Stress responses and changes in protein metabolism in carp Cyprinus carpio during cadmium exposure

Stress responses and changes in protein metabolism were studied in common carp Cyprinus carpio exposed to 0, 0.8, 4, and 20 microM cadmium (Cd) over a 29-day period. Blood and other tissue samples were taken after 4 and 29 days of exposure. The highest Cd concentration proved to be lethal to the fish, resulting in 100% mortality after 21 days of exposure. Cd accumulated in the tissues in the following order: kidney>liver>gills. Blood hematocrit, blood hemoglobin, plasma glucose, plasma lactate, and tissue total protein contents were not significantly altered. The concentrations of Cd and zinc (Zn) binding metallothioneins ((Cd, Zn)-MTs) were in the following order=liver>kidney>gills. An increase in (Cd, Zn)-MTs was observed at all exposure concentrations at days 4 and 29 in kidney and at Day 29 in gills. No significant changes in (Cd, Zn)-MT contents were found in liver. The concentrations of free amino acids and the activities of proteases were increased at Day 4 in gills, liver, and kidney of carp exposed to 4 and 20 microM Cd, and in gills and kidney at Day 29 in carp exposed to 4 microM Cd. The observed increases in the activities of aspartate aminotransferase and alanine aminotransferase suggest that the observed proteolysis is intended to increase the role of proteins in the energy production during Cd stress. However, this increased activity of both aminotransferases was not found in gills during exposure to the lethal Cd concentration, indicating that Cd may also cause an inhibitory effect on the activity of these enzymes above a certain level.     

Effect of cadmium administration and aging on the concentration of essential metals in liver and kidney

To investigate the changes in the concentration of essential metals in organs caused by exposure to cadmium (Cd) and by aging, Cd was administered subcutaneously in single doses of 0.3, 0.9 and 2.7 nig/kg to female rats 10 and 40 weeks of age. The animals were sacrificed on the 7th day after the administration. The concentration of Cd, zinc (Zn), copper (Cu), iron (Fe) and manganese (Mn) in the liver and the kidney was determined and the relations between the concentration of Cd and that of other metals were investigated.1) In 10-week-old rats, the amount of Cd accumulated in the liver and the kidney increased linearly with increasing doses of Cd, while in 40-week-old rats, suppressed accumulation of Cd in the liver and increased accumulation of Cd in the kidney were found after administration of the high dose.2) The concentration of Zn in the liver and the kidney both increased with increasing doses of Cd. There was no age-related difference.3) The concentration of Cu in the liver increased in the animals which received the intermediate and the high dose, irrespective of age. The concentration of Cu in the kidney showed no changes caused by Cd administration or by aging.4) The concentration of Fe in the liver increased in both 10-week-old and 40-week-old rats which received the high dose. The concentration was higher in 40-week-old rats than in 10-week-old rats. The Fe concentration in the kidney and the Mn concentration in the liver and the kidney was not affected by Cd administration or by aging.5) Discriminant analysis, by age, suggested that the amount of metals in the liver and the kidney was more likely to be affected by exposure to Cd in young individuals and less likely to be affected by exposure to Cd with the increase of age.     

Cadmium turnover and changes of zinc and copper body status of rats continuously exposed to cadmium and ethanol

