Acute Cadmium Intoxication Research Articles

Individual Characteristic and Cadmium Level in Blood on Tradisional Metal Foundry Workers

Cadmium is one type of seriously hazardous heavy metal if inhaled. Acute cadmium poisoning may result from exposure of cadmium oxide vapor during metal melting process. This study aims to determine the factors ofindividuals characteristic associated with levels of cadmium in the blood of workers. This research is an analytic observation research with cross sectional approach. Samples were taken purposively from 30 metal casting workers. The research variables are smoking habit, BMI, working hours, duration of work and occupation as independent variables and cadmium levels in the blood as dependent variables. Blood cadmium levels were measured using Atomic Absorbtion Spectophotometer (AAS). Data were analyzed using chi-square. Although there was no correlation between smoking habit and working hours on cadmium blood level (p value> 0, 05) but there was correlation between nutritional status, duration of work and occupation to cadmium in blood (P value <0.05). There is a relationship between BMI, duration of work and type of work with cadmium levels in the blood of metal casting workers, for modification of workplace ventilation and the use of personal protective equipment to increase fume of cadmium in workplace.

Cadmium Toxicity: Oxidative Stress, Inflammation and Tissue Injury

Cadmium is a known environmental pollutant targeting various organs. Often implicated in cadmium toxicology is the formation of reactive oxygen species, overwhelming the free radical scavenging mechanisms and inducing oxidative stress. Acute cadmium intoxication has been shown to reduce antioxidant enzyme activity and induce oxidative stress. However, chronic intoxication has obscure outcomes in oxidative stress while the cell makes adjustments to overcome the toxicant load. Also linked with the occurrence of oxidative stress is inflammation. Stimulation of acute or chronic inflammation is mediated by different cascades. However, key events include activation of transcription factor, NF-κB and release of pro-inflammatory cytokines. Both oxidative stress and inflammation are implicated simultaneously in pathogenesis and induction of multi-organ tissue damage under cadmium exposure. This article reviews the impact of acute and chronic cadmium intoxication on inducing oxidative stress, inflammation and thereby inflicting tissue damage.

Protective effects of synbiotic diets of Bacillus coagulans, Lactobacillus plantarum and inulin against acute cadmium toxicity in rats

BackgroundCadmium is a heavy metal that causes oxidative stress and has toxic effects in humans. The aim of this study was to investigate the influence of two probiotics along with a prebiotic in preventing the toxic effects of cadmium in rats.MethodsTwenty-four male Wistar rats were randomly divided into four groups namely control, cadmium only, cadmium along with Lactobacillus plantarum (1 × 109 CFU/day) and inulin (5% of feedstuff) and cadmium along with Bacillus coagulans (1 × 109 spore/day) and inulin (5% of feedstuff). Cadmium treated groups received 200 μg/rat/day CdCl2 administered by gavage. During the 42-day experimental period, they were weighed weekly. For evaluation of changes in oxidative stress, the levels of some biochemicals and enzymes of serum including SOD, GPX, MDA, AST, ALT, total bilirubin, BUN and creatinine, and also SOD level of livers were measured at day 21 and 42 of treatment. The cadmium content of kidney and liver was determined by using atomic absorption mass spectrophotometry. Data were analyzed using analysis of variance (ANOVA) followed by Duncan’s post hoc test.ResultsTreatment of cadmium induced rats with synbiotic diets significantly improved the liver enzymes and biochemical parameters that decreased AST, ALT, total bilirubin, BUN and metal accumulation in the liver and kidney and increased body weight, serum and liver SOD values in comparison with the cadmium-treated group. No significant differences were observed with MDA and GPX values between all groups (p > 0.05).ConclusionsThis study showed that synbiotic diets containing probiotics (L. plantarum and B. coagulans) in combination with the prebiotic (inulin) can reduce the level of cadmium in the liver and kidney, preventing their damage and recover antioxidant enzymes in acute cadmium poisoning in rat.

