ISSN:0731-5724    

DOI:10.1080/07315724.1985.10720061

出版商:Routledge    

年代:1985

数据来源: Taylor

ISSN:0731-5724    

DOI:10.1080/07315724.1985.10738064

出版商:Routledge    

年代:1985

数据来源: Taylor

摘要:

Protein-calorie malnutrition is associated with impaired immunocompetence and increased susceptibility to infection. Clinically evident nutritional deficiency syndromes, however, are composite of deficits of many essential nutrients, each of which may exert an important regulating effect on immunity. Among other nutrients, several trace elements have been shown to regulate immune responses, particularly cell-mediated immunity. Zinc undernutrition results in lymphoid atrophy and reduced capacity to respond to many T-cell-dependent antigens. Plaque forming cell response to heterologous erythrocytes is decreased, as is the function of B cells. In zinc deficient rodents, the generation of cytotoxic lymphocytes in the spleen is reduced. Antibody-dependent cell-mediated cytotoxicity is largely unchanged. In acrodermatitis enteropathica, lymphocyte proliferation response to mitogens is decreased and there are significant changes in delayed hypersensitivity responses and in the proportion of various T cell subsets. Neutrophil function is not changed by zinc deficiency. Iron deficiency results in a slight decrease in the number of rosette-forming T cells and a significant impairment of lymphocyte response to mitogens and antigens. Polymorphonuclear leukocytes are unable to kill ingested bacteria and fungi in an efficient manner. Copper deficiency impairs cell-mediated immunity, as does selenium deficiency when it is associated with vitamin E lack. Several pathogenetic mechanisms may underlie such alterations in immunity. Many heavy metals impair immune responses. These effects of trace elements on immunity may have important fundamental and practical implications.

ISSN:0731-5724    

DOI:10.1080/07315724.1985.10720062

出版商:Routledge    

年代:1985

数据来源: Taylor

摘要:

Over the past 30 years human magnesium (Mg) deficiency has become an accepted fact in most medical circles. Our index patient had striking neurological manifestations including generalized tremulousness, grimaces and fibrillary twitches of facial muscles, athetoid and choreiform movements of upper extremities, dysphagia, inability to speak, repeated convulsions, and confusion. She had received glucose in water and saline intravenously for several months. A patient with chronic alcoholism was noted to have almost identical symptoms and signs as the index patient. He also responded dramatically to MgSO4 injections. This resulted in a series of studies on patients with chronic alcoholism. The evidence of Mg deficiency in alcoholism includes the following: significant hypomagnesemia, strongly positive Mg balance during recovery, significant decrease in muscle Mg, a deficit of total exchangeable 28Mg quantitatively similar to deficit by balance studies, often a dramatic response of symptoms to therapy with Mg, and diuresis of Mg produced by ingestion of alcohol. Lipolysis with high levels of long-chain free fatty acids (FFA) occurs in withdrawal of alcohol in chronic alcoholism, withdrawal of certain addictive drugs, after trauma, surgery, administration of adrenergic compounds or theophylline, exposure to cold, and an adverse environment as in grass staggers. Concentrations of Mg fall when FFA increase in all of the above circumstances. This phenomenon has wide implications in health and disease. Better awareness of Mg deficiency in a wide variety of clinical conditions will result in life-saving treatment and less morbidity of other patients.

ISSN:0731-5724    

DOI:10.1080/07315724.1985.10720063

出版商:Routledge    

年代:1985

数据来源: Taylor

摘要:

We examined interaction of the trace element zinc with copper and lead. In sickle cell anemia, the usual situation is one of mild to moderate zinc deficiency owing to renal loss of zinc. Zinc deficiency seems to produce a mild overburden of copper and an increased ceruloplasmin level, probably by enhancing copper absorption. With zinc therapy, this process is reversed. Pharmacological doses of zinc, when administered in a way to ensure effectiveness (without food) will usually lead to copper deficiency. We have taken advantage of the copper-depleting effect of zinc to design a new therapy for Wilson's disease. Zinc, by inducing intestinal metallothionein, inhibits absorption of copper from food, and inhibits reabsorption of endogenously secreted copper, thereby producing a negative copper balance in Wilson's disease. Once we are certain that zinc blocks accumulation of copper in the liver of Wilson's disease patients, zinc therapy will be available as one approach for treating this fatal disease. The animal literature indicates that zinc protects against lead toxicity when both elements are given orally, no doubt through the intestinal metallothionein mechanism. In preliminary experiments in rats, we have not been able to show that toxicity from lead that arrives into the body through a nonoral route is affected by oral zinc supplements.

ISSN:0731-5724    

DOI:10.1080/07315724.1985.10720064

出版商:Routledge    

年代:1985

数据来源: Taylor

摘要:

Genetic trace metal disturbances can be at three levels. Trace metals play an important role in the metabolism of genetic macromolecules and the information transfer system. Deficiency or excess of trace metals caused either by dietary or genetic factors will affect the normal functioning of the whole organism. The roles of trace metals in carcinogenesis/mutagenesis and ageing are typical of this category. The second level of genetic trace metal disturbances affect the metabolic pathway of the trace metal itself. Biochemical derangement resulting from genetic defects cause aberrant metabolism of the element and thus disease symptoms. Diseases caused by abnormal metabolism of copper, zinc, iron, and molybdenum are discussed. Trace metal disturbances can also be the result of other genetic diseases. This aspect of genetic trace metal disturbances is least investigated. However, information should be important for improving the existing treatment protocol for the more common inborn errors of metabolism, such as phenylketonuria.