The effects of continuous exposure to cadmium (Cd) and ethanol on Cd turnover and zinc (Zn) and copper (Cu) body status of male Wistar rats were studied. The animals received an aqueous solution of 10% (w/v) ethanol and/or 50 mg Cd/l as the only drinking fluid for 12 weeks. The concentrations of Zn, Cu and Cd in the serum (or blood), liver, kidneys, spleen, brain, heart, femoral muscle and femur as well as in 24-h urine and faeces specimens were assessed by atomic absorption spectrometry (AAS). Ethanol alone had no effect on Cd accumulation or excretion. By contrast, co-administration of ethanol with Cd influenced the turnover of this toxic metal. Long-term consumption of ethanol alone caused a decrease in femur Zn and liver Cu concentrations. Moreover, the urinary loss of both bioelements decreased, whereas their faecal excretion was increased. Exposure to Cd resulted in an increase in liver and kidney and in a decrease in femur and 24-h urine Zn concentrations. An increase in Cu concentration in the kidney and a decrease in the brain were also noted. Moreover, Cd increased the total pool of Zn in organs (kidneys, liver, spleen, heart and brain), but did not influence that of Cu. Zn concentration in the liver, kidney and spleen of rats co-exposed to Cd and ethanol were increased, but were decreased in the brain and femur, compared to controls. The concentrations of Cu in livers and brains of these rats were decreased, whereas those in kidney, spleen and heart were increased. The urinary excretion of the elements was decreased, whereas their faecal excretion was increased. Moreover, the total amount of Cu in organs decreased below the control value and that of Zn was in the normal range. These changes in Zn and Cu levels could be explained by different effects of both toxic substances, differences in bioelement intakes (due to reduced consumption of drinking solutions and food), and the modifying effect of ethanol on Cd turnover. Our results suggest that alcoholics may be more susceptible to Cd accumulation and its effects on body Zn and Cu.     

Metallothionein levels in liver and kidney of Canadians--a potential indicator of environmental exposure to cadmium

Liver and kidney cortex samples were obtained from 89 human autopsies for the determination of metallothionein (MT), cadmium (Cd), zinc (Zn), and copper (Cu). An age-dependent increase of Cd, Zn, and Cd/Zn was observed in the kidney; increases peaked at mid-age and were followed by a decline. Cadmium was present at a low constant level in the liver at all ages. The mean concentrations of Cd and Zn were 18.0 and 40.1 micrograms/g wet weight, respectively, in the kidney, and for the liver the values for Cd and Zn were 2.0 and 79.0 micrograms/g wet weight, respectively. A positive linear relationship was observed between Cd or Zn and MT in the kidney and between Zn and MT in the liver. No other correlation was found between Cu and MT in either organs. Similar values were obtained for MT when estimated by Ag-hem and Cd-hem methods.     

Toxicity,fertility, teratogenicity,and dominant lethal tests in rats administered cadmium subchronically: I. Toxicity studies

In order to obtain an overall understanding of the toxicity of cadmium (Cd), a single experimental series was designed to investigate the diverse effects of Cd. Four groups of Sprague-Dawley rats, each of which consisted of 14 male and 14 female rats, were administered Cd (CdCl₂) orally at dose levels of 0, 0.1, 1.0, 10.0 mg/kg/day for 6 weeks. After this, the animals were mated for 3 weeks, changing partners every week, for fertility and teratogenicity tests. Cd was given during this mating period. Females were administered Cd during gestation and sacrificed on the 20th day of gestation for fetal examination. After a total of 9 weeks administration, males were subjected to dominant lethal tests by mating 2 females per male per week for 6 weeks. Pregnant females were killed on the 13th day of gestation to test for dominant lethality. This paper reports the results of the general toxicity tests. The main toxic signs, seen only in the 10 mg/kg group, were repression of food intake and body weight gain, depilation, whitening of the incisors, and salivation. Hematological analyses showed that the number of RBC increased while hemoglobin and hematocrit levels decreased, and the number of WBC increased, mainly as a result of neutrophilia. Serum biochemical analyses indicated increased levels of GPT and creatinine, reflecting damage to the liver and kidneys. Increased glucose levels were seen in males. A major change found at the time of autopsy by macroscopic observation of organs was hypertrophy of the jejunum and ileum with a darkish-brown color in nonpregnant females of the 10 mg/kg group. Microscopically, hyperplasia with a high frequency of mitotic figures was seen in the lamina propria mucosae. The weight of the thymus decreased and the weight of the adrenals increased in both males and females. The weight of the ovaries decreased. Major histopathological changes were focal necrosis in the liver and hyperplasia of the adrenal cortices with patchy necrosis in nonpregnant females of the 10.0 mg/kg group. Determination of Cd in the liver and kidneys suggested that excretion of the accumulated Cd was slow. Two aspects of Cd toxicity, i.e., the inhibition of nutrient resorption by unresorbed Cd and the toxicity expressed by resorbed Cd, as well as the causative factors of the adrenal hyperplasia, are discussed.     

