Ppm CdCl2 Research Articles

Curcumin Treatment Ameliorates Hepatic Insulin Resistance Induced by Sub-chronic Oral Exposure to Cadmium LOAEL Dose via NF-κB and Nrf2 Pathways.

Cadmium (Cd) is a global pollutant, and its accumulation in the liver causes oxidative stress, inflammation, insulin resistance (IR), and metabolic complications. This study investigated whether curcumin treatment could alleviate hepatic IR in Wistar rats exposed to sub-chronic cadmium and explored the underlying molecular pathways. Male Wistar rats were divided into a control group (standard normocaloric diet + cadmium-free water) and a cadmium group (standard normocaloric diet + drinking water with 32.5ppm CdCl2) for 30days. Oral glucose tolerance, insulin response, and IR were assessed using mathematical models. Liver tissue was analyzed for markers of oxidative stress, inflammation, and key regulatory pathways, including NF-κB, Nrf2, MAPKs (JNK and p38), and the IRS1-Akt pathway. We established an effective curcumin dose of 250mg/kg for 5days orally. Results demonstrated that after 30days of exposure, cadmium accumulated in the liver, inducing an oxidative and inflammatory state. This was characterized by increased expression of NF-κB, JNK, and p38, along with diminished Nrf2 expression, hepatic IR, hyperglycemia, and hyperinsulinemia. Curcumin treatment effectively alleviated these metabolic disorders by restoring the balance between NF-κB and Nrf2 in the liver, modulating the MAPK pathway, and, consequently, improving oxidative and inflammatory balance. In conclusion, this study suggests that cadmium induces hepatic IR through an imbalance between NF-κB and Nrf2 signaling pathways. Curcumin treatment appears to improve these pathways, thereby ameliorating hepatic IR.

Pancreatic Antioxidative Defense and Heat Shock Proteins Prevent Islet of Langerhans Cell Death After Chronic Oral Exposure to Cadmium LOAEL Dose.

Cadmium, a hazardous environmental contaminant, is associated with metabolic disease development. The dose with the lowest observable adverse effect level (LOAEL) has not been studied, focusing on its effect on the pancreas. We aimed to evaluate the pancreatic redox balance and heat shock protein (HSP) expression in islets of Langerhans of male Wistar rats chronically exposed to Cd LOAEL doses, linked to their survival. Male Wistar rats were separated into control and cadmium groups (drinking water with 32.5 ppm CdCl2). At 2, 3, and 4 months, glucose, insulin, and cadmium were measured in serum; cadmium and insulin were quantified in isolated islets of Langerhans; and redox balance was analyzed in the pancreas. Immunoreactivity analysis of p-HSF1, HSP70, HSP90, caspase 3 and 9, and cell survival was performed. The results showed that cadmium exposure causes a serum increase and accumulation of the metal in the pancreas and islets of Langerhans, hyperglycemia, and hyperinsulinemia, associated with high insulin production. Cd-exposed groups presented high levels of reactive oxygen species and lipid peroxidation. An augment in MT and GSH concentrations with the increased enzymatic activity of the glutathione system, catalase, and superoxide dismutase maintained a favorable redox environment. Additionally, islets of Langerhans showed a high immunoreactivity of HSPs and minimal immunoreactivity to caspase associated with a high survival rate of Langerhans islet cells. In conclusion, antioxidative and HSP pancreatic defense avoids cell death associated with Cd accumulation in chronic conditions; however, this could provoke oversynthesis and insulin release, which is a sign of insulin resistance.