ISSN:0731-5724    

DOI:10.1080/07315724.1985.10720065

出版商:Routledge    

年代:1985

数据来源: Taylor

摘要:

Zinc deficiency may complicate many gastrointestinal malabsorptive states. Zinc deficiency may manifest itself in a myriad of ways, ranging from skin lesions to immune dysfunction. This paper reports many of the ways in which zinc deficiency may appear in malabsorption syndromes and possible mechanisms for the development of this zinc deficiency.

ISSN:0731-5724    

DOI:10.1080/07315724.1985.10720066

出版商:Routledge    

年代:1985

数据来源: Taylor

摘要:

During the past two decades, essentiality of zinc for man has been established. Deficiency of zinc in man attributable to nutritional factors and several diseased states has been recognized. High phytate content of cereal proteins decreases availability of zinc; thus the prevalence of zinc deficiency is likely to be high in the population subsisting mainly on cereal proteins. Zinc deficiency has been noted to occur in patients with malabsorption syndrome, chronic renal disease, cirrhosis of the liver, sickle cell disease, AE (acrodermatitis enteropathica), and other chronically debilitating diseases. Growth retardation, male hypogonadism, skin changes, poor appetite, mental lethargy, and delayed wound healing are some of the manifestations of chronically zinc-deficient human subjects. In severely zinc-deficient patients, dermatological manifestations, diarrhea, alopecia, mental disturbances, and intercurrent infections predominate. If untreated, the condition becomes fatal. Zinc deficiency affects testicular functions adversely in man and animals. This effect of zinc is at the end-organ level. It appears that zinc is essential for spermatogenesis. Zinc is involved in many biochemical functions. Several zinc metalloenzymes have been recognized in the past decade. Zinc is required for each step of cell cycle in microorganisms and is essential for DNA synthesis. The effect of zinc on protein synthesis may be attributable to its vital role in nucleic acid metabolism. The activities of many zinc-dependent enzymes have been shown to be affected adversely in zinc-deficient tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

ISSN:0731-5724    

DOI:10.1080/07315724.1985.10720067

出版商:Routledge    

年代:1985

数据来源: Taylor

摘要:

Essentiality of zinc in nutrition of higher animals was established in 1934. Dietary zinc deficiency in humans was recognized in 1961. Dietary requirements for zinc have been estimated factorially and by balance studies. Factors that influence dietary zinc requirement include dietary and other substances that either facilitate or inhibit absorption and retention of zinc; and metabolic phenomena that influence retention or excretion of the element. These determinants must be considered in estimating the requirement and the recommended dietary allowance for this essential element. An approach that has been used to assess requirement is the measurement of dietary zinc retention by men fed diets providing sufficient energy to meet the needs of each individual and containing other nutrients in proportion to energy content. By measurement of chemical balance and subsequent analysis of the data by multiple regression, dietary factors influencing requirement have been identified and amounts of dietary zinc essential for needs calculated. Using this approach, 83% of the variance (P less than 0.0001) in requirement was accounted for by the dietary content of phosphorus and nitrogen when data from 157 twenty-eight to thirty day studies were analyzed. The equation, Intake = 1.466 + 0.23 (Zn balance) + 5.19 (P intake) + 0.40 (N intake)−0.30 (P intake−1.389) (N intake - 14.646), was used to estimate zinc requirement of persons who participated in the most recent USDA Food Consumption Survey. For all age groups, ages 9 to greater than 75y, males and females, the mean (range) difference between the estimated intakes and calculated requirements were: males 1.5% (−6.5 to + 8.1), females 11.3% (−1.1 to + 20.3). Thus, mean intakes were generally within the 95% confidence limits of the estimated requirements. Of some interest was the finding that the mean intake of none of the groups was equivalent to the Recommended Dietary Allowance. The mean intake of males ranged from 9.32 mg in men 75y and older to 13.53 mg in persons 15–18y. The mean intake of the females ranged from 7.04 mg in women 75y and older to 9.22 mg in persons 12–14 y.

ISSN:0731-5724    

DOI:10.1080/07315724.1985.10720068

出版商:Routledge    

年代:1985

数据来源: Taylor

摘要:

Veterinary nutritional science has embraced the study of copper for decades, but copper has languished as an orphan among human nutritionists because of the obscurity of clinical copper-deficiency states in man. As medical investigators, we may have gone down a long road, missing the forest for the trees. Indeed, overt copper-deficiency syndromes in humans have been recognized since the 1960s, and the list of contributing factors is expanding. Unwise self-medication with megadoses of zinc, for instance, might produce a mini-epidemic of copper deficiency. Moreover, induced copper deficiency may someday prove to be a legitimate therapeutic intervention in some disease states. But, the influence of subtle differences in dietary intakes of copper on human health may be much more important than frank copper depletion. Moreover, the recognition of disordered copper metabolism simulating a deficiency state--as occurs in Menkes' KHS and in variant Elhers-Danlos syndrome--has important implications. The full description of the relationship that thionein and other intracellular proteins might have in the etiology of these alterations has yet to be written. The elegance of the interplay of biochemical defects, physiological dysfunction, and clinical manifestations in copper metabolism is virtually unmatched in nutritional biology; yet, our present abilities to determine human copper status are limited. Now that it is clear that intracellular redistribution as well as total-body depletion can effect the disruption of copper-dependent functions, a concerted effort to improve status assessment through the use of functional indices should become a high priority. Finally, the pursuit of the bases of copper's involvement in host defenses, antiotoxidant protection and carbohydrate metabolism--functions in which clear links to established mammalian cuproenzyme are at present elusive--should provide exciting substrate for investigators for years to come.

ISSN:0731-5724    

DOI:10.1080/07315724.1985.10720069

出版商:Routledge    

年代:1985

数据来源: Taylor