Protective Effects of Long Term Administration of Zinc on Bone Metabolism Parameters in Male Wistar Rats Treated with Cadmium

Background: Acute cadmium (Cd) intoxication can be caused by eating foods or drinks that are packed in metal containers coated with Cd. The exposure to Cd enhanced resorption and inhibited formation of the bone tissue resulting in its decreased mineralization and thus may lead to various complications. Zinc supplement can reduce Cd absorption as well as neutralize the Cd-induced toxicity. This study aimed to investigate the protective effect of zinc on bone metabolism parameters in male rats treated with Cd. Materials and Methods: In this experimental study, a total of 48 male Wistar rats were randomly allocated into eight groups: group 1 received 0.5 mL of normal saline, group 2 received 0.5 mg/kg zinc, three Cd groups that received three different Cd concentrations (0.5, 1 and 2 mg/kg) and the other three groups received three Cd concentrations and zinc simultaneously. Blood samples were taken over a 30-day period and factors related to bone metabolism were measured. Results: The results showed that administration of three different doses of Cd chloride (0.5, 1 and 2 mg/kg) increased the activity of alkaline phosphatase, calcium, phosphorus and magnesium and decreased the albumin concentration compared to the control group. Moreover, the simultaneous use of three concentrations of Cd chloride with zinc reduced the activity of alkaline phosphatase, calcium, phosphorus, magnesium and increased the albumin concentration (P<0.05). Conclusion: Zinc supplementation can have protective effects against the toxicity caused by Cd on parameters of bone metabolism.

ChemInform Abstract: Metal‐Dithiocarbamate Complexes: Chemistry and Biological Activity

AbstractReview: 122 refs.

Metal-dithiocarbamate complexes: chemistry and biological activity

Dithiocarbamates are highly versatile mono-anionic chelating ligands which form stable complexes with all the transition elements and also the majority of main group, lanthanide and actinide elements. They are easily prepared from primary or secondary amines and depending upon the nature of the cation can show good solubility in water or organic solvents. They are related to the thiuram disulfides by a one-electron redox process (followed by dimerisation via sulfur-sulfur bond formation) which is easily carried out upon addition of iodide or ferric salts. Dithiocarbamates are lipophilic and generally bind to metals in a symmetrical chelate fashion but examples of other coordination modes are known, the monodentate and anisobidentate modes being most prevalent. They are planar sterically non-demanding ligands which can be electronically tuned by judicious choice of substituents. They stabilize metals in a wide range of oxidation states, this being attributed to the existence of soft dithiocarbamate and hard thioureide resonance forms, the latter formally resulting from delocalization of the nitrogen lone pair onto the sulfurs, and consequently their complexes tend to have a rich electrochemistry. Tetraethyl thiuramdisulfide (disulfiram or antabuse) has been used as a drug since the 1950s but it is only recently that dithiocarbamate complexes have been explored within the medicinal domain. Over the past two decades anti-cancer activity has been noted for gold and copper complexes, technetium and copper complexes have been used in PET-imaging, dithiocarbamates have been used to treat acute cadmium poisoning and copper complexes also have been investigated as SOD inhibitors.

Oxidative stress in rat liver during acute cadmium and ethanol intoxication

The aim of our study was to investigate the effects of binge drinking on prooxidant/antioxidant system in rat liver in acute cadmium (Cd) intoxication. In experiment male Wistar rats were used and divided into following groups: 1. control, 2. ethanol-treated group, in five subsequent doses of 2 g/kg administered by orogastric tube, 3. Cd-treated group in a single dose of 2.5 mg/kg intraperitoneally, 4. group that received Cd 12 hours after the last dose of ethanol. Blood and liver samples were collected for determination of oxidative stress parameters, 24 hours after treatment. When administered in combination, ethanol and Cd induced a more pronounced increase in serum and liver malondialdehyde level than either of these substances alone (p&lt;0.01). Liver manganese superoxide dismutase (MnSOD) activity was increased both in ethanol and Cd-treated group (p&lt;0.01), while liver copper/zinc superoxide dismutase (Cu/ZnSOD) activity was elevated in Cd group only. However, when administered in combination, ethanol and Cd induced a more pronounced decrease in liver MnSOD and Cu/ZnSOD activity 24 hours after treatment (p&lt;0.01). Based on our study, it can be concluded that ethanol may act sinergistically with Cd in inducing lipid peroxidation and reduction in liver SOD activity.

Bradykinin potentiating factor isolated from Buthus occitanus venom has a protective effect against cadmium-induced rat liver and kidney damage

