Pregnant rats were fed liquid diet to determine the influence of maternal ethanol intake on maternal and pup liver copper when dietary copper was low. The diets, which contained either 0.75(low) or 3.75(control)mg copper/1 with or without 30% of kcal from ethanol, were fed throughout gestation and the first 15 days of lactation. maternal calorie intake and body weight were unaffected by dietary treatment. Ethanol intake depressed maternal liver copper concentration only when diet copper was low(interactive effect P<0.05). Although ethanol intake depressed total pup liver copper concentration regardless of dietary copper level, the interactive effect observed in maternal liver was reflected incopper content of the pup liver metallothionein fraction eluted from a Sephadex G-75 column. The zinc content of metallothionein was inversely related to copper content of metallothionein. Results suggest that pregnancy and lactation is a special period to develop a copper deficiency when low copper intake and ethanol ingestion are combined not only in mothers but also in their offspring.
The purpose of this study was to analyse copper intake and effect ofZn(30mg ZnSO4/d) supplementation on plasma copper level of Korean adults. Daily Cu intakes were studied in ninety subjects aging 20-20 years. Among them twenty four subjects participated in 6 weeks Zn supplementation study. The men consumed 1.47($\pm$0.64)mg of Cu and the women consumed 0.98($\pm$0.43)mg of Cu daily. the most abundant sources of Cu was meat, fish, egg and soybean group, the second was cereal and grain group and the third was vegetable group. These three groups supplied about 90% of copper in the subjects. The plasma copper level of the subjects was not changed much until two weeks of Zn supplementation. However, after two weeks of Zn supplementation plasma copper level was reduced continuously during the experiment. There was no significant difference in plasma Cu level between control and supplement group of the men, while the supplemented women showed significantly lower plasma Cu level than control group at week 4(p<0.01) and week 6(p<0.05). Although plasma Cu level of the subjects was slightly changed, its concentration in plasma was still in normal range in all groups and no one showed clinical Cu deficiency. Therefore the Zn supplementation of RDA level doesn't seem to cause any adverse effect on Cu status.
Plants need essential mineral elements to favorably develop and to complete their life cycle. Despite the irreplaceable roles of microelements, they are often ignored due to the relative importance of macroelements with their influence on crop growth and development. We focused on the changes in primary metabolites in the leaves and roots of bell pepper plants under 6 microelements-deficient conditions: Copper (Cu), Zinc (Zn), Iron (Fe), Manganese (Mn), Boron (B) and Molybdenum (Mo). Bell pepper plants were grown in hydroponic containers, and individual elements were adjusted to 1/10-strength of Hoagland nutrient solution. A remarkable perturbation in the abundance of the primary metabolites was observed for the Fe and B and the Mn and B deficiencies in the leaves and roots, respectively. The metabolites with up-accumulation in the Fe-deficient leaves were glucose, fructose, xylose, glutamine, asparagine and serine. In contrast, the Mn deficiency also resulted in a higher accumulation of glucose, fructose, xylose, galactose, serine, glycine, β-alanine, alanine and valine in the roots. The B deficiency noticeably accumulated alanine, valine and phenylalanine in the roots while it showed a substantial decrease in glucose, fructose and xylose. These results show that the primary metabolism could be seriously disturbed due to a microelement deficiency, and the alteration may be either the specific or adaptive responses of bell pepper plants.
This study was performed to investigate the biochemical status of iron, zinc and copper for 125 preschool children (Males : 69, Females : 56) residing in a low-income area of Seoul. The number of subjects aged, 3, 4, 5 and 6 were 19, 41, 41 and 24, respectively. The hemoglobin level of the children aged 3 was 11.8 g/dl and was lower thant hat of the other groups(p<0.05). Similar results were found for hematocrit and serum zinc. The percentage of children with an iron deficiency assessed by Hb(3-5) years : <11.0g/dl, 6 years: <11.5g/dl), Hct(3-6 years : 33%, 6 years : <35%), serum transferrin(<16%) and serum ferritin(<10ng/ml) were 4.3%, 9.5%, 8.2% and 17.7%, respectively. The mean serum zinc was 67.9$\mu\textrm{g}$/dl and urinary zinc was 0.1300mg/day. Low serum zinc (61.0$\mu\textrm{g}$/dl) occurred in 28.0% of the children. The mean serum copper was 110.5$\mu\textrm{g}$/dl and urinary copper was 0.0126mg/day. The prevalence of children with elevated serum copper($\geq$ 130$\mu\textrm{g}$/dl) was 54.8%, which was higher than 7.4%, the prevalence of low serum copper(<70$\mu\textrm{g}$/dl). Children with higher status, more weight, larger girth of chest, or larger midarm circumference showed higher values of Hb. The height and weight of children also showed a positive crrelation with serum zinc(P<0.001-P<0.05).
