Effect of zinc on human body

1. Zinc is an essential element for the normal development of human body. All organs of human body contain zinc, especially skin, bones, hair, prostate, gonads and eyeballs. Zinc participates in the synthesis of carbonic anhydrase, alkaline phosphatase and KL. Polymerase and other enzymes; Accelerate growth and development and increase the repair of traumatic tissue; Participate in the regulation of taste, vision and sexual function; Participate in energy, cell decomposition and metabolism of other substances; Coordinate immune response and maintain reproduction. Therefore, the content of zinc in human body is very important to health, and supplementing zinc, an essential trace element for human body, has attracted wide attention. 2 related knowledge background of zinc 2. 1 Physical and chemical properties of zinc Zinc is widely distributed in nature, with M8! -Status exists, M8! -it is a strong Lewis acid (n1I: >; 45:@) or electron acceptor. Zinc has strong binding force with thiol and amine electron donors, and has the function of rapid ligand exchange, which is of great significance in the catalysis of metalloenzymes. The chemical properties of zinc in cells mainly involve mercaptan and imidazole ligand, and the combination of zinc and mercaptan is considered to be an important mechanism to regulate the cellular level of this trace element [%]. These physical and chemical properties of zinc are the basis of specific physiological functions of zinc, and all functions related to zinc, such as structural active center or catalytic regulation function, are related to this. 2.2 Distribution of Zinc in Organisms Zinc is distributed in all tissues and organs, body fluids and secretions of the human body, and zinc is more than any other trace elements except iron. However, zinc cannot be stored in adipose tissue like energy, and there is no special storage mechanism of zinc in the body. Zinc content in skin, skeletal muscle, hair, viscera, prostate, gonads, nails, eyeballs and so on is high. And it is very low blood. Zinc mainly exists in the form of enzymes in the body. 2.3 Absorption of Zinc 2.3. 1 Absorption site The absorption of zinc in the gastrointestinal tract generally needs to form a complex with the ligands in chyme in an acidic environment in the stomach, and the main absorption site is in the small intestine. Normal people absorb the most in the duodenum and jejunum. Zinc is rarely absorbed, and less than 10% of zinc in food can be absorbed by the body. 2.3.2 Factors affecting the absorption and utilization of zinc The factors affecting the absorption and utilization of zinc are: (1) Zinc intake: The zinc content in the diet itself will affect the absorption of zinc in the body. The absorption rate of zinc decreased with the increase of dietary zinc content. (2) protein: The complex of zinc and protein with low molecular weight and low affinity will promote the absorption of zinc, and the absorption rate of zinc will increase with the increase of protein content in food, showing obvious positive correlation. (3) Low molecular ligands and chelates: When zinc forms a complex with low molecular ligands or chelates, the solubility of zinc can be increased, thus promoting the absorption of zinc. It is suggested that ligands or chelates (such as EDTA), amino acids (such as histidine) and organic acids (such as malic acid, citric acid and lactic acid) can promote the absorption of zinc. (4) Iron: Taking a certain amount of iron from supplements every day can reduce the absorption of zinc. Comparatively speaking, when iron intake is low, zinc absorption will increase. 2.4 Physiological Function of Zinc 2.4. 1 Catalytic Function Zinc is closely related to the composition and activity of enzymes. About 100 specific enzymes contain zinc, and the activity of these enzymes depends on the presence of zinc. Zinc-dependent metalloenzymes can be found in all six enzyme systems. At present, RNA polymerase, alcohol dehydrogenase, carbonic anhydrase and alkaline phosphatase are widely studied. If zinc is deficient, it will lead to a series of metabolic disorders and pathological changes, and the activities of various zinc-containing enzymes will decrease, such as metabolic disorders of cystine, methionine, leucine and lysine. The possible relationship between zinc-containing metalloenzymes and diseases, including the relationship between zinc deficiency and alcohol dehydrogenase in alcoholic liver disease, and the decrease of thymidine kinase mRNA activity can partly explain the growth retardation of zinc-deficient animals. 2.4.2 Structure and Function Some regions inherent in protein can combine with zinc to produce some bioactive molecules in protein, and most protein, including cysteine and histamine acid residues, can chelate with zinc to form zinc finger protein. Zinc finger protein was first confirmed in frog oocyte transcription factor TF ⅲ a in 1985. The existence of zinc finger proteins and their key biochemical functions theoretically determine the importance of strict steady-state control of zinc metabolism. In the in vitro experiment of a transcription factor, it was found that the removal of zinc from zinc finger protein by zinc MT (demethylsulfhydryl protein) may lead to the loss of real function. At present, the relationship between zinc nutrition and zinc finger protein in diet has not been widely demonstrated. 