To investigate the effect of cadmium and cadmium binding protein on the electron transport system and conformational changes of rat kidney mitochondria, various cadmium concentration were treated in vitro and respiration rate, NADH-CoQ reductase activity were measured. Ultrastructural changes at state IV respiration were also observed. CdBP was isolated from the rat liver by Sephadex G-75 column fractionation and treated in vitro with cadmium. Also mitochondrial state IV respiration rate was measured. When cadmium was treated in vitro, state IV respiration and enzyme activity were decreased and ultrastructural transformation of mitochondria from a condensed to an orthodox conformation was inhibited under state IV respiration. In case cadmium and CdBP were treated together, oxygen consumption was more increased than cadmium only. Conformational changes of mitochondria from a condensed to orthodox conformation were also observed. This indicates that CdBP have a protective effect against cadmium toxicity.
Mulberry leaf sprayed on at the various concentrations of cadmium (Cd) was fed on the just molted fifth instar through the 6th day of the fifth instar and content of cadmium and zinc in the feces, organs and tissues involved were analyzed by spectrophotometer. Along with the effect of those heavy metals on development of the relevant organs and tissues sexwise. 1. The residual content of cadmium on mulberry leaf was about 50% of the total cadmium and the weight of feces disposed from the cadmium fed larvae was less than the control. There was distinctive differences in female-wise disposal of feces between cadmium treatment and control ; cadmium treatment female larvae disposed less feces than female of control. 2. Fourteen percent of the total dry weight of the anterior plus the middle silkgland and of the posterior silkgland in cadmium 100ppm treatment was decreased in female but only 9% of the anterior plus middle silkgland in male was made, showing no decrease the weight of the posterior silkgland in male. 3. Decrease of the dry weight of the silkgland, fat body and hindgut was made in cadmium 100ppm treatment and contrarily the weight of midgut and malphihian tube were increased. The total larval weight of the female and male were decreasd in cadmium 100ppm treatment and the decreasing ratio was higher in famale. 4. There wasa no detection of cadmium in all of the organs and tissues of the control and in those of the cadmium treatment the high residual content was in order of the midgut, hindgut, malphighian tube and head. A slight accumulation of cadmium was shown in fat body and silkgland. 5. Cadmium accumulation in the midgut was higher than in female but in the fat body, malphighian tube, trachea and integument was contrarily high in the female than male. 6. The total zinc content of the larvae was below 60ppm in the control and 80ppm in cadmium 100ppm treantment. The increase of zinc content in cadmium treatment was made on silkgland, malphigian tube and midgut but contrarily the decrease of zinc content in fat body was resulted. 7. In cadmium treatment, much more cadmium accumulation took place in the female and zinc accumulation was made much more in the male.
An animal experiment was performed to investigate the effects of dietary cadmium on growth rates and cadmium accumulations in internal organic tissues and blood by feeding mice with dietary $cdcl_2$ additives and/or brown rice with high cadmium content as during a 12-week feeding period. The results were as follows : Mice weights decreased with increasing levels of dietary cadmium at the end of a 9-week feeding period. The weights of mice organs in the cadmium-free feeding group were higher than in the cadmium-added groups, and the weights of mice organs did not show any significant differences among feeding groups with different levels of dietary cadmium. The concentrations of cadmium in kidney and liver were much higher than in other internal organs and blood, and the next higher concentration was in the heart. The cadmium accumulation in all internal organs and blood increased with increasing dietary cadmium levels, respectively. The ratios of cadmium accumulation in organ tissues and total blood of cadmium-added groups increased with decreasing dietary cadmium levels.
This study was performed to investigate the effect of chitosan and NOCC from different sources and of different molecular weights on cadmium toxicity. Sprague-Dawley rats were blocked into 26 groups according to body weight, and were raised for 4 weeks. Cadmium chloride was given at the level of 0 or 400 ppm in diet. Various forms of chitosan and NOCC were given at the level of 0 or 4%(w/w) of diet. Cd toxicity was alleviated by various chitosan and NOCC supplements. However, the alleviating effects were different with fiber source(crab and shrimp), type(chitosan and NOCC), and molecular weight (low, medium, and high). Molecular weight had no significant effect. Compared with shrimp-source-fiber-fed groups, crab-source-fiber-fed groups showed lower Cd concentrations in blood and kidney, lower kidney metallothionein concentration, and lower liver and kidney MT-Cd contents. Compared with NOCC -fed groups, chitosan-fed groups showed lower intestine and liver Cd concentrations, lower liver and kidney MT concentrations and MT-Cd content, and higher fecal Cd excretion. Among cadmium-exposed group, low molecular weight shrimp chitosan group showed low Cd concentrations of liver and kidney, high fecal Cd excretions, and the lowest intestine and liver MT concentrations and liver MT-Cd content. In summary, a crab source fiber was more effective than shrimp source fiber, chitosan was more effective than NOCC, and the most effective one in alleviating Cd toxicity was low molecular weight shrimp chitosan.