Journal of the Korean Society of Food Science and Nutrition
/
v.27
no.6
/
pp.1244-1252
/
1998
The purpose of this study is to evaluate the nutritional status of vitamin and minerals in the patients with alcoholic liver disease and to obtain the materials for nutritional education for alcoholics. The subjects consist of 80 patients with alcoholic liver cirrhosis(ALC) and 12 patients with alcoholic fatty liver(AFL). The control group included 57 alcoholics without liver disease(A), 32 patients with viral liver cirrhosis(VLC) and 194 normal men(NL). Biochemical evaluation of nutritional status was investigated by the analysis of blood samples. The frequency of vitamin B1 deficiency in the ALC, AFL and A groups as indicated by the erythrocyte transketolase activity coefficient were 46.0%, 66.7% and 57.9% respectively. The frequency of vitamin B2 deficiency in the ALC, AFL and A groups as indicated by the erythrocyte glutathione reductase activity coefficient were 9.8%, 8.3% and 38.6% respectively. Vitamin A deficiency was not detected in the alcoholic subjects. The frequency of vi tamin E deficiency in ALC, AFL and A were 96.3%, 66.7% and 86.0% respectively. The levels of plasma lipid peroxidation products were significantly higher in the alcoholic subjects than in the normal subjects. The frequency of subjects below normal range of hemoglobin were 85.0% in ALC, 50.0% in AFL and 31.6% in A. The frequency of copper deficiency in the ALC, AFL and A groups were 48.4%, 16.7% and 17.5% respectively. The frequency of zinc deficiency in the ALC, AFL and A groups were 83.8%, 41.7% and 66.7% respectively. Overall, the vitamin and minerals status of the alcoholic subjects in this study was evaluated to be very poor on the basis of biochemical assessments. The results suggest that alcohol abuse and poor dietary intake could cause malnutrition and may be important risk factors in causing alcoholic liver disease in alcoholics. In addition, vitamin B1, vitamin B2, Cu, Fe and antioxidant supplementation may be effective in nutritional therapy for chronic alcoholics.
Anemia is a usual finding in advanced malignant diseases. Various mechanisms were reported as to be involved in the development of anemia of this kind, and they may differ in individual cases. Tumor anemias may be due, for instance, to chronic blood loss, shortened life span of the red blood cells or a decreased hemopoiesis in the bone marrow. The serum iron and copper levels, total iron binding capacity, apparent half survival of $^{51}Cr$-labelled red blood cells were measured along with the ferrokinetic studies using $^{59}Fe$ in 64 patients with various malignant tumors. Following were the results: 1. The serum iron levels were decreased in all cases. There existed no correlation between the serum iron levels and the severity of the diseases. 2. The serum copper levels were increased, particularly in lung cancer, rectal cancer, hepatoma and various sarcomas. There was also no correlation between the serum copper levels and the severity of the diseases. 3. The serum iron levels appeared to be inversely proportional to the serum copper levels. 4. The total iron binding capacities were within normal limits in all cases. There were also no correlations between the total iron binding capacities, serum iron levels and the severity of the diseases. 5. The patients could be classified according to the ferrokinetic patterns, namely, that of iron deficiency anemia in 10 cases, that of refractory anemia in 6 cases, normal in 1 case and that of atypical abnormal in 9 cases. 6. Apparent half survival time of $^{51}Cr$-labelled red blood cells were definitely shortened in half of the cases.
Purpose : Anticonvulsants have a number of side effects and some of them may be attributed to a disturbance of serum trace metal homeostasis. Although they are minor building components in tissues, they play important functional roles in the peripheral and central nervous system. We measured serum copper and zinc levels in epileptic children who were treated with anticonvulsants to know the effects of anticonvulsants on serum copper and zinc levels. Methods : Serum copper and zinc levels were determined in 64 epileptic patients receiving anticonvulsant therapy in Chungnam National University Hospital, and in 20 normal controls. Sixty-four epileptic patients were divided into three groups : 16 patients who were treated with valproic acid monotherapy; 26 patients who were treated with valproic acid in addition to other anticonvulsants; and 22 patients who were treated with anticonvulsants except for valporic acid. Results : All patients receiving anticonvulsants had significantly lower serum copper levels($80.21{\pm}19.42{\mu}g/dL$) in comparison to the normal controls($102.12{\pm}32.8{\mu}g/dL$). Serum zinc levels in patients receiving anticonvulsants($79.78{\pm}21.88{\mu}g/dL$) were not statistically different from those of controls ($85.26{\pm}29.81{\mu}g/dL$). There were no significant difference of serum copper and zinc levels among the three groups. Conclusion : In this study, we clearly showed that anticonvulsants decreased serum copper levels. Although we did not observe any clinical findings related to copper deficiency, we should pay attention to potent copper deficiency in patients with anticonvulsant treatment.