Availability and toxicological effects of low levels of biologically bound cadmium

Rats were fed a casein based diet containing Cd biologically bound in ryegrass (Lolium multiflorum L. ssp. italicum) for eight weeks. The grass portion in the diet was 20% (w/w). Cd concentrations of the respective diets were (g/g diet): 0.24 (control group Cd=0), 0.85 (group Cd=1) and 2.25 (group Cd=2). After six weeks on the diets, food intake and body weight were reduced by the low dietary Cd concentration (Cd=1), while in treatment group Cd=2 this occurred after 2 weeks. After an 8-week feeding period the concentrations of Cd, Cu, Zn, Fe and Ca in selected organs, tissues and in the excreta of rats beside whole body element contents were determined. While no elevated Cd levels due to the Cd intoxication were found in skin, lung, blood, testes, muscle and urine, Cd concentrations in liver, kidney and spleen increased in a dose-dependent manner. This was also true for whole body Cd and Cd in faeces, the latter being 27.6 fold higher in the high Cd load (Cd=2) as compared to the controls (Cd=0). Highest Cd concentrations were recorded in liver and kidney. Calculated as percentage of the whole body metal content liver Cd increased from 1.49% (Cd=0) to 7.41% (Cd=2) and kidney Cd from 0.65% to 4.87%. While no changes of the Ca levels in all organs and tissues investigated were observed, liver Zn increased and blood Cu decreased. Copper and Zn increased in faeces and decreased in urine. With the exception of skin and lung, a significant loss of Fe was observed in all organs and tissues, which was most evident in treatment group Cd=2. Depending on the Cd dose applied, reduced fecal and urinary Fe excretion occurred. Hematological parameters (hemoglobin, hematocrit, blood glucose) and serum enzyme activities (alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, -glutamyl transferase) were not affected by Cd in a biologically bound form. Serum alanine amino transferase showed slightly lower activities in treatment groups Cd=1 and Cd=2. Analysis of the glucose concentration and the activity of alkaline phosphatase in urine did not reveal any changes due to the Cd intoxication. Accumulation and toxicological effects of Cd biologically bound in ryegrass are discussed in relation to inorganic forms of the metal administered to mammals.     

Cadmium,zinc, and copper in horse liver and in horse liver metallothionein: Comparisons with kidney cortex

Cadmium, zinc, and copper were determined in liver and in kidney cortex samples obtained from 33 normal Swedish horses. Cadmium concentrations in liver ranged from 0.002 to 0.165 mmole/kg and in kidney from 0.01 to 2.15 mmole/kg. There was a significant correlation between liver and kidney concentrations of cadmium. The average kidney concentration of cadmium was about 15 times that of liver. Zinc concentrations increased with increasing cadmium concentrations in both liver and kidney. The relative increase of zinc with cadmium was more pronounced in liver than in kidney. However, the absolute increase of zinc was larger in kidney due to the much higher concentration of cadmium in kidney compared to liver. Any significant correlation between copper and cadmium, or copper and zinc, could not be revealed. Sephadex gel filtration was performed on supernatants from homogenates of kidney and liver from 19 of the horses. In both organs the major part of cadmium was recovered in protein fractions corresponding to metallothionein (MT), in which the increase of zinc also took place. The molar ratio between zinc and cadmium was higher in MT fractions obtained from liver than in MT fractions obtained from kidney.     