Effect of Zinc supplementation on haematology, oxidative stress and plasma biochemical parameters in cadmium exposed goats

The present study was designed to assess the effect of zinc supplementation on haematology, oxidative stress and plasma biochemical parameters in Cd induced lactating goats. Eighteen crossbred lactating goats were divided into three groups (Control, T1 and T2). In T1 and T2 groups, goats were given 10 ppm Cdcl2, while in T2, Zinc @100ppm was also supplemented for period of 120 days. At the end of study, blood glucose, TLC, neutrophil % and AST, ALT were increased significantly in T1 group and except glucose, Zn supplementation in T2 group showed its protective effect on TLC, neutrophil %, lymphocyte %, AST and ALT. There was significant decrease in lymphocyte %, Hb and plasma total antioxidant activity in T1 group. At 30 days, the activity of SOD was increased in T1 and T2 but thereafter activities were significantly decreased at 120 days in T1 but in T2 it was similar to control. The activity of catalase was increased on 30 and 60 days and thereafter decreased from 90 days onwards but the rate of decline was comparatively less in T2. Total immunoglobulin and lymphocyte stimulation index were significantly decreased in T1 group whereas in Zn supplemented group decline trend was less. Henceforth, it was concluded that 100 ppm Zn is helpful in reducing burden of Cd induced biochemical and oxidative stress in goats.

Phytotoxic Effect of Cadmium Induced Stress on LAI, CGR and Yield of Rice Plant (Oryza sativa L.)

Background: Cadmium is a noxious heavy metal that is commonly found in the soil while its concentration is increasing in soil because of industrialization at the global level. It does not only reduce the yield of crops but also adulterates food and underground drinkable water. The availability of Cd beyond the threshold level may cause many problems in human beings. Exposure to Cd for a short period causes inhalation, muscle pain and lung damage while for a longer time, it may cause bone and kidney-related issues. The present study aimed to study the phytotoxic effect of Cadmium-induced stress on morphological changes and their impact on the yield of rice plants. Methods: Present piece of research work was carried out on the Research Farm of Lovely Professional University, Department of Agronomy, School of Agriculture, in 2019-20. A range of five different concentrations of CdCl2 was comprised with statistical design CRD. The range of 100 to 300 ppm CdCl2 was considered to induce Cd-based stress. The standard procedures were followed to measure the growth parameters at regular intervals while the SPSS software was used to analyze the significance of the data. Result: Cadmium-induced stress was created artificially in an experiment to analyze the detrimental effect on the growth and yield of rice plants. As the externally imposed cadmium stress increased from the control set (T0), all the growth parameters along with grain yield, Biological yield hill-1 (g) and harvest index (%) started to decline till the maximum concentrations of CdCl2, i.e. 300 ppm. As per the DAT is concerned, % reduction of each parameter was also calculated to the known intensity of toxicity where the maximum % reduction was recorded at 50 DAT in the leaf area and LAI (38.47% and 38.38%) while the maximum % reduction of CGR was recorded at 50-75 DAT (35%). However, the % reduction in grain yield, biological yield hill-1 (g) and harvest index % were recorded at the highest concentration of CdCl2 (31.87, 28.70 g and 11.1%).

Cadmium exposure decreases fasting blood glucose levels and exacerbates type-2 diabetes in a mouse model.

Although the effects of cadmium (Cd) on the development of diabetes have been extensively investigated, the relationship between Cd exposure and the severity of established diabetes is unclear. Herein, we investigate the effects of long-term exposure to Cd in a streptozotocin-induced mouse model of type-2 diabetes mellitus (T2DM) and the underlying mechanism. C57BL/6 Mice were divided into the following four groups: (1) control group; (2) Cd-exposed group; (3) diabetic group; (4) Cd-exposed diabetic group. Cd exposure was established by the administration of 155 ppm CdCl2 in drinking water. After 25 weeks of treatment, serum fasting glucose and insulin were measured. Meanwhile, the liver and pancreas specimens were sectioned and stained with Hematoxylin and eosin. Gluconeogenesis, glycolysis, lactate concentration, and fibrosis in liver were evaluated. Clinical signs attributable to diabetes were more apparent in Cd-exposed diabetic mice, while no effects of Cd exposure were found on non-diabetic mice. Cd exposure significantly decreased fasting blood glucose (FBG) levels in diabetic group. We further demonstrated that the glycolysis related hepatic enzymes, pyruvate kinase M2 (PKM-2) and lactic dehydrogenase A (LDHA) were both increased, while the gluconeogenesis related hepatic enzymes, phosphoenolpyruvate-1 (PCK-1) and glucose-6-phosphatase (G6Pase) were both decreased in Cd exposed diabetic mice, indicating that Cd increased glycolysis and inhibited gluconeogenesis in diabetic model. Moreover, lactate accumulation was noted accompanied by the increased inflammation and fibrosis in the livers of diabetic mice following Cd exposure. Cd exposure disturbed glucose metabolism and exacerbated diabetes, providing a biological relevance that DM patients are at greater risk when exposed to Cd.

