• Journal of Nutrition and Health
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• v.33 no.7
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• pp.725-732
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• 2000

The purpose of this study was to investigate the effects of green tea catechin on renal dysfunction and blood presure change 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 raids for 20weeks. Cadmium were supplied as drinking water of 50ppm Cd2+ Morphological changes shown through a light microscope and an electro-microscope revealed the mitochondria and tubule epithelial cell edema in Cd -0C group but they were alleviated in catechin supplementation. The urinary $\beta$2-microglobulin that measured to observe the glomerular injury were higher in Cd-poisoned groups than in normal group but they was lowered by catechin supplementation. Glomerular filtration ratios(GFR) in Cd-poisoned groups were significantly lower than in normal group but that of catechin supplementation group was similar to normal group. This suggested that catechin protected the kidney from the functional damage. Angiotensin converting enzyme(ACE) activity and blood pressure(BP) in Cd-poisoned groups were significantly higher than in normal group. Heart rate was tended to increase in Cd-poisoned groups. The results indicate that green tea catechin supplementation on chronic cadmium-poisoned rats normalized the renal dysfunction and blood pressure system.

• The Korean Journal of Pharmacology
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• v.15 no.1_2 s.25
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• pp.29-37
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• 1979

The tension-length relationships and reactivity of vascular smooth muscle in longitudinal strips from portal vein ana in helical strips from thoracic aorta and pulmonary artery of normotensive control and cadmium-hypertensive rabbits were studied in vitro. 1. The mean arterial pressures of non-poisoned control rabbits was $87.0{\pm}4.7 mmHg$. However, Cd-poisoned group revealed the significant increase in pressure by $109.04{\pm}2.8 mmHg$ (p<0.005). 2. By tension-length studies, strips from portal vein of Cd-poisoned group stretched a greater percent increase in length in response to an applied resting force from 0.25 to 5 g than did those from non-poisoned group. On the contrary, strips from thoracic aorta of Cd-poisoned group showed less compliant than those from control, i.e. the former underwent a less percent increase in length than the latter. Passive tension-length relations of pulmonary artery was unaffected by Cd-hypertension. 3. The force of contraction(active tension) was significantly lowered in strips from aorta of Cd-hypertensive group throughout the range of $0.5{\sim}2g$ passive tension. However, there was no significant difference in the development of active tension of portal vein or pulmonary artery of both groups. 4. The $K^+$-contraction in the portal vein, aorta and pulmonary artery of Cd-poisoned group made no difference in the active force from those of control group. 5. The force of contraction in the strips from aorta of Cd-poisoned group was significanty decreased compared to that of control. The results suggested that the alterations in vascular reactivity to contracting substances and in distensibility to passive tension were induced in the Cd-hypertensive rabbits.

• Journal of Nutrition and Health
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• v.34 no.8
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• pp.881-886
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• 2001

The purpose of this study was to Investigate the effects of green tea catechin on changes of mineral contents in chronic cadmium-poisoned rats. Sprague-Dawley male rats weighing 100 $\pm$ 10g were randomly assigned one of 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 raised for 20 weeks. Cadmium was supplied in drinking water which contained 50ppm Cd$^{2+}$. Effects of catechin were analyzed on changes of mineral contents in chronic cadmium poisoned rats by determining the calcium accumulation in bones, blood, urine and faces and phosphorus In blood and urine. Cd-poisoning inducted the decrease of red blood cell(RBC), white blood cell(WBC), contents of blood hemoglobin and hematocrit, but the levels of those indices were increased by catechin supplementation. The contents of tibia and femur in Cd-0C group was significantly lower than in normal group, but those of catechin supplemetation group was similar to normal group. The calcium contents of urine and faces were higher in Cd-poisoned groups than in normal group, but they was lowered by catechin supplementation. The phosphorus contents of blood and urine in Cd-0C group was significantly lower than in normal group, but that of catechin supplementation group was similar to normal group. Catechin supplementation improved the calcium metabolism in chronic cadmium poisoned rats by increasing the contents of minerals such as calcium and phosphorus in blood and femur and by lowering the urinary and fecal calcium.m.