Effects of oral copper administration to pregnant heterozygous brindled mice on fetal viability and copper levels

Copper (6 ppm) was administered to pregnant heterozygous brindled and normal mice from 13 to 18 days gestation. The copper and zinc concentrations in the cerebrum, cerebellum, liver, and kidneys of mothers and their fetuses were determined. The placental concentrations in fetuses of heterozygous mothers administered copper were also determined. The heterozygous mothers had smaller numbers of live fetuses than the normal mothers, but had the same number as normal mothers when copper was administered. The hepatic copper concentration in the heterozygous mothers was lower than that in the normal mothers and was not increased by the administration. The body and tissue wet weights of all fetuses were unaffected by the maternal genotype or drinking fluid. The cerebral copper concentrations in hemizygous and heterozygous fetuses were increased by the copper administration but did not reach normal levels. The hepatic and renal concentrations remained unchanged. The cerebral copper concentrations in normal fetuses of both heterozygous and normal mothers were increased by the copper administration. The copper administration increased the copper concentrations in liver of normal fetuses of heterozygous mothers and in kidneys of normal fetuses of normal mothers. The placental copper concentration in hemizygous fetuses was higher than those in heterozygous and normal fetuses. These results suggested that oral copper administration to pregnant females could improve an abnormal copper distribution in hemizygous and heterozygous fetuses without affecting fetal growth.     

The tissue disposition of zinc and copper following repeated administration of cadmium and selenium to rats

Female rats were divided into four groups of five rats each including one control group (C). The animals were administered Na2SeO3 (Se), (CdCl2 Cd), and Na2SeO3 + CdCl2 (Cd + Se). Sodium selenite was given intragastrically at a dose of 0.5 mg Se/kg every day and cadmium chloride was injected subcutaneously every other day at a dose of 0.3 mg Cd/kg for 2 weeks. Exposure of rats to Cd caused an increase in the concentration of copper in the kidneys, blood, and liver and a decrease in the lung, but increased the concentration of zinc in the liver and brain and diminished it in the muscles and bones. In animals exposed to Se an increase in the copper concentration was observed in blood and brain; zinc was increased in the blood, heart, brain, and stomach, but decreased in the kidneys. Exposure of rats to Cd + Se resulted in an increase of copper in the kidneys and a decrease in the spleen, lungs, stomach, muscles and bones. Se prevented the cadmium-induced diminution of the zinc levels in the muscles and bones.     

Toxicity,fertility, teratogenicity,and dominant lethal tests in rats administered cadmium subchronically: II. Fertility,teratogenicity, and dominant lethal tests

Four groups of Sprague-Dawley rats, each of which consisted of 14 males and 14 females, were administered 0, 0.1, 1.0, and 10.0 mg/kg/day of cadmium (Cd) for 6 weeks. Males and females within each group were mated 6 days a week for 3 weeks, changing partners every week if necessary. Cd was administered during the mating period. Pregnant females were administered Cd during the gestation period and killed on the 20th day of gestation for teratogenicity tests. Males were mated with 2 virgin females per male per week for 6 weeks. Pregnant females were killed on the 13th day of gestation for dominant lethal tests. Numbers of total implants and live fetuses in the 1.0 mg/kg group decreased slightly, but there was no significant difference from the control. Numbers of total implantations and live fetuses decreased significantly in the 10.0 mg/kg group. In this group, the number of resorbed fetuses increased significantly and the number of corpora lutea decreased without showing a significant difference from the control. Fetuses from the 10.0 mg/kg group showed decreased body weight, body length, and tail length and increased placental weight. About one-third of fetuses were subjected to visceral examination, but no specific anomalies considered to be due to Cd toxicity were found. Skeletal examination was performed for the remaining two-thirds of the fetuses. Delayed ossification of the sternebrae and caudal vertebrae was observed. No dominant lethality was found under the conditions used here. Although physiological deterioration caused by 10.0 mg/kg of Cd has an adverse effect on mating performance, mating ratio, the number of total implants, the number of live fetuses, and the ossification of fetuses, Cd induced neither teratogenicity nor dominant lethality.     