Oral Subacute Exposure to Cadmium LOAEL Dose Induces Insulin Resistance and Impairment of the Hormonal and Metabolic Liver-Adipose Axis in Wistar Rats.

Cadmium is a nonessential transition metal considered one of the more hazardous environmental contaminants. The population is chronically exposed to this metal at low concentrations, designated as the LOAEL (lowest observable adverse effect level) dose. We aimed to investigate whether oral subacute exposure to cadmium LOAEL disrupts hormonal and metabolic effects of the liver-adipose axis in Wistar rats. Fifty male Wistar rats were separated into two groups: control (standard normocalorie diet + water free of cadmium) and cadmium (standard normocalorie diet + drinking water with 32.5 ppm CdCl2). After 1 month, zoometry, a serum lipid panel, adipokines, and proinflammatory cytokines were evaluated. Tests of glucose and insulin tolerance (ITT) and insulin resistance were performed. Histological studies on structure, triglyceride distribution, and protein expression of the insulin pathway were performed in the liver and retroperitoneal adipose tissue. In both tissues, the cadmium, triglyceride, glycogen, and proinflammatory cytokine contents were also quantified. The cadmium group developed dyslipidemia, glucose intolerance, hyperinsulinemia, hyperleptinemia, inflammation, and selective insulin resistance in the liver and adipose tissue. In the liver, glycogen synthesis was diminished, while de novo lipogenesis increased, which was associated with low GSK3β-pS9 and strong expression of SREBP-1c. Dysfunctional adipose tissue was observed with hypertrophy and lipolysis, without changes in SREBP-1c expression and low glycogen synthesis. Both tissues accumulated cadmium and developed inflammation. In conclusion, oral subacute cadmium LOAEL dose exposure induces inflammation, insulin signaling modifications, an early insulin resistance stage (insensibility), and impairment of the hormonal and metabolic liver-adipose axis in Wistar rats.

Chronic Cadmium Exposure Alters Cardiac Matrix Metalloproteinases in the Heart of Sprague-Dawley Rat.

The aim of this study was to evaluate the role of chronic cadmium exposure in modulating cardiac matrix metalloproteinases (MMPs) in the heart of rats. Adult male Sprague-Dawley rats were exposed to 15 ppm CdCl2 in drinking water for 10 weeks followed by withdrawal of cadmium treatment for 4 weeks. Following the completion of the treatment, gene expression of inflammatory mediators (IL-1β, IL-6, IL-10, TNF-α and NF-κB), protein expression of MMP-2, MMP-9 and their respective inhibitors- TIMP-1 and TIMP-2, and gelatinolytic activity of MMP-2 and MMP-9 were determined. At the protein level, cadmium incites a differential effect on the expression and activity of gelatinases and their endogenous inhibitors in an exposure-dependent manner. Results also show that the administered cadmium dose elicits an inflammatory response until week 10 that slightly diminishes after 4 weeks. This study provides evidence of cadmium-induced imbalance in the MMP-TIMP system in the cardiac tissue. This imbalance may be mediated by cadmium-induced inflammation that could contribute to various cardiovascular pathologies.

