This study was performed to investigate the effect of chlorella on cadmium (Cd) toxicity in Cd-administered rats. Sixty male Sprague-Dawley rats (14 week-old) were blocked into 6 groups. Cadmium chloride was given at levels of 0 or 325 mg (Cd: 0, 160 ppm), and chlorella powder at levels of 0, 3 and 5%. Cadmium was accumulated in blood and tissues (liver, kidney and small intestine) in the Cd-exposed groups, while the accumulation of Cd was decreased in the Cd-exposed chlorella groups. Fecal and urinary Cd excretions were remarkably increased in Cd-exposed chlorella groups. Thus, cadmium retention ratio and absorption rate were decreased in the Cd exposed chlorella groups. Urinary and serum creatinine, and creatinine clearance were not changed in experimental animals. In addition, metallothionein (MT) synthesis in tissues was increased by Cd administration. The Cd-exposed chlorella groups indicated lower MT concentration compared to the Cd-exposed groups. Moreover, glomerular filtration rate (GFR) was not changed by dietary chI orella and Cd administration. According to the results above, this study could suggest that Cd toxicity can be alleviated by increasing Cd excretion through feces. Therefore, when exposed to Cd, chlorella is an appropriate source which counteracts heavy metal poisoning, to decrease the damage of tissues by decreasing cadmium absorption.
The purpose of this study was to investigate the effects of green tea catechin on the cadmium accumulation in body, cadmium excretion and detoxification functions in chronic cadmium poisoned rats. Sprague-Dawley male rats weighing 100$\pm$10g were randomly assigned to one normal group and three cadmium poisoned groups. Cadmium groups were classified to catechin free diet (Cd-0C group), 0.25% catechin diet(Cd-0.25C group) and 0.5% catechin diet(Cd-0.5C group) according to the levels of catechin supplement. Animals were maintained on 0, 0.25 and 0.5% catechin diets for 20 weeks and simultaneously administered 50ppm Cd(sup)2+ dissolved in the drinking water. Body weight, food intakes and food efficiency ratio in Cd-0C group was lower than the normal group. The accumulation of cadmium in rat liver, kidney, and blood was reduced by catechin supplementation. The excretion of cadmium in urine and feces was increased by catechin supplementation. The metallothionein(MT) contents in liver and kidney were increased in all cadmium groups compared with that of normal group. The ratios of cadmium absorption and retention ratios were significantly decreased in catechin supplementation groups. Accordingly, catechin supplementation resulted to an excretion of cadmium in urine and feces and a lowered accumulation of cadmium in liver and kidney by increasing methallothionein synthesis that led to the significant decrease in cadmium absorption and retention ratios.(Korean J Nutrition 34(4) : 384~392, 2001)
This study was undertaken to find out the effect of persimmon leaves on histopathological changes of cadmium toxicity in mice. Seventy two BALB/c mice of male were divided into a control group(A) and five experimental groups (B, C, D, E, F) : group A received tap water and basal diet, group B received tap water and diet supplemented with 3% persimmon leaves alone, group C received basal diet and 300 ppm cadmium, group D, E and F received basal diet supplemented with 1, 3% and 7% persimmon leaves and 300 ppm cadmium respectively. Cadmium dissolved in tap water was used, and the persimmon leaves were mixed with feed. All mice were dissected on the 84th day. Pathological changes in liver, kidney, cortical osseous tissue of femoral shaft, bone trabecular of femur, and epiphyseal cartilage plate of femur were observed. Group B showed no significant changes as the control group. But group C showed the unclearness of specific cells in liver, the loss of architecture and necrosis of hepatocyte, degeneration and necrosis of renal convoluted tubules, desquamation and vacuolization of the greater part of the renal tubular epithelium, marked thinning of the cortical osseous tissue in femoral shaft, reduction of cancellous bone volume and decreaswe of trabecular number, and marked thinning of epiphyseal cartilage plate in femur. On the other hand, persimmon leaves-treated group showed a little convalescent changes an maintained their normal architectures in liver, kidney, cortical osseous tissue of femoral shaft, bone trabecular of femur, and epiphyseal cartilage plate of femur.
The welders and car painters are frequently exposed to heavy metals such as lead, zinc, cadmium and chromium, and those are a major source of heavy metal poisoning. This study was carried out to investigate the relationship of the heavy metal level in blood by age, working duration, and smoking status among 105 industrial workers and 88 general people in Gyeongnam province from October 2003 to October 2004. The heavy metal level in blood was analyzed by atomic absorption spectrophotometer. Mean blood lead level in exposed group and control group was 8.40±4.67μl/dl, 1.82±1.35μl/dl, respectively. Mean blood zinc level in exposed group and control group was 9.43±5.38 ㎍/ml, 2.89±1.79㎍/ml, respectively. Mean blood cadmium level in Exposed group and control group was 1.53±1.05μl/dl, 0.60±0.49 μl/dl, respectively. Mean blood chromium level in exposed group and control group was 0.89±0.76μl/dl, 0.68±0.63μl/dl, respectively. Lead, zinc, cadmium and chromium level in blood of exposed group was significantly higher than that of control group. In the comparison of smoking status, lead, zinc and cadmium level of smoker's was significantly higher than that of non-smoker's. Comparison of heavy metal level by age, lead, zinc, cadmium level in 40's, 50's (exposed group) in blood significantly higher than that of 20's, 30's. In exposed group, working duration has no significant difference. In conclusion, smoking was the most hazardous factor to elevate in blood heavy metal levels.