镉急性染毒各器官含量及致死机制研究

目的研究镉急性染毒时，机体重要器官镉分布及致死机制。方法通过静脉分别注射1．0．1．5mg氯化镉后，同步测定重要器官镉含量和功能。结果心、肝、肾、脑、血有一稳定的镉浓度，但镉对肝、肾功能的损害作用低于心功能的损害。结论镉急性染毒镉主要分布在肝和肾，但动物死亡原因不是肝、肾损害引起。而是由于心功能衰竭。     

Effect of diet on urinary and fecal excretion of cadmium,copper, and zinc from rats preaccumulated heavily with cadmium

The effects of diets on urinary and fecal excretion of cadmium (Cd), copper (Cu), and zinc (Zn) were examined after loading Cd to a maximum concentration in the livers of rats. The amount of diet and volume of water taken upad libitum by the rats were also traced throughout. The amount of Cd excreted into urine was dramatically increased immediately after changing to a low protein diet, while that excreted into the feces was slightly decreased (not significant). Zn and Cu excreted into the urine were highly and significantly increased in amount by Cd loading but less affected by diets (not significant). However, Zn and Cu excreted into the feces were lowered by the low protein diet due to the low content of the two metals in this diet. Thus, Cd, selectively released from the liver after changing to a low protein diet, was excreted primarily in the urine.     

Reduced cadmium body burden in cadmium-exposed calves fed supplemental zinc

The objectives of this study were to evaluate the use of practical supplemental dietary zinc to modify the cadmium content in edible bovine tissues and to identify copper interactions with cadmium and zinc. The effect of supplemental zinc (200 or 600 μg/g) on the concentrations of cadmium, zinc, and copper in liver, kidney cortex, muscle, and blood of calves fed 50 μg/g cadmium for 60 days was evaluated. Blood samples were collected before and eight times after starting to feed cadmium or cadmium plus zinc. Liver, kidney, and muscle samples were collected when calves were slaughtered (baseline, at beginning of experimental feeding; cadmium-fed, at end of 60 days feeding). The cadmium concentrations of all sample types collected were markedly increased by the feeding of cadmium. Feeding 600 μg/g supplemental zinc significantly increased the zinc concentrations of liver, kidney cortex, and blood and decreased the cadmium accumulation in these organs as well as muscle. The copper concentrations of muscle or blood were not altered by feeding cadmium with or without zinc but those of liver and kidney cortex were significantly increased by higher dietary levels of zinc and cadmium. The potential use of dietary zinc salts in reducing cadmium body burden in food animals suspected or known to have high cadmium intakes is suggested.     

The effect of cadmium pretreatment on the disposition and excretion of methylmercury and trace elements (zinc, copper) in rats

Cadmium chloride (Cd) was injected s.c. into male rats at a dose rate of 3 mg Cd/kg 3 times a week for 4 weeks. The animals were maintained for administration of methylmercury (203 Hg) chloride at a dose of 3 mg CH3Hg/kg given p.o. 3 times a week for 2 weeks, followed by 3 weeks of recovery period. Animals were sacrificed 24 h after the final dose of MeHg, or 5 weeks after cessation of Cd administration. Cd-pretreatment significantly decreased total Hg concentration in the kidney and RBC and almost completely inhibited demethylation of MeHg in the kidney (from 32% to 3% of inorganic Hg). Cd-pretreatment did not affect urinary excretion of total Hg, but significantly increased daily excretion of total Hg in feces. MeHg given alone significantly increased renal but not hepatic copper levels and decreased copper in the plasma and brain. In Cd-pretreated rats, both renal and hepatic copper concentration were in the normal ranges. Zinc levels in Cd-pretreated rats significantly increased in the kidney, liver and brain but decreased in plasma (compared to control and MeHg-alone treated animals). From these results it can be concluded that Cd-pretreatment may decrease MeHg toxicity by increasing the fecal mercury excretion and by inhibiting the formation of inorganic mercury in the kidney, which is a more potent renal toxin than MeHg.     

