Tissue Accumulation Of Cadmium Research Articles

Oxidative response to accumulation of trace metals in tissue of two bivalves, the Asian green mussel Perna viridis and the blood cockle Tegillarca granosa, living in Pattani Bay, Thailand.

Using bivalves to indicate aquatic pollutants was favorable for discerning the negative effects of high levels of metal accumulation in tissue. We investigated the correlation between trace metal accumulation and the tissue oxidative response of two bivalves. The Asian green mussel Perna viridis and the blood cockle Tegillarca granosa were sampled along with seawater and sediments from three locations around Pattani Bay, Thailand. Accumulation of nine trace metals (cadmium, cobalt, copper, chromium, nickel, manganese, iron, zinc, and lead) in seawater, sediments, and tissue and the oxidative tissue response were evaluated. Metal bioaccumulation factor, biota-sediment accumulation factor, and histopathology were also indicated. The present study found that P. viridis and T. granosa were macroconcentrators and bioaccumulative of cadmium, and their tissue accumulation of cadmium was strongly related to lipid peroxidation activation. Perna viridis exhibited a higher oxidative response than T. granosa, as indicated by malondialdehyde, catalase, and reduced glutathione levels. The present study indicated that P. viridis and T. granosa were macroconcentrators and bioaccumulative of cadmium, and their tissue accumulation of cadmium was strongly related to lipid peroxidation activation. Research has shown discernible negative effects of a high level of metal accumulation in tissue, and deformed and damaged tissues were present in the gills, digestive glands, intestines, and feet of P. viridis and T. granosa.

Bioaccessibility as a determining factor in the bioavailability and toxicokinetics of cadmium compounds

Cadmium toxicity occurs where there is absorption and accumulation of cadmium ions (Cd2+) in tissues beyond tolerable levels. Significant differences in the release of Cd2+ from cadmium compounds in biological fluids, like gastric fluid, may indicate differences in bioavailability and absorption. This means that direct read-across from high solubility cadmium compounds to lower solubility compounds may not accurately reflect potential hazards. Here, the relative bioaccessibility in gastric fluid of cadmium telluride and cadmium chloride was evaluated using in vitro bioelution tests whilst the toxicokinetic behavior of these two compounds were compared after dietary administration for 90 days in male and female Wistar Han rats following OECD TG 408. Cadmium chloride was highly bioaccessible, whilst cadmium telluride showed low solubility in simulated gastric fluid (90 % and 1.5 % bioaccessibility, respectively). This difference in bioaccessibility was also reflected by a difference in bioavailability as shown by the difference in the liver and kidney concentrations of cadmium after repeat oral exposure. Feeding at doses of 750 and 1500 ppm of cadmium telluride did not result in tissue cadmium levels above the lower limit of quantification (LLOQ). In contrast, feeding with a lower test substance concentration yet higher concentration of bioaccessible cadmium (30 ppm cadmium chloride) resulted in tissue accumulation of cadmium. Only slight, non-adverse changes in hematology and clinical chemistry parameters were seen at these doses, indicating an absence of significant cadmium mediated toxicity towards target organs (kidney and liver), reflected in minimal cadmium accumulation in these organs.This study demonstrates that bioelution tests can help determine the bioaccessibility of cadmium, which can be used to estimate the potential for target tissue toxicity based on known toxicokinetic profiles and threshold levels for cadmium toxicity, while reducing and refining animal testing.

Influence of microplastics on the accumulation and chronic toxic effects of cadmium in zebrafish (Danio rerio)

As the accumulation of microplastics (MPs) in the environment continues to rise, more concerns focus on the health risk of combined exposure to MPs and other contaminants. The aim of this study is to investigate the influences of MPs on the tissue-accumulation of cadmium (Cd) in zebrafish and explore the related chronic toxic effects induced by combined exposure of Cd and MPs. After co-exposure to MPs and Cd for 3 weeks, 20 and 200 μg/L MPs increased the accumulation of Cd in zebrafish livers (46% and 184%), guts (10% and 25%) and gills (9% and 46%). The Cd accumulation was gill > gut > liver. Comprehensive analyzes of biochemical biomarkers, histopathological observation and functional gene expression firstly demonstrated that the presence of MPs enhanced the toxicity of Cd on zebrafish and the combined exposure caused oxidative damage and inflammation in zebrafish tissues. Collectively, our results highlight the chronic effects of combined exposure to MPs and heavy metals.

Effect of hemolytic and iron-deficiency anemia on intestinal absorption and tissue accumulation of cadmium

Abnormal iron (Fe) metabolism induces iron-deficiency anemia (FeDA) and also affects body cadmium (Cd) accumulation. However, whether hemolytic anemia also affects Cd metabolism is not known. We compared the intestinal absorption and tissue accumulation of Cd after oral administration of Cd to mice with hemolytic anemia induced by treatment with phenylhydrazine (PHA mice) to that in mice with FeDA. Although the hematocrit decreased significantly in mice with either type of anemia, the Fe concentration decreased in the livers and kidneys of FeDA mice, but increased in those of PHA mice. After an oral administration with various amounts of Cd, hepatic and renal Cd concentrations significantly increased in both FeDA and PHA mice. An intraduodenal injection of Fe raised the hepatic Fe content in FeDA mice to the control level and raised the hepatic Fe content in PHA mice to 2.4 times that in control mice. Intestinal divalent metal transporter 1 (DMT1) expression increased significantly in mice with both types of anemia. These data indicate that, despite the accumulation of hepatic Fe associated with PHA, PHA also significantly increases hepatic and renal Cd accumulation according to an stimulation of intestinal DMT1 expression, as occurs in FeDA mice. This suggests that anemia may be a risk factor for Cd accumulation.