• Journal of Nutrition and Health
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• v.29 no.1
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• pp.70-76
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• 1996

This study was undertaken to investigate the effect on the Cd accumulation in long-term Cd poisoned rats. 40 male weaning Sprague Dawley rats weighting 80-90g were divided into 4 groups (LCuLFeCd : low Cu, Fe and Cd group, ACuLFeCd : adequate Cu, low Fe and Cd group, ACuAFeCd : adequate Cu, adequate Fe and Cd group) according to Cu and Fe levels (Cu 0.5ppm, 8.5ppm : Fe 6ppm, 40ppm) for 12 weeks. There were no significant difference in water intake, feed intake, and body weight gain according to dietary Cu and Fe consumption. But the mean food intake and body weight gain of adequate Fe groups(LCuAFeCd, ACuAFeCd) were higher than those of deficient Fe groups (ACuLFeCd, LCuFeCd)in long-term Cd poisoned rats. The mean Cd levels of serum, liver, kidney, and urine in ACuAFeCd group were lower than those of Cu and /or Fe deficient groups. But the mean fecal Cd excretion of ACuAFeCd group was higher than that of Cu and/or Fe deficient groups. And the mean Cd retention amount of ACuAFeCd group was lower than those of Cu and/or Fe deficinet groups. In conclusion, these results provide an evidence that adequate Cu and Fe intakes can decrease Cd accumulation in rats. Therefore, in the point of increasing environmental Cd contamination, adequate Cu and Fe intakes must be suggested to prevent Cd accumulations.

• YAKHAK HOEJI
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• v.44 no.6
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• pp.552-557
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• 2000

In order to investigate the effects of Yukmijihwang-Tang on the hepatic microsomal function of Cd-poisoned rats, 3 mg/kg of cadmium (Cd) and 500 mg/kg of Yukmijihwang-Tang extract (YJT), a herbal hepatoprotective medicine, were administered concurrently to rats for 4 weeks. The levels of protein, aniline hydroxylase (AH) and malondialdehyde (MDA) were increased in Cd-treated group. This increase was suppressed by treatment or YJT. The levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), glucose-6-phosphatase (G-6-P) and ${\delta}-aminolevulinic$ acid dehydratase (ALAD) of Cd-treated group were decreased. This decrease was inhibited by treatment of YJT. Treatment with YJT significantly protects cadmium-induced hepatotoxicity.

• The Korean Journal of Pharmacology
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• v.18 no.1
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• pp.23-31
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• 1982

1) Experiments were undertaken to elucidate the mechanism which elevates the systemic arterial blood pressure by cadmium (Cd). 2) The mean arterial pressure and peripheral resistance of central ear artery in Cd-poisoned rabbit were significantly increased in comparison with those in control. 3) The vascular pressure response to electrical stimulation in Cd-poisoned group was less than that in control. However, in the former group it showed the supersensitivity to norepinephrine. 4) The response to electrical stimulation was diminished by sodium arachidonate in the ear artery, on the contrary, it was rather enhanced in the vessel of Cd-poisoned group. The responses in both groups were reduced by pretreatment with either $PGE_2\;or\;PGF_{2{\alpha}}$. 5) The response to electrical stimulation was not affected in control, but enhanced in Cd-poisoned group by pretreatment with indomethacin. 6) When the ear artery of control group was perfused with physiological salt solution (PSS) the response to electrical stimulation was not changed by indomethacin, it was much enhanced without affecting on the response to norepinephrine when $K^+-free\;PSS$, was used. These results demonstrate the evidence that the alteration of regulatory mechanism on the vessels was causally related to the elevation of arterial pressure and the increase in peripheral resistance in Cd-poisoned rabbits.

• Journal of the Korean Society of Food Science and Nutrition
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• v.28 no.6
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• pp.1355-1363
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• 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.

• Journal of Nutrition and Health
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• v.27 no.7
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• pp.709-716
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• 1994

This study was undertaken to investigate the effect of dietary Fe levels on Cd accumulation in Cd poisoned rats. Forty male weaning Sprague Dawley rats weighing 80-90g were divided into 4 groups(LFe : low Fe, LFeCd : low Fe and Cd, AFe : adequate Fe, AFeCd : adequate Fe and Cd) according to Cd administration(Cd : 0 or 50ppm in drinking water) and Fe levels (Fe : 6 or 40ppm in diet) for 12 weeks. The food intake and weight gain of LFe and LFeCd were significantly lower than those of AFe and AFeCd(p<0.01, p<0.001). The water intake was not affected significantly by Cd and Fe, therefore Cd intake was no significant difference between groups. The Cd accumulation of kidney in LFeCd was significantly higher than those of AFeCd(p<0.001). But the Cd accumulations of brain, liver and spleen were not significantly different between Cd groups and without Cd groups. The serum Cd content and urinary Cd excretion of LFeCd was significantly higher than those of AFeCd(p<0.01, p<0.01). But the fecal Cd excretion of LFeCd was significantly lower than that of AFeCd(p<0.001). The Cd retention, Cd retention rate, and apparent Cd digestibility of LFeCd were significantly higher than those of AFeCd(p<0.001, p<0.001, p<0.001). It was concluded that adequate Fe supplementation have protective effects on the long term Cd poisoning in rats.