Zinc is one of the essential trace elements in the living organism for growth and health. The first identified metalloenzyme, carbonic anhydrase, is a zinc compound and several others have been described since. Among zinc deficiency syndromes in animals porcine parakeratosis has been successfully treated with zinc supplements, and in man a syndrome of anemia, hypogonadism, hepatosplenomegaly, and dwarfism, prevalent in parts of Iran and Egypt, has been ascribed to lack of zinc in the diet. Dietary zinc excess in the rat is manifested by a hypochromic, microcytic anemia, poor growth, reduction in liver catalase and cytochrome oxidase. The present study is an attempt to delineate the changes of tissue contents of trace elements, especially of iron, copper and zinc in liver and kidneys of the rats. Weanling albino rats, weighing 60 to 80gm. were used in this experiments. The rats were housed in cages with aluminum floors and received feed and distilled water ad libitum. Animals were divided into three groups, control, low zinc diet and high zinc diet groups. The high zinc diet group was subdivided into 0.5% Zn and 0.7%Zn groups. The supplementary copper or iron was added to the high dietary zinc groups. The animals were sacrificed and the tissues were washed several times with deionized water. The wet digested samples were analyzed by Hitachi Model 207 atomic absorption spectro-photometer for the determination of iron, copper and zinc in the liver and kidney. Hemoglobin level in the blood was measured by cyanmethemoglobin method. The results of this study are as follows: 1) All rats fed high zinc diets and low zinc diets gained less weight than control. Weight gain was not improved by the supplementary copper or iron and both. 2) Hemoglobin concentration was decreased significantly in the rats fed high zinc diets and less in the low zinc diet. Supplementary copper and iron to the higher zinc diet appeared to give some improvement of anemia. 3) The iron contents of the liver and kidneys were significantly decreased in the high zinc groups and the reduction was more significantly in the rats receiving higher zinc diet (0.7%). The supplementary copper caused a further depression of liver iron. On the other hand, the iron, added to the high zinc diet lessoned the severity of the decrease in liver iron and caused kidney iron to be maintained almost at the level found in the rats fed by zinc and supplementary copper diet. 4) High zinc diets did not change copper content of the liver and kidney. Supplementary copper elevated the concentration in the liver and kidney and added iron had no effect on the accumulation of copper in the liver and kidneys. 5) The high zinc diets caused marked increases of zinc content in the liver and kidney. Supplementary iron to the high zinc diet caused increases of zinc contents of liver and kidneys.
Wilson's disease is an autosomal recessive disorder of copper metabolism consequence of which leads to accumulation of copper in the liver, brain, cornea and other tissues. The manifestations are more likely to be hepatic in the early childhood and neurological in the adolescents. In addition, the abnormalities that develop during disease progression may result in other manifestations such as hematologic, endocrine, or renal findings. We report a thirteen year-old girl who manifested tetany shortly after the initial diagnosis of Wilson's disease. Despite aggressive calcium, magnesium and vitamin D replacement, the hypocalcemia and hypomagnesemia did not respond to the therapy promptly. It took more than three weeks for blood levels of the minerals to be normal. We concluded that tetany occurred in our patient because of hypoparathyroidism as a rare complication of Wilson disease, vitamin D deficiency resulting from various conditions, and inconclusive hypomagnesemia.
Purpose: Patients with chronic gastrointestinal disease are at risk for trace element deficiency due to impaired absorption and gastrointestinal loss. The aim of this study was to evaluate the trace element status of patients with gastrointestinal disease by blood and hair analysis, and to determine the usefulness of hair mineral analysis for diagnosing trace element deficiency not detected by a blood test. Methods: An analysis of hair minerals was performed and compared with blood mineral analysis in 13 patients with chronic gastrointestinal disease. The concentration of each element in the hair and blood was compared in the subgroups based on parenteral nutritional support or clinical symptoms. Results: Almost all patients had trace element deficiency. The trace elements deficient in the blood or hair analysis included zinc, selenium and copper. The hair zinc concentration was significantly lower in the group receiving parenteral nutritional support. The hair selenium concentration was statistically associated with the clinical symptoms of hair loss, brittle hair and loss of hair pigmentation. Conclusion: The results of this study suggest that patients with chronic gastrointestinal disease should receive adequate zinc and selenium replacement to avoid trace element deficiency especially when treated with long-term parenteral nutrition. Hair mineral analysis is useful as a complementary tool for the detection of a trace element deficiency.
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