Tissue accumulation of cadmium following oral administration to metallothionein-null mice

To verify the roles of intestinal metallothionein (MT) as a barrier against ingested cadmium (Cd) and as a transporter of mucosal Cd to the kidneys, the distribution of orally administered Cd was compared between normal and MT-I and -II knock-out (MT-null) mice. Following single administration of a low dose of Cd (0.1 mg/kg), hepatic Cd levels and the sum of total Cd in the liver and kidney (K+L) were significantly less in the controls than in MT-null mice. The ratio of Cd in the kidney to the liver (K/L) was significantly lower in the MT-null mice. On the other hand, at a high Cd dose (2.0 mg/kg), K+L and K/L were not significantly different between the two groups. However, following oral pretreatment with zinc (Zn) to the high dose control mice, K+L significantly decreased and K/L significantly increased. No such effects of Zn pretreatment were observed in MT-null mice. Similar differences in K+L and K/L were also observed between the control and MT-null mice groups following the Zn pretreatment. Repeated administration of Cd for 4 weeks resulted in significantly larger K/L distribution in control mice over null mice. These results suggest that MT in the intestinal mucosa functions both as a protective barrier against Cd absorption and as an extracellular transporter of Cd to the kidney.

Effect of co-exposure to ethanol and cadmium in rats.

Metabolism and toxicity of heavy metals may be influenced by certain factors such as protein malnutrition, essential element deficiency or alcoholism. Ethanol has been found to enhance the absorption of lead in body and alcoholics have been reported to be more susceptible to lead intoxication. As alcoholism may be common among industry workers and a significant section of population, who may be exposed to cadmium, it was considered of interest to investigate the influence of ethanol-cadmium co-exposure on cadmium sensitive hepatic, renal and serum enzymes, tissue accumulation of cadmium, essential trace element status and cadmium induced hepatic metallothione in synthesis in rats.

Tissue accumulation of cadmium as a function of blood concentration

We have provided data relating Cd concentration in tissue to about a 40-fold range in blood Cd concentration. Osmotic pumps containing cadmium chloride were subcutaneously implanted in male New Zealand white rabbits. The pumps continuously delivered either 0.15 or 1.5 mg Cd/d. Blood and plasma levels of Cd were measured weekly throughout the study. After 28 d, the rabbits were killed and tissue concentrations of Cd determined by atomic absorption spectrophotometry. Less than 10% of the total Cd in the blood was carried in the plasma, the remainder was associated with the blood cells, where it was bound mainly to metallothionein. We found the blood and tissue levels of Cd were correlated for each tissue we investigated. There was a wide range in affinity of the tissues for Cd; liver and kidney had the highest Cd uptake, whereas brain affinity was about 500 times less than liver.

Effects of Diet on Tissue Accumulation of Cadmium and Its Toxicological Indicators (Regular Presentations) (Proceedings of the 11 th Symposium on Environmental Pollutants and Toxicology)

Effects of Diet on Tissue Accumulation of Cadmium and Its Toxicological Indicators (Regular Presentations) (Proceedings of the 11 th Symposium on Environmental Pollutants and Toxicology)

Effects of dietary zinc, manganese, and copper on tissue accumulation of cadmium by Japanese quail.

The beneficial effects of a combined dietary supplement of Zn, Cu, and Mn in decreasing Cd absorption was previously reported. The purpose of this study was to investigate the individual and combined effects of these three elements. In the first two experiments, day-old Japanese quail were fed basal diets containing either requirement amounts of Zn (30 ppm) and Mn (12 ppm) and slightly above requirement levels of Cu (5 ppm). From Day 7 birds were fed either the basal diet or diets containing combinations at twice these concentrations; a 2 X 2 X 2 factorial design was used. 109Cd content and Cd concentration of these diets were 100 mu Ci and 145 micrograms/kg, respectively. In the third experiment, day-old birds were fed either the basal diet or a basal diet containing 109Cd and single additional supplements of either Zn, Cu, or Mn. All birds were killed at 14 days of age. The Cd concentration was determined for the duodenum, jejunum-ileum, liver, and kidney. When the experimental diets were fed for 7 days, only Zn had a protective effect against Cd. Whereas none of the elements reduced the Cd concentration of the duodenum, Zn reduced the Cd in the jejunum-ileum, liver, and kidney by approximately 66, 21, and 11%, respectively. Cu and Mn caused occasional increases of Cd in some tissues. Feeding the experimental diets for 2 weeks resulted in similar responses. Zn nutrition appears to play an important role in protecting against dietary Cd absorption.

Effect of cadmium administration on growth, excretion, and tissue accumulation of cadmium and histological alterations in calcium-sufficient and -deficient rats: An equalized feeding study

To clarify the effect of cadmium on rats, excluding the influence of decrease in food consumption, animals were separated into three groups and fed three different semisynthetic diets by equalized dietary regimens. The first group was fed a normal diet, 50 ppm of cadmium was added to the diet of the second group, while the third group was fed a calcium-deficient diet to which 50 ppm of cadmium was added. In cadmium-treated rats, growth was depressed, cadmium concentration in liver and kidney increased, and histological abnormalities in liver, kidney, and bone were prominent. These abnormalities were more significant in calcium-deficient-cadmium-treated rats than in calcium-sufficient-cadmium-treated rats. The results indicate that these abnormalities are not associated with the decrease in food consumption but rather are related only to cadmium poisoning.