Studies on the effect of sodium arsenate & cadmium chloride on Pithophora oedogonia (Mont.) Wittrock 1877

Cadmium and Arsenic are heavy metals although not common in our environment, its threat in certain places are aggravated due to anthropogenic factors. To know its critical role on plants the investigation was made using Na2HAsO4 and CdCl2 treatment on Pithophora oedogonia (Mont.) Wittrock 1877. The observations were made after 14 days of treatment. The changes were noted. In both cases, the treated cells exhibited gradual disruption of cell wall and cell membrane. The chlorophyll content initially increased and finally decreased due to the notable destruction of chloroplasts in both treated cells. A profuse number of akinetes were observed at 100 ppm and 150 ppm of Na2HAsO4 and CdCl2 treated media. Decrease in protein content was started at 100 ppm in both cases. The lipid content initially decreased at 50 ppm and at 100 ppm lipid profile increased in terms of toleration to the Na2HAsO4 and CdCl2 stress. Pithophora oedogonia (Mont.) Wittrock 1877 exhibited more sensitivity to CdCl2 stress & showing abrupt changes in chlorophyll-a and chlorophyll-b production. The carotenoid production shown more sensitivity in Na2HAsO4 stress. Total phenol production was decreased initially and at 200 ppm CdCl2 stress had shown significant enhancement than the control set but at the 200 ppm of Na2HAsO4 shown inhibitory effect.

Cadmium Exacerbates Acetic Acid Induced Experimental Colitis in Rats

Background: Increase in the incidences of inflammatory bowel disease (IBD) in developing countries is a pointer to the role metal toxicants may play in its pathogenesis. Cadmium (Cd) has been implicated in the etiology of diseases involving several tissues including the colonic mucosa. This present study aimed at investigating the effects of oral cadmium exposures on healing of acetic acid (AA)-induced colitis in rats. Methods and Findings: Male Wistar rats (100-120 g) were grouped and exposed to cadmium as follows: Control (water), Cd25 (25 ppm CdCl2), Cd50 (50 ppm CdCl2), Cd100 (100 ppm CdCl2) for four weeks. Colitis was induced by intrarectal administration of 2 ml 4% acetic acid. Rats were sacrificed and colons were resected on days 0, 3, 7 and 14 of colitis induction. Weekly body weight, diarrheal and macroscopic scores, organ weights, neutrophil/lymphocyte ratio (NLR), malondialdehyde (MDA) concentration, and regeneration in colonic tissues were studied microscopically. Cadmium significantly (p<0.05) decreased weight gain (%) at weeks 3 and 4 in Cd100 group, significantly (p<0.05) increased stool consistency scores on day 5 in Cd100 group, increased colon macroscopic scores in Cd100 group on days 3 and 7, significantly (p<0.05) increased neutrophil/ lymphocyte ratio on days 0 and 7 in Cd50 and Cd100, and colonic MDA concentrations in each of Cd25, Cd50 and Cd100 from day 3 till day 14. Colon histopathology persisted till day 14 in Cd100 group. Conclusions: These data indicate that cadmium delayed healing of acetic acid induced colitis and inflammatory pathways may be implicated.

Possible molecular mechanism underlying cadmium-induced circadian rhythms disruption in zebrafish