Cadmium accumulation in rat organs after extended oral administration with low concentrations of cadmium oxide

Rats were exposed to dietary cadmium oxide (CdO) (2.80 and 7.15 ppm Cd) for 60 days. Between days 20 and 36 of the feeding experiment, only 7.15 ppm Cd significantly reduced body weight, while an improved food utilization was recorded at both dietary Cd concentrations between days 36 and 50. After 40 and 60 days of exposure, Cd concentrations of selected organs and tissues and the excreta were recorded by atomic absorption spectroscopy. Compared to the control animals, Cd levels of hair, bone (femur), blood, and testes did not increase. Soft tissues (liver, kidney, lung, and spleen) displayed significantly elevated Cd concentrations after 40 and 60 days in both dosage groups. An increased level of Cd in muscle was observed in one group only (7.15 ppm, day 40). Maximum Cd levels were 11.6 ppm in liver and 9.75 ppm in kidney on a dry weight basis, reflecting a 68- and 50-fold accumulation of the metal compared to the controls. Only absolute weights of lung and liver decreased slightly in the higher dosage group, while relative weights of all organs investigated were not affected by Cd. The ratios in fecal Cd levels between control and CdO-treated animals partly reflected the Cd concentration ratio between the respective diets. No increase in the urinary Cd level was found during the feeding trial. The significance of Cd accumulation in organs, tissues, and excreta and their value as indicators for CdO exposure are discussed.     

Distribution of cadmium and zinc in tissues and organs,and their age-Related changes in striped dolphins,Stenella coeruleoalba

Cadmium and zinc concentrations were determined in the tissues and organs, including the fetus, of striped dolphins. The kidney showed the highest cadmium concentration and the hepatic cadmium concentration was also relatively high. A similar distribution pattern among soft tissues was also observed with zinc, where its concentration varied less than that of cadmium. A significant positive correlation between zinc and cadmium was found in both the kidney and the liver; the increase of zinc concentration with cadmium was more marked in the liver (Zn:Cd 3∶1 on molar basis) than kidney (Zn:Cd 1∶1). Negligible cadmium concentration in the fetus suggested that cadmium is not transferred to the fetus via the placenta from the mother. Organ-specific age trends of cadmium and zinc concentrations were presented in detail for muscle, liver, kidney, pancreas, brain, and blood. Both metals showed rapid change during the periods of the fetus and weaning.     

Copper levels in maternal and fetal tissues of rabbits bearing intrauterine copper wires

A study was undertaken to determine if copper wire, placed within the uterine lumen after implantation and kept in situ throughout pregnancy, results in an excessive accumulation of the metal in maternal and/or fetal tissues; and if so, what effect if any, such an accumulation may have on both mother and offspring. Copper wires were inserted into the uterine cavities, near the utero-tubal junction, of rabbits on Day 7 of pregnancy and were allowed to remain in situ until Day 28, at which time the animals were sacrificed. Tissues from mother and offspring were subjected to routine histological examinations and their copper content was determined. A parallel series of sham-operated animals served as the control. Copper was released from the intrauterine copper wires at an average daily rate of 38.81 plus or minus 7.26 mcg. Histological examination of maternal adrenal, brain, heart, kidney, liver, lung, ovary, spleen, and uterus revealed no anatomical abnormalities. There was no increase in copper in any of the tissues except the uteri and placentae of animals bearing intrauterine copper wires. There were no anatomical abnormalities in either fetal brain, heart, kidney, liver, or lung. There was an increase in the amount of copper found in the liver of fetuses obtained from animals bearing intrauterine copper wires. As there were no histological differences between livers of the control and experimental groups, and no evidence of teratological effects due to copper, it is assumed that this small but significant increase in fetal liver copper is insufficient to produce any toxic effects on the offspring.     