Bradykinin and its related peptides are widely distributed in venomous animals, including scorpion. A peptide fraction isolated from the venom of the Egyptian scorpion Buthus occitanus was proved to have a bradykinin-potentiating activity. The aim of the present study was conducted to investigate whether the treatment with bradykinin potentiating factor (BPF) offers more beneficial effects in reversing cadmium-induced oxidative stress in rat liver and kidney. Adult male rats, equally divided into control and two treated groups, 10 animals in each group. group (I) was orally given (1 ml) saline and served as a control group; group (II) of rats was given cadmium chloride (4 mg/kg) alone, once daily an oral dose for 7 successive days; group (III) of rats was given ip injection (1 ml) BPF, once daily a dose for 7 successive days prior to CdCl 2 treatment and on the next 7 successive days with the same dose of cadmium as group II. Both organs were subjected to histopathological analysis with the light microscope. The activities of alanine aminotransferase (ALT), asparate aminotransferase (AST) and alkaline phosphatase (ALP) in serum were measured as indicators of the liver function. As parameters of the kidney function, creatinine, uric acid and urea concentrations in serum were determined. Also, malondialdehyde (MDA), reduced glutathione (GSH), super oxide dismutase (SOD) and catalase (CAT) were determined in both tissues. Cd exposure caused a significant decrease or inhibition in the activities of GSH, SOD, and CAT, with significant increase in the level of MDA, in versus to control groups in both liver and kidney. Also, when Cd was treated in co-administration with BPF induced increase or stimulation in the activity of GSH, SOD, and CAT, with significant decrease in the level of MDA when compared to Cd group in both organs. Histopathological changes of liver and kidney were also in accordance with the biochemical findings. Our data showed that Cd treatment induced histopathological alteration in the liver, severe hydropic degeneration in centrolobular zones. Inflammatory cells infiltration around the congested central vein and an obvious injury in some renal tubules. Bradykinin potentiating factor (BPF) administration prevented the histopathological alterations which observed in Cd-groups and both liver and kidney had essentially normal appearance in histopathological examination. In conclusion, BPF markedly ameliorated cadmium-induced liver and kidney tissue damage as evidenced by histological and biochemical examinations and acts as a potent scavenger of free radicals to protect the liver and kidney against the deleterious effect of acute cadmium intoxication.

Possible role of oxidative stress in acute cadmium hepatotoxicity in rats

It is known that cadmium induces a variety of functional disorders, especially liver and kidney dysfunction. The main mechanism involved in cadmium hepatotoxicity is its binding to sulfhydryl groups and initiation of inflammation. Additionally, oxidative stress, due to a decrease in antioxidative capacity, plays a role in chronic cadmium hepatotoxicity. The role of oxidative stress in acute cadmium intoxication is still not clear. The aim of our study was to investigate the role of reactive oxygen species and efficiency of antioxidant protection in rat liver in acute cadmium intoxication. Male Wistar rats (n=16) were divided into the following groups: 1. control group (n=7), treated with saline, 2. cadmium-treated (n=9) with a single dose of 2.5 mg/kg intraperitoneally. After administration (24 hours), blood samples from the right side of the heart and liver samples were collected for the determination of oxidative stress parameters. In our study malondialdehyde concentration was elevated both in plasma and liver after cadmium administration (p<0.01). Moreover, superoxide dismutase activity was increased in the cadmium-treated group, mainly due to increasean in copper/zinc superoxide dismutase activity (p<0.01). Reduced glutathione level in liver and plasma and concentration of sulfhydryl groups were not significantly changed by cadmium. The present study suggests that lipid peroxidation plays an important role in acute cadmium-induced liver injury. Antioxidant capacity of hepatocytes is partly increased due to an adaptive increase of superoxide dismutase activity.

Protective role of carnosine in mice with cadmium-induced acute hepatotoxicity

The hepatoprotective effect of carnosine was investigated against cadmium-induced acute liver injury in mice. Hepatotoxicity was induced by a single i.p. injection of cadmium chloride (6.5 mg/kg). Carnosine treatment (10 mg/kg/day, i.p.) was applied for three consecutive days, starting one day before cadmium administration. Carnosine significantly decreased the cadmium-induced elevations in serum aminotransferases. Carnosine suppressed lipid peroxidation and restored the deficits in the antioxidant defense mechanisms (reduced glutathione level, and catalase and superoxide dismutase activities) in liver tissue resulted from cadmium administration. Also, the reductions in hepatic nitric oxide and zinc ion levels, and the increases in hepatic cadmium ion concentration, and myeloperoxidase and caspase-3 activities following cadmium exposure were significantly attenuated by carnosine treatment. In addition, carnosine markedly ameliorated cadmium-induced liver tissue damage as evidenced by light and electron microscopic examinations. It was concluded that carnosine can be considered a potential candidate to protect the liver against the deleterious effect of acute cadmium intoxication.

Renal superoxide dismutase activity in mice exposed to acute and subacute cadmium intoxication: The role of magnesium pretreatment

Renal superoxide dismutase activity in mice exposed to acute and subacute cadmium intoxication: The role of magnesium pretreatment

Effect of magnesium pretreatment on reduced glutathione levels in tissues of mice exposed to acute and subacute cadmium intoxication: a time course study.