This study was aimed to explore the mechanisms underlying cadmium-induced circadian rhythms disruption. Two groups of zebrafish larvae treated with or without 5 ppm CdCl2 were incubated in a photoperiod of 14-h light/10-h dark conditions. The mRNA levels of clock1a, bmal1b, per2 and per1b in two groups were determined. Microarray data were generated in two group of samples. Differential expression of genes were identified and the changes in expression level for some genes were validated by RT-PCR. Finally, Gene Ontology functional and KEGG pathway enrichment analysis of differentially expressed genes (DEGs) were performed. In comparison with normal group, the mRNA levels of clock1a, bmal1b, and per2 were significantly changed and varied over the circadian cycle in CdCl2-treated group. DEGs were obtained from the light (84 h, ZT12) and dark (88 h, ZT16) phase. In addition, G-protein coupled receptor protein signaling pathway and immune response were both enriched by DEGs in both groups. While, proteolysis and amino acid metabolism were found associated with DEGs in light phase, and Neuroactive ligand-receptor interaction and oxidation-reduction process were significantly enriched by DEGs in dark phase. Besides, the expression pattern of genes including hsp70l and or115-11 obtained by RT-PCR were consistent with those obtained by microarray analysis. As a consequence, cadmium could make significant effects on circadian rhythms through immune response and G protein-coupled receptor signaling pathway. Besides, between the dark and the light phase, the mechanism by which cadmium inducing disruption of circadian rhythms were different to some extent.

Preferential Elimination of Older Erythrocytes in Circulation and Depressed Bone Marrow Erythropoietic Activity Contribute to Cadmium Induced Anemia in Mice.

Feeding cadmium chloride (50 or 1000 ppm CdCl2 in drinking water, ad libitum) to C57BL/6 mice resulted in a significant and sustained fall in blood erythrocyte count and hemoglobin levels that started 4 and 3 weeks after the start of 50 and 1000 ppm cadmium doses respectively. A transient yet significant reticulocytosis occurred during the first 4 weeks of cadmium treatment. Using the recently developed double in vivo biotinylation (DIB) technique, turnover of erythrocyte cohorts of different age groups was simultaneously monitored in control and cadmium treated mice. A significant accumulation of younger erythrocytes and a concomitant decline in the relative proportions of older erythrocytes in circulation was observed in both 50 and 1000 ppm cadmium groups indicating that older erythrocytes were preferentially eliminated in cadmium induced anemia. A significant increase in the erythropoietin levels in plasma was seen in mice exposed to 1000 ppm cadmium. Levels of inflammatory cytokines (IL1A, IL6, TNFα, IFNγ) were however not significantly altered in cadmium treated mice. A significant increase in cellular levels of reactive oxygen species (ROS) was observed in older erythrocytes in circulation but not in younger erythrocytes. Erythropoietic activity in the bone marrows and spleens of cadmium treated mice was examined by monitoring the relative proportion of cells belonging to the erythroid line of differentiation in these organs. Erythroid cells in bone marrow declined markedly (about 30%) in mice in the 1000 ppm cadmium group but the decline was not significant in the 50 ppm cadmium group. Cells representing various stages of erythroid differentiation in bone marrow and spleen were enumerated flow cytometrically by double staining with anti-Ter119 and anti-transferrin receptor (CD71) monoclonal antibodies. Decline of erythroid cells was essentially confined to pro-erythroblast and erythroblast-A, along with a concurrent increase in the splenic erythroid population indicating a stress response. In short cadmium exposure causes preferential clearance of older erythrocytes from circulation along with a depressed erythropoietic activity at higher doses.

