Cd²⁺ on α-glucosidase.