The study was designed to investigate the role of magnesium (Mg) pretreatment on reduced glutathione (GSH) levels in kidney, liver and testis of mice intoxicated with cadmium (Cd). Animals were divided into four groups: I--controls, II--Cd group: mice intoxicated with Cd, III--Mg+Cd group: mice given Mg 1 h before Cd, and IV--Mg group: mice given only Mg. In acute time--response studies, the single oral dose of Cd was 20 mg Cd/kg b.w. and 40 mg Mg/kg b.w. GSH levels were determined after 4, 6, 12, 24, and 48 h. In subacute experiments, mice were given 10 mg Cd/kg b.w. orally every day and 20 mg Mg/kg b.w., and GSH content was determined in investigated organs after 1 and 2 weeks. Acute cadmium intoxication significantly decreased the GSH content in liver 4, 6 and 12 h after Cd administration and increased GSH in kidney after 12, 24 and 48 h, but did not cause significant GSH alterations in testis. Mg pretreatment reduced the observed changes of GSH content in kidney and liver. Subacute Cd intoxication induced diminished renal GSH levels compared with the controls while the increased GSH levels were observed in liver and testes after 2 weeks Cd treatment. Mg pretreatment was efficient in restoring renal and testis GSH levels towards the control group, but had no effect on hepatic GSH.

Quantitative TLC of toxic elements on inorganic ion-exchangers. VI. Separation and determination of cadmium

Increasing contamination of drinking water, food, and the environment with toxic elements has led to a demand for fast and selective analytical methods [1–4]. Interest in cadmium is increasing because of its fatal toxicity [5]. The effects of acute cadmium poisoning are manifested in a variety of different symptoms including high blood pressure, kidney damage, and destruction of red blood cells [6]. Exposure to small doses of cadmium also slowly causes emphysema, anosmia, and nephropathy [7]. Separation and determination of cadmium in biological and environmental matrices have therefore aroused much interest [3]. Effective HPLC methods for detection and determination of cadmium have recently been reported [8, 9]. A theoretical model have also been established for predicting the retention behavior of EDTA-complexed anions of toxic metals [9]. Much of the chromatography of metal complexes and other difficult ionic separations will remain unpredictable, however, until definite studies of their retention behavior have been made. Use of new synthetic inorganic ion-exchangers as adsorbents in thin-layer chromatography has transformed this technique into a rapid and selective means of separation and determination of metal ions [10–16]. In continuation of our studies on chromium [16], we report here rapid and selective TLC method using titanium silicate [17], an inorganic ion-exchanger, for separation and determination of cadmium in the presence of numerous elements. 2 Experimental

Acute cadmium intoxication induces alpha-class glutathione S-transferase protein synthesis and enzyme activity in rat liver

Acute cadmium intoxication affects glutathione S-transferase (GST) in rat liver. It has been found that 24 h after i.p. cadmium administration to rats, at a dose of 2.5 mg CdCl 2 kg −1 body weight, the activity of this enzyme in liver cytosol increased by 40%. A less stimulatory effect persisted till 48 h and thereafter the enzyme activity normalized. Since, GST isoenzymes belong to different classes in mammalian tissues, we used quantitative immunoassays to verify which family of GST isoenzymes is influenced by this intoxication. Only alpha-class glutathione S-transferase (α-GST) proteins were detected in rat liver cytosol and their level increased by about 25%, 24 h after cadmium treatment. No pi-GST isoforms were found in liver cytosol from either normal or cadmium-treated rats. Co-administration of actinomycin D with cadmium normalized both the protein level and the activity of α-GST, suggesting that some effect occurs on enzyme transcription of these isoenzymes by this metal. On the other hand, it seems unlikely that the stimulatory effect is due to the high level of peroxides caused by lipid peroxidation, since Vitamin E administration strongly reduced the TBARS level, but did not cause any GST activity decrease.

Prevention of acute cadmium toxicity by Picroliv

The potential of Picroliv, a herbal extract against acute cadmium (Cd) intoxication, was evaluated in male rats. Biochemical and histopathological profile in rats pretreated with Picroliv (12 mg/kg, oral) followed by a single dose of Cd as cadmium chloride (CdCl2) (3 mg/kg, ip) revealed marked suppression of oxidative stress in liver and testes. The Cd-induced enhanced levels of lipid peroxidation, membrane fluidity and reduced levels of nonprotein sulphydryls and Na(+)K(+)ATPase were significantly restored to near normal by Picroliv pretreatment. In addition, the Cd-induced serum levels of glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, gamma glutamyl transpeptidase and lactate dehydrogenase were restored to near basal levels. Hepatic and testicular histopathological damage was also minimized. The results strongly suggest definite hepato- and testicular protection by Picroliv. The antioxidant potential of the herbal extract in the major part, and not its chelating property, seems to be responsible for its ameliorative action.