Cadmium exposure inhibits MMP2 and MMP9 activities in the prostate and testis

Matrix metalloproteinases (MMPs) are zinc (Zn2+) and calcium (Ca2+) dependant endopeptidases, capable of degradation of numerous components of the extracellular matrix. Cadmium (Cd2+) is a well known environmental contaminant which could impair the activity of MMPs. In this sense, this study was conducted to evaluate if Cd2+ intake inhibits these endopeptidases activities at the rat prostate and testicles and if it directly inhibits the activity of MMP2 and MMP9 at gelatinolytic assays when present in the incubation buffer. To investigate this hypothesis, Wistar rats (5 weeks old), were given tap water (untreated, n = 9), or 15 ppm CdCl2 diluted in drinking water, during 10 weeks (n = 9) and 20 weeks (n = 9). The animals were euthanized and their ventral prostate, dorsal prostate, and testicles were removed. These tissue samples were processed for protein extraction and subjected to gelatin zymography evaluation. Additionally, we performed an experiment of gelatin zymography in which 5 μM or 2 mM cadmium chloride (CdCl2) was directly dissolved at the incubation buffer, using the prostatic tissue samples from untreated animals that exhibited the highest MMP2 and MMP9 activities in the previous experiment. We have found that CdCl2 intake in the drinking water led to the inhibition of 35% and 30% of MMP2 and MMP9 (p < 0.05) at the ventral prostate and testis, respectively, in Cd2+ treated animals when compared to controls. Moreover, the activities of the referred enzymes were 80% and 100% inhibited by 5 μM and 2 mM of CdCl2, respectively, even in the presence of 10 mM of CaCl2 within the incubation buffer solution. These important findings demonstrate that environmental cadmium contamination may deregulate the natural balance in the extracellular matrix turnover, through MMPs downregulation, which could contribute to the toxic effects observed in prostatic and testicular tissue after its exposure.

Acute enhancement of non‐rapid eye movement sleep in rats after drinking water contaminated with cadmium chloride

Cadmium (Cd) is a heavy metal widely used or effused by industries. Serious environmental Cd pollution has been reported over the past two centuries, whereas the mechanisms underlying Cd-mediated diseases are not fully understood. Interestingly, an increase in reactive oxygen species (ROS) after Cd exposure has been shown. Our group has demonstrated that sleep is triggered via accumulation of ROS during neuronal activities, and we thus hypothesize the involvement of Cd poisoning in sleep-wake irregularities. In the present study, we analyzed the effects of Cd intake (1-100 ppm CdCl₂ in drinking water) on rats by monitoring sleep encephalograms and locomotor activities. The results demonstrated that 100 ppm CdCl₂ administration for 28 h was sufficient to increase non-rapid-eye-movement (non-REM) sleep and reduce locomotor activities during the night (the rat active phase). In contrast, free-running locomotor rhythms under constant dim red light and their re-entrainment to 12:12-h light/dark cycles were intact under chronic (1 month) 100 ppm CdCl₂ administrations, suggesting a limited influence on circadian clock movements at this dosage. The relative amount of oxidized glutathione increased in the brain after the 28-h 100 ppm CdCl₂ administrations similar to the levels in cultured astrocytes receiving H₂O₂ or CdCl₂ in culture medium. Therefore, we propose Cd-induced sleep as a consequence of oxidative stress. As oxidized glutathione is an endogenous sleep substance, we suggest that Cd rapidly induces sleepiness and influences activity performance by occupying intrinsic sleep-inducing mechanisms. In conclusion, we propose increased non-REM sleep during the active phase as an index of acute Cd exposure.

The metallohormone cadmium modulates AhR-associated gene expression in the small intestine of rats similar to ethinyl-estradiol

Cadmium (Cd) affects the expression of estrogen receptor (ER) and aryl hydrocarbon receptor (AhR)-associated genes in rat uterus and elicits estrogen-like activity in vitro. The small intestine is highly exposed to dietary Cd which may mimic or antagonize estrogen action in this tissue. We investigated the effects of Cd and 17-alpha-ethinylestradiol (EE₂) on AhR-associated gene expression after oral exposure of ovariectomized female Wistar rats, and metallothionein (Mt1a) expression as a typical metal-response marker. Mt1a in the small intestine was strongly induced by co-treatment with CdCl₂ at 2 mg/kg b.wt (Cd 2) and 0.1 mg/kg b.wt EE2 than by the single compound (3-day gavage). The Cd 2-induced down-regulation of Cyp1a1, Gsta2, and Nqo1 mRNA was not antagonized by pure anti-estrogen (2.5 mg/kg b.wt ZK191703 s.c., ZK). Interestingly, the EE₂-induced down-regulation of Cyp1a1, Gsta2, and Nqo1 mRNA was antagonized by Cd 2 in vivo and in colon cancer cell lines (HT-29 and CaCo-2, treated 5 days with Cd 1 µM and/or E₂ 0.01 µM) with low or no ER-beta expression. Dose dependency was studied after Cd exposure with drinking water (5 and 50 ppm CdCl₂ equivalent to 0.4 and 4 mg/kg b.wt; Cd 0.4, Cd 4) for 28 days and EE₂ as reference. Intestinal Mt1a expression was dose dependently induced, while AhR target genes were down-regulated by Cd 0.4 similar to EE₂ and more pronounced than by Cd 4. We propose that Cd modulates intestinal AhR-associated gene expression similar to estrogens, but (contrary to its effects in uterus) via ER-independent and/or ER-beta-mediated mechanisms. Our new data suggest interference of Cd with estrogen and AhR signaling in the small intestine.