Copper, manganese, zinc, nickel, cadmium and lead in human foetal tissues

1. Concentrations of copper, manganese, zinc, nickel, cadmium and lead were measured in samples of liver, kidney, brain, heart, lung, skeletal muscle and vertebral bone from forty foetuses of 23-43 weeks gestation. 2. Cu concentrations in the liver were up to 100 times those in other tissues, but only those in the brain showed a significant increase with gestational age. 3. Mn concentrations were similar in all tissues; the over-all range was 0.35-9.27 microgram/g dry matter (DM). 4. Concentrations of Zn in the liver were much higher than in other tissues and decreased with gestational age, whereas levels in skeletal muscle increased. 5. In all tissues Ni concentrations were within the range 0.04-2.8 microgram/g DM and levels in kidney and muscle decreased significantly with age. 6. Cd was detected in most of the tissue samples and concentrations were within the range 0.01-0.58 microgram/g DM. 7. Concentrations of Pb, where it was detected, varied from 0.1 to 2.4 microgram/g DM in the soft tissues and from 0.4 to 4.3 microgram/g DM in the bone samples.     

The effect of low doses of dietary cadmium oxide on the disposition of trace elements (zinc,copper, iron), hematological parameters,and liver function in rats

The Zn, Cu, and Fe concentrations in selected organs, tissues and in the excreta of male Wistar rats, exposed to dietary CdO (2.80 and 7.15 ppm) for 40 and 60 days, were investigated. Concomitantly hematological values and serum enzyme activities were recorded. Zn levels of spleen, kidney, testes, muscle and feces were not affected by the Cd treatment. After 40 days of Cd exposure, the Zn concentration in the hair decreased, while the Zn level of the lung slightly increased. During the feeding trial, Cd produced an increase of liver Zn by about 24%. Femur Zn decreased and Zn in urine increased after 60 days of exposure to 7.15 ppm Cd. Except in hair and urine, the Cu concentration in all organs and tissues investigated remained unchanged. Hair Cu levels decreased after 40 days of Cd exposure but increased after 60 days. At this time, elevated Cu concentration in urine was recorded. After exposure to 7.15 ppm Cd, the Fe content of the lung, liver, spleen, testes, muscle, femur and blood decreased significantly. After 60 days on the 7.15 ppm diet, highest reductions (30%–60%) of Fe content were recorded in the lung, liver, and spleen. Similar to Zn and Cu, the Fe concentration in urine increased at that time. No changes were found in the Fe content of hair, kidney, and feces. In spite of a disturbed Fe metabolism, an anaemic response of Cd-treated rats was not observed. Hematocrit and hemoglobin remained unchanged and the number of red blood cells slightly increased after 40 days of Cd exposure. While the activity of serum alkaline phosphatase was not affected by dietary Cd, the activities of serum-GOT and serum-GPT increased after exposure to 7.15 ppm Cd indicating disturbed hepatic functions.     

Zinc-vitamin A interaction in pregnant and fetal rats: supplemental vitamin A does not prevent zinc-deficiency-induced teratogenesis

The influence of a higher-than-normal intake of vitamin A on the detrimental effects of zinc deficiency on vitamin A metabolism was investigated in pregnant Sprague-Dawley rats. At mating, rats were fed diets containing 100 (control), 4.5, or 0.5 micrograms/g zinc combined with 4 (control) or 8 micrograms retinyl acetate/g. Low intake of zinc, but not of vitamin A, caused food intake, total body weight change, fetal weight and placental weight to be low. Incidence of teratogenic effects was more pronounced in low zinc groups than in controls. Concentrations of vitamin A in maternal plasma and liver were affected by the amount of zinc in the diet. Dietary vitamin A, however, did not affect either of these parameters. Maternal plasma zinc concentration was affected only by low dietary zinc, whereas plasma copper and iron were unaffected by the dietary treatments. Maternal liver iron was higher in zinc-deficient rats than in controls; however, maternal liver zinc and copper concentrations were not altered by dietary treatments. No significant differences in vitamin A concentration of fetal liver, fetal plasma, or placenta were seen among the groups. Fetuses from zinc-deficient dams had significantly lower levels of liver vitamin A and liver zinc than did controls. Fetal liver iron was higher in zinc-deficient fetuses than in controls, whereas fetal liver copper was not affected by dietary treatment. These data suggest that supplemental dietary vitamin A does not ameliorate the effect of zinc deficiency on vitamin A metabolism during pregnancy.