Tolerance to toxic effects of cadmium (Cd), including lethality has been shown following pretreatment with cadmium and zinc. This study was designed to determine if tolerance also develops to Cd-induced hepatotoxicity and renal toxicity. Three groups of rats (A, B, C), each consisting of 108 rats, were studied and each group was divided into three subgroups (1, 2, 3), 12 rats for each subgroup. Rats were subcutaneously pretreated with saline (A), CdCl$_2$ (0.5 mg/kg, B), and ZnCl$_2$ (13.0 mg/kg, C) during time periods of 5 days. At the end of the period, rats were challenged with CdCIa (3.0 and 6.0 mg/kg) by intraperitoneal injection. As for the cadmium levels in rat tissues after pretreatments, it was highest in the liver. Then kidney, heart, blood and muscle followed it in that order. After 24, 48 and 96 hours of intraperitoneal injection by challenge doses the concentration of cadmium in liver and kidney increased proportionally to the increase of challenge dosage. However metallothioneins in liver and kidney were increased by the pretreatment of cadmium and zinc. These data indicate the liver is a major target organ of acute Cd poisoning, and suggest that cadmium induced hepatic injury, via release of Cd-MT, may play and important role in the nephrotoxicity observed in response to short-term exposure to cadmium. This result suggests that increasing cadmium concentrations, gradually accumulating in liver and kidney as the result of the pretteatmerit, served to induced the synthesis of metallothionein, thus making them resistant to the challenge from cadmium.
Tolerance to toxic effects of cadmium(Cd), including lethality has been shown following pretreatment with cadmium and zinc. This study was designed to determine if tolerance also develops to Cd-induced hepatotoxicity and renal toxicity. Three groups of rats(A, B, C), each consisting of 52 rats, were studied and each group was divided into three subgroups(1,2,3), 28 rats for each subgroup. Rats were subcutaneously pretreated with saline(A), $CdCl_2$(0.5 mg/kg, B), and $ZnCl_2$(13.0 mg/kg, C) during time periods of 5 days. At the end of the period, rats were challenged with $CdCl_2$(3.0 and 6.0 mg/kg) by intraperitoneal injection. As for the cadmium levels in rat tissues after 1,3,5,6 days of pretreatments, it was highest in the liver. Then kidney, heart, blood and muscle followed it in that order. After 24, 48 and 96 hours of intraperitoneal injection by challenge doses the concentration of cadmium in liver and kidney increased proportionally to the increase of challenge dosage. However metallothioneins in liver and kidney were increased by the pretreatment of cadmium and zinc. These data indicate the liver is a major target-organ of acute Cd poisoning, and suggest that cadmium induced hepatic injury, via release of Cd-MT, may play an important role in the nephrotoxicity observed in response to short-term exposure to cadmium. This result suggest that increasing cadmium concentrations, gradually accumulating in liver and kidney as the result of the pretreatment, served to induce the synthesis of metallothionein, thus making them resistant to the challenge from cadmium.
This research was conducted to determine the effects of chitosanoligosaccharide on liver poisoning induced by cadmium (Cd). Three groups of mice were used in this research. The first group was only injected with cadmium (5.0 mg/kg; i.p.) (group Cd) and the second one with cadmium and chitosanoligosaccharide (0.5% solution) at the same time (group Cd+Chi). The third one which had already been injeted with chitosanoligosaccharide (0.5% Solution) aweek before (group Ch7+Cd) was used. In order to investigate the inhibitory action of chitosanoligosaccharide on liver damage, enzyme activity in serum, glutathione peroxidase (GSHPx) activity and glutathione reductase (GR) activity were relatively measured. In addition, histological observations were made to determine the morphologic injury of liver tissues. As the result of enzyme activity in serum, the activity of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) in chitosanoligosaccharide-injected groups Cd+Chi and Chi7+Cd was lower than in group Cd. GSH-Px activity was sharply increased in groups Cd+Chi and Chi7+Cd compared to group Cd. GR activity was conspicuously decreased in groups Cd+Chi and Chi7+Cd compared to group Cd. As the result of light microscopic observation, liver cell necrosis caused by cadmium poisoning was obseved in liver cells. The finding of group Cd+Chi and Chi7+Cd was similar total on of normal groups. As the result of electron microscopic observation, mitochondria in group Cd showed a severe swelling phenomenon, RER fragment and ribosome dropout. However, in groups Cd+Chi and Chi7+Cd, mitochondria wiht high electron density were distributed and RER forming a typical lamellae with ribosome was observed. From these results, cadmium toxicity on rat liver tissues could be lessened by chitosanoligosaccharide.