Efficacy of 2,3-dimercapto-1-propanesulfonic acid (DMPS) and diphenyl diselenide on cadmium induced testicular damage in mice

The deleterious effect of acute cadmium-intoxication in mice testes was evaluated. Animals received a single dose of CdCl 2 (2.5 or 5 mg/kg, intraperitoneally) and a number of toxicological parameters in mice testes were examined, such as δ-aminolevulinic acid dehydratase (δ-ALA-D) activity, lipid peroxidation, hemoglobin and ascorbic acid contents. Furthermore, the parameters that indicate tissue damage such as plasma alanine aminotransferase (ALT), aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) were also determined. Thus, a possible protective effect of 2,3-dimercapto-1-propane-sulfonic acid (DMPS) and diphenyl diselenide (PhSe) 2 were studied. The results demonstrated an inhibition of δ-ALA-D activity, a reduction of ascorbic acid and an increase of lipid peroxidation induced by cadmium, indicating testes damage. Furthermore, we observed an increase of plasma LDH, AST and ALT activities. DMPS (400 mol/kg) and (PhSe) 2 (100 μmol/kg) partially protected from the inhibitory effect of 2.5 mg/kg CdCl 2 on δ-ALA-D and from the increase of TBARS (thiobarbituric acid reactive species) levels. (PhSe) 2 therapy was effective in ameliorate ascorbic acid content when the cadmium dose was 2.5 mg/kg. Treatment with DMPS and (PhSe) 2, individually or combined, was inefficient in reducing cadmium-induced plasma LDH and ALT activity increase. The use of combined therapy (DMPS plus (PhSe) 2) proved to be efficient in decreasing cadmium levels in testes and in ameliorating plasma AST activity from animals that received the highest dose of cadmium.

Plasma Antioxidants Changes after Acute Cadmium Intoxication in Rats

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506 Protective effect of IP administered olive oil in acute cadmium intoxication

506 Protective effect of IP administered olive oil in acute cadmium intoxication

Parkinsonism after acute cadmium poisoning

A 64-year-old man suffered from acute exposure to cadmium, followed by multiple organ failure. Three months after exposure, the patient developed parkinsonian features. The case suggests that cadmium intoxication may damage the basal ganglia, resulting in parkinsonism.

Effect of monoisoamyl meso-2,3-dimercaptosuccinate on the pathology of acute cadmium intoxication.

The ability of monoisoamyl meso-2,3-dimercaptosuccinate (Mi-ADMS) to offset the characteristic organ pathology of intraperitoneally administered cadmium chloride (CdCl2) and that of the cadmium-cysteine complex has been examined in male Wistar rats. The tissues examined for damage were the testes, kidney, liver, pancreas, and bone marrow. At a high dose of CdCl2 (0.03 mmol/kg, ip) testicular damage was completely prevented by Mi-ADMS (0.50 mmol/kg, ip) given immediately. A decrease in the protective ability of the antagonist was observed following delayed administration of Mi-ADMS given at 1, 2, 4, and 24 h post CdCl2. At a lower dose of CdCl2 (0.006 mmol/kg, ip), Mi-ADMS furnished essentially full protection from testicular damage when given (0.50 mmol/kg, sc) at 0 and 1 h after CdCl2. The administration of cadmium-cysteine complex (0.01 mmol/kg, ip) induced notable renal tubular damage, which was antagonized by the administration of Mi-ADMS (0.50 mmol/kg, ip) as late as 4 h after the complex. At a 24-h delay, extensive tubular necrosis was found on sacrifice after 4 d. The administration of cadmium-cysteine complex ip reduced, but did not eliminate, the characteristic damage of the seminiferous tubules found for cadmium alone. There is a progressive reduction of testicular weight as the interval between cadmium and antagonist administration increases. The average kidney weights of the animals given CdCl2-cysteine complex were increased in comparison to normal controls. The antagonistic effects of Mi-ADMS treatment on cadmium intoxication in the kidneys and the testes of rats is very similar to that found for effective dithiocarbamate antagonists. In order to obtain complete protection of the testes from the deteterious effects of cadmium, such antagonists must be administered no later than about 1 h after the cadmium.