Absorption, translocation, and remobilization of cadmium supplied at different growth stages of rice

Cadmium (Cd) is absorbed by rice root and transferred into the other rice organs including grain. A solution-culture experiment was conducted to investigate the absorption and distribution of Cd supplied at different growth stages of rice. Two rice cultivars, a japonica ‘Chucheong’ and a tongil-type ‘Milyang23’ that exhibit high and low ability of Cd absorption by root and accumulation in grain were grown in culture solution and subjected to 2 ppm CdCl2 treatment for 2 weeks at four different growth stages: before panicle initiation stage (BPI), after panicle initiation stage (API), early ripening stage (ER), and mid-ripening stage (MR). Cd concentration and accumulation in rice organs were measured at harvest. The two rice cultivars accumulated two to three times greater amounts of Cd in grain in the two Cd treatments before heading (BPI and API treatments) than in the Cd treatment after heading (ER and MR treatment). The higher grain Cd accumulation in BPI and API treatments was not attributed to the higher Cd uptake but to the higher translocation from root to shoot and the higher redistribution from shoot to grain than ER and MR treatments These results imply that the remobilization of Cd through phloem during leaf senescence is the major process for Cd accumulation in rice grain rather than direct transport of absorbed Cd through the xylem-phloem transfer to grain. ‘Milyang23’ absorbed significantly smaller amount of Cd than ‘Chucheong’. However, ‘Milyang23’ accumulated more than a three times larger amount of Cd in grain compared to ‘Chucheong’ as the former exhibited the higher root-shoot translocation and shoot-grain remobilization as well. It indicates that the greater Cd translocation from root to shoot and subsequent higher Cd remobilization from shoot to grain, not the higher absorption ability, have led to the higher Cd accumulation and concentration in grain of ‘Milyang23’.

Selection and Identification of Differential Proteins of Liver Revealed with Proteomics in Achatina Fulica Under Induction of Cadmium

Abstract In comparison with direct lysis, acetone/trichloroacetic acid (TCA) precipitation was selected to optimize and separate whole protein from the liver tissue of Achatina fulica (AF), and approximately 600 protein spots were obtained in gel. Using the cabbage exposed to 0.05 ppm CdCl2 as AF food, the liver was selected to reveal the stress proteins in the AF exposed to acute cadmium toxicity. Fourteen of differential protein spots in AF liver were obtained by proteomics, and then seven of these spots were further identified by both peptide mass fingerprint and database search, which indicated that these proteins in part were identified to be heat shock protein, methyltransferase, ABC transporter, molybdate transporter subunit, and phosphoglycerate mutase. We suggest that these significant proteins are connected with metabolism pathway of cadmium, biomarkers for monitoring the contamination level of the cadmium, and evaluating the crisis level of both food and soil.

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.