• Journal of the East Asian Society of Dietary Life
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• v.4 no.2
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• pp.9-16
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• 1994

This study was undertaken to investigate the effects of dietary low (Fe) levels on Fe metabolism of cadmium(Cd) poisoned rats. 40 male Sprague weaning Dawley rats weighing 80-90g were divided into 4 groups(LFe:low Fe, LFeCd:low Fe and Cd, AFe: adequate Fe, AFeCd: adequate Fe and Cd) according to Cd administration(0, 50ppm in drinking water) and Fe levels(Fe:6ppm, 40ppm in diet)for 12 weeks. The food intake and body weight gain of Cd group with low Fe(LFeCd) were significantly lower than those of without Cd group with adequate Fe(AFe)(p<0.01, P<0.05). But there was no significantly difference between Cd groups and without Cd groups in water intake. The blood levels of hemoglobin, hematocrit, and serum levels of Fe of LFeCd were significantly lower than those of AFe(p<0.01, p<0.05, p<0.001). The urinary and fecal excretion of Fe of LFeCd was significantly lower than that of AFe(p<0.05, p0.05). The levels of Fe of liver, spleen in LFeCd were lower than those of AFeCd(p<0.05, p<0.05). These results indicates that adequate iron supplementation to Cd pretreated rats induce protective effects on the reduction of Fe status by Cd poisoning.

• Nutritional Sciences
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• v.6 no.4
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• pp.223-228
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• 2003

This study was carried out to investigate the effects of vitamin E on the cadmium contents of bone and on the calcium and phosphorous contents of the blood, urine and feces. Male Sprague-Dawley rats weighing 100$\pm$10g were randomly assigned to one normal group and three cadmium poisoned groups. The cadmium poisoned groups consisted of a vitamin E free diet (Cd-0E) group; a 40 mg vitamin E /kg diet (Cd-40E) group; and a 400 mg/kg diet (Cd-400E) group. Experimental animals were maintained on their respective diets for 20 weeks and were simultaneously administered 50 ppm $Cd^{2+}$ dissolved in the drinking water. At the end of the trial, the average hematocrit value in the Cd-0E group was 28.13% lower than in the normal group. However, the average hematocrit value in the Cd-400E group was significantly higher than in the Cd-0E and Cd-40E groups. WBC levels in the cadmium-poisoned groups were lower than in the normal group, but Cd-400E group levels were significantly higher than in the Cd-0E and Cd-40E groups. The contents of calcium of tibia has no significant difference between normal group and cadmium exposed group at $10^{th}$ week After 20 weeks, the calcium contents of the tibia in the Cd-0E and Cd-40E groups were lower than in the normal group by 25.5% and 22.1 %, respectively, although the calcium contents of the tibia in the Cd-400E group were higher than in the normal group. After 10 weeks, the calcium contents of the femur in the Cd-0E and Cd-40E groups were 19.25% and 15.45% lower than in the normal group, respectively, but the calcium contents of the femur in the Cd-400E group were at the same levels as in the normal group. The levels of calcium in the femur after 20 weeks were similar to the 10-week levels. Calcium levels of the urine in the Cd-0E and Cd-40E groups were 3.92 fold and 2.92 fold higher, respectively, than in the normal group, but levels in the Cd-400E group were significantly lower than in either the Cd-0E group or the Cd-40E group. Calcium levels of the feces in cadmium-poisoned groups were significantly higher than in the normal group, although levels in the Cd-400E group were significantly lower than in the Cd-0E and Cd-40E groups. Phosphorous levels of the blood in the Cd-0E group were 17% lower than in the normal group, although levels in the Cd-400E group were significantly higher than in the Cd-0E group. Phosphorous levels of the urine in the Cd-0E and Cd-40E groups were significantly higher than in the normal group, while Cd-400E group levels were found to be at the same level as in the normal group. Cadmium contents of the tibia in the Cd-40E and Cd-400E groups were 13% and 17% lower, respectively, than in the Cd-0E group. Regarding cadmium levels in the femur, only the Cd-400E group achieved lower levels (10% lower) than the Cd-0E group. In conclusion, vitamin E supplementation resulted in a suppression of the release of calcium from bone, and a reduction in the excretion of calcium via the urine and feces, thus having a normalizing effect on calcium metabolism in rats with chronic cadmium poisoning.