Kim, Tae-Kyung;Park, Bum-Ho;Lee, Sang-Il;Kim, Soon-Dong
Food Science and Preservation
/
v.15
no.1
/
pp.161-168
/
2008
The effects tea beverages (TBs) prepared from powdered green tea (Gt), oolong tea (Ot), black tea (Bt), or pure tea (Pt) with lemon, orange, grenadine etc on cadmium toxicity in rats were investigated Sensory evaluations of the TBs are better than those of each water extracted teas. Cadmium (50 ppm) was administered to experimental rats fed a basic diet, or a diet with various TBs (15% w/v), for 5 weeks. Although body weight gains, feed intakes, and fecal weights in all Cd-treated groups were lower than those in the normal control group (NC), feed efficiency ratio, urine volumes, liver weights, and kidney weights did not differ significantly between groups. The serum ALT and AST levels in the Cd-treated control group (Cd-Co) were higher than those in the NC animals. Serum ALT and AST levels in all Cd-treated rats fed TB-supplemented diets were lower than in animals of the Cd-Co group. Tibia and femur weights in Cd-Co animals were lower than those in NC rats. Tibia and femur weights in Cd-treated rats fed TB-supplemented diets were higher than those in Cd-Co animals. There were no between-group differences in tibia lengths; animals in the NC and TB-supplemented diet groups showed femur lengths longer than those of Cd-Co rats. Although the contents of crude ash and cadmium in the femurs of Cd-Co mts was markedly higher than in the femurs of NC animals, the cadmium content in femurs of Cd-Co rats was significantly lower than that in the femurs of NC animals. The changes in mineral levels caused by Cd administration were alleviated by every TB-supplemented diet tested Whereas fecal calcium excretion by Cd-Co animals was significantly higher than that of NC rats, calcium excretion by Cd-treated rats fed TB-supplemented diets was significantly lower than that of Cd-Co animals. Fecal cadmium excretion by all Cd-treated rats fed TB-supplemented diets was significantly higher than that of Cd-Co animals. In conclusion, this study provides experimental evidence that various TBs may regulate cadmium-induced organ toxicity by reducing cadmium accumulation in tissues through the mechanism of increasing the fecal excretion of cadmium.
The purpose of this study was to investigate the metallothionein of acute cadmium poisoning mice as a Cadmium index. Forty male ICR mice were injected with cadmium chloride solution from 1/8LD50 to 1/2LD50 dose. At 24 hours after exposed Cd, I examined Cd and metallothionein (MT) intissues(liver and kidney) and fluids(whole blood and urine) and also measured low molecular proteins, N-acetyl-D-glucosaminidase(NAG) and 2- microglobuline (2-MG) in urine. The concentration of Cd and MT of liver kidney whole blood and urine were increased with dose dependent manner. Urinary Cd and urinary MT and very good significance (p<0.01) and urinary MT had good significance with kidney Cd and NAG but not 2-MG Conclusionally MT in urine was very correlated with kidney Cd and urine Cd, So MT maybe useful as a Cd poisoning index.
The present study was undertaken to investigate the protective role of taurine (2-aminoethanesulfonic acid) against cadmium (Cd) induced oxidative stress in murine erythrocytes. Cadmium chloride ($CdCl_2$) was chosen as the source of Cd. Experimental animals were treated with either $CdCl_2$ alone or taurine, followed by Cd exposure. Cd intoxication reduced hemoglobin content and the intracellular Ferric Reducing/Antioxidant Power of erythrocytes, along with the activities of antioxidant enzymes, glutathione content, and total thiols. Conversely, intracellular Cd content, lipid peroxidation, protein carbonylation, and glutathione disulphides were significantly enhanced in these cells. Treatment with taurine before Cd intoxication prevented the toxin-induced oxidative impairments in the erythrocytes of the experimental animals. Overall, the results suggest that Cd could cause oxidative damage in murine erythrocytes and that taurine may play a protective role in reducing the toxic effects of this particular metal.
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