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 study was performed in order to investigate the effects of taurine on cadmium poisoning in muscle, gill, and bone tissues of wild goldfish. For this experiment, 80 wild goldfish were divided into four experimental groups: 0.3 mg/L of cadmium and 0 mg/L of taurine (Group I), 0.3 mg/L of cadmium and 20 mg/kg of taurine (Group II), 0.3 mg/L of cadmium and 40 mg/L of taurine (Group III), and 0.3 mg/L of cadmium and 80 mg/L of taurine (Group IV). The results were as follows: The cadmium concentration in muscle tissue of wild goldfish was 0.65-3.21 mg/kg wet wt in Group I, whereas it decreased in Group IV. Levels of cadmium in gill tissue of wild goldfish were 16.57-42.39 mg/kg wet wt in Group I, 15.23-43.01 mg/kg wet wt in Group II, 15.11-39.56 mg/kg wet wt in Group III, and 13.15-38.55 mg/kg wet wt in Group IV (P < 0.05), suggesting that the cadmium concentration decreased in the experimental groups compared to control. The cadmium concentration in bone tissue of wild goldfish after 28 days was 0.52-9.75 mg/kg in Group II, whereas it increased in Group III (P < 0.05). In conclusion, taurine may have a preventive effect against cadmium accumulation in biological tissues.
Journal of the Korean Society of Food Science and Nutrition
/
v.28
no.6
/
pp.1355-1363
/
1999
The purpose of this study was to investigate the effects of vitamin E on liver microsomal cytochrome P450 contents and xanthine oxidase activity in acute cadmium poisoned rats. Sprague Dawley male rats weighing 100$\pm$10g were randomly assigned to one normal and three cadmium injected groups. Cadmium injected groups were fed vitamin E free diet(0E Cd group), 40mg vitamin E per kg diet(40E Cd group) or 400mg vitamin E per kg diet(400E Cd group). Vitamin E level of normal group was 40mg per kg diet. Animals were injected intraperitoneally with 2.0mg Cd2+/kg bw for 4 days after the rats were fed diets with three different levels of vitamin E for 2 and 4 weeks. Body weight, food intake and feed efficiency ratio of cadmium injected animals, were decreased compared with those of normal group. The weights of liver and kidney in cadmium injected groups were not different from those of normal group. Cadmium contents of liver in cadmium groups were 160 fold higher those that of normal group. Accumulation of cadmium poisoned rat liver was reduced by vitamin E supplementation. Contents of blood hemoglobin and hematocrit in 0E Cd groups were decreased to 2~ 14% of those of the other groups. Contents of serum triglyceride in all experimental groups were not significantly different each other. Levels of serum total cholesterol, LDL cholesterol and antherogenic index in 0E Cd and 40E Cd groups were higher than those of normal group, while the contents of HDL cholesterol in 0E Cd and 40E Cd groups were lower than those of normal group. Xanthine oxidase(XOD) activity and cytochrome P450 contents in the liver were significantly increased in cadmium injected groups but these were reduced by vitamin E supplementations. The present results indicate that acute cadmium poisoning in rats causes increasing free radical generation systems in the liver and that leads to liver tissue damage. But these abnormalities can be reduced by dietary vitamin E supplementations.
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.
To investigate the cadmium (Cd) toxicity on the testis, male rats were treated with 1, 2, 4 and 8 mg/kg of Cd by IP. According to histochemical studies, Cd-treated testis tissue showed death of spermatozoa, death of Sertoli cells, death of all the spermatogenic cells, and finally disappearance of basal lamina of seminiferous tubules with increasing doses, and showed decreased ground substances and Leydig cells, increased inflammatory cells and fibroblasts, and fibroblasts, and finally disappearance of ground substances and all the cells except fibroblasts within interstitial tissues with increasing doses. According to biochemical studies, two kinds of proteins, 25 and 45 kDa, were dramatically disappeared from the total protein of rat testis treated with Cd comparing to normal testis. The result of electrophoresis of total protein suggests that actin (45 kDa), presumed on its mmolecular weight and amount, in the testis-cells is the primary target of Cd poisoning. Although its exact mechanism is not clear, the disappearance of two proteins when testis is exposed to Cd should give some clues to understnad the mechanism of necrosis of testis tissue crumbling by heavy metal pollutant such as Cd.
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