Biochemical and Haematological Study in Rats Exposed to Cadmium Chloride in Drinking Water

The objective of this study was investigate the Physiological effect ofdifferent concentrations of cadmium chloride in drinking water on somebiochemical and haematological parameters of male rats. Animals in thisexperiment were randomly divided into four equal groups and treated for 15weeks as follows : Rats in control group were offered ordinary tap water ,while animal in M1 , M2 , and M3 were received 10 , 20 , 30 ppm Cdcl2 indrinking water, respectively. The activity of Alanine aminotransferase(ALP), Aspartate aminotrasferase (AST) and alkaline phosphatase (ALP) inserum were measured. Further mor, hemoglobin concentration (Hb) andwhite blood cells count (WBCs) were detected. The result revealed thataddition of cadmium chloride in different concentrations in drinking watercaused a significant increase in activity of serum of ALT in treated group(M1 , M2 , M3 ) as compound with control. Within the time the activity ofserum AST was significantly increased in three treated group as comparedwith pretreatment period. On the other hand , significant increase in serumALP concentration were show in both M1 and M3 treated groups at 12th and15th week of the treatment as compared with control group. Significantdecrease in haemoglobin concentration were observed in M1 , M2 , M3 from9th week to the end of experiment comparing to control. While cadmiumchloride treatment caused significant increase in total white blood cells countin treated groups as compared with control group. On Conclusion, it seemslikely that exposure of male rats to cadmium chloride at level above thepermissive one had induced clear biochemical and haematological changes.

Salicylic Acid Alleviates the Cadmium Toxicity in Chinese Cabbages (Brassica chinensis)

To test the effects of Salicylic Acid (SA) on physiological changes of plants under cadmium stress one cultivar of Chinese cabbage (Brassica chinensis) cadmium resistance, Changkenxiaobaicai (tolerance) were studied with pots cultures. Like other organisms Plants have adaptatives mechanisms whereby they are able to respond to both nutrient deficiency and toxicities. Plants materials were originated from the vegetable market in Wuhan, Hubei China. The seeds were tested on the pot cultures in the green house. The results of our experiments were quite different between the treatments. The combined treatment Cd 5 ppm + SA 500 mmol L(-1) during our experiment showed that the activity of peroxidase and superoxidase dismutase in the cabbages were induced, the total chlorophyll content increased significally by 25.38%, chl a/b about 43.01% and total biomass about 41.67%, both in comparison with the control. The soluble sugar content increased significantly to about 25.47% in comparison with the control. The electrolyte leakages were less affected. Under SA treatment only, the chlorophyll content, chl a/b content increased to about 18.85%, in comparison with the control. Plant biomass increased about 18.90% with the addition of SA in the culture. SA treatment can increase or decrease the Chinese cabbages metabolism. Plants were exposed to 5 ppm CdCl2 for 5 days under natural light. Then they were cultivated with Hoagland nutrient solution, which served as control, nutrient solution supplemented with 5 ppm CdCl2. Five days after Cd treatment, seedlings were harvested. The experiment was performed in triplicate.

Immunohistochemical and ultrastructural changes in the renal cortex of cadmium-treated rats.

The aim of this study was to determine the cadmium-induced immunohistochemical and morphological changes in the renal cortex of adult male rats exposed to high doses of cadmium for 30 d. Animals used as controls received a standard diet and water ad libitum. The animals used for this study received 15 ppm CdCl2 in their drinking water for 1 mo. The mean arterial pressure (MAP), the mean blood Cd level, and the mean tissue Cd content were significantly higher when compared to controls (p < 0.01). Immunohistochemical studies demonstrated a weak labeling to type IV collagen and laminin, but a strong labeling to fibronectin in the renal cortex of the Cd-treated animals when compared to controls. The ultrastructural alterations found in Cd-treated rats were a diminution in the amount of filtration slits, increased fusion of foot processes in epithelial cells of the glomeruli, increase of lysosomal structures and pinocytic vesicles as well as large mitochondria in proximal tubule cells, and degenerated cells in distal tubules. Additionally, the glomerular basement membrane was slightly thickened. In conclusion, cadmium toxicity results in alterations in the renal extracellular matrix and tubular or glomerular cells, which could play an important role in renal dysfunction.