2.4.3 The regulatory function is the expression of metallothionein, and the mechanism of regulating metallothionein expression includes that metal-binding transcription factor (MTF 1) obtains zinc in intracellular cytosol tuberculosis, and then reacts with metal response element (MRE) to activate gene transcription. Animal experiments show that the null mutation of MTF 1 gene will have a fatal effect on mouse embryos, which indicates that MTF 1 definitely plays a regulatory role in some key genes. There is evidence that zinc can exert its regulatory function by affecting apoptosis and the activity of protein kinase cells. In addition, zinc's participation in normal synaptic signal transduction is also a part of its regulatory function. 3 The relationship between zinc and health and disease 3. 1 zinc and coronary heart disease Zinc is closely related to the occurrence of heart disease. Zinc can competitively inhibit the catalytic effect of iron thiol complex on oxygen free radicals, thus protecting the normal metabolism, structure and function of myocardial cells. Zinc is also related to human serum cholesterol levels. The content of zinc in mitochondria, microsomes and soluble proteins of myocardial cells in the dead zone of myocardial infarction and around * * * is significantly higher than that of normal myocardial cells, and there are a large number of zinc-containing alkaline phosphatase aggregates in the myocardial infarction and necrosis zone, which indicates that zinc enzyme participates in the repair process and plays an important role in the pathogenesis of coronary heart disease. The research data confirmed that the zinc content in the heart of patients with cardiovascular diseases such as coronary heart disease decreased, the zinc concentration in angina pectoris decreased obviously, and increased obviously after remission, but it was still lower than that in the control group. It is suggested that the excessive consumption of serum zinc during myocardial injury leads to the transfer of serum zinc to traumatic tissue, which leads to the decrease of serum zinc concentration. It is reported that zinc deficiency can affect the activity of antioxidant enzymes, reduce the free radical scavenging rate, increase lipid peroxidation, cause arteriosclerosis, and then lead to cardiovascular diseases. 3. The study of1zinc and liver cirrhosis found that the blood zinc concentration of patients with liver cirrhosis decreased obviously, which suggested that the decrease of blood zinc was of great significance in the occurrence and development of liver cirrhosis. Because hepatocyte necrosis is the main cause of liver fibrosis, zinc deficiency will reduce the ability of human body to scavenge free radicals, resulting in cell membrane damage during lipid peroxidation, thus aggravating hepatocyte necrosis and promoting the persistence of fibrosis factors. Therefore, the decrease of serum zinc is the related factor of the transformation from hepatitis to cirrhosis and liver cancer. In short, zinc deficiency will affect the immune function of the body and aggravate the immune dysfunction of liver cirrhosis. 3.3 Zinc is closely related to diabetes and diabetes. Some researchers reported that the blood zinc concentration of stable type 2 diabetes decreased, and the urinary zinc loss of all diabetic patients with hypoglycemia increased, so it should be supplemented in time. There are two zinc atoms in each insulin molecule, which helps glucose move on the cell membrane, so zinc is related to insulin activity. Zinc can regulate and prolong the hypoglycemic effect of insulin. If zinc is deficient in the body, the conversion rate of proinsulin will decrease, which will lead to the decrease of insulin level in serum and the utilization of glucose by muscle and fat cells. A large amount of glucose will remain in the blood, which will increase the blood sugar concentration and lead to diabetes. 3.4 Zinc and male reproductive system diseases In recent years, it has been found that the relationship between zinc and pituitary function is particularly important, and it plays an important role in maintaining the coordination of thalamus-pituitary-gonad axis. Zinc deficiency can inhibit the release of pituitary gonadotropin and make gonadal dysplasia or gonadal reproductive endocrine dysfunction; Zinc is directly involved in the process of sperm formation, maturation, activation or capacitation, and plays an important role in sperm vitality, metabolism and stability. Zinc can delay the lipid oxidation of sperm membrane, maintain the integrity and stability of cell membrane, and keep sperm vitality. Sperm absorbs zinc from seminal plasma and combines with sulfhydryl groups of nuclear chromosomes to prevent chromosome disaggregation and promote sperm-egg combination, which is beneficial to fertilization. Zinc can change the speed of testicular spermatogenesis and has an important influence on sperm metabolism. Zinc participates in the synthesis of lactate dehydrogenase and carboxypeptidase A, which are coenzymes of many enzymes. Zinc deficiency will affect the activity of enzymes, and then affect reproduction. It has been proved that testis, prostate and epididymis tissues, especially semen, are rich in zinc, and the increase of sperm density is often accompanied by the increase of zinc content, which can increase the number of sperm. The content of zinc in semen of incomplete liquefaction infertility group decreased, especially in inflammatory group and azoospermia group. Zinc deficiency can make testicular tissue atrophy, abnormal changes, seminiferous tubule basement membrane thinning, abnormal sperm growth and decreased motility, accompanied by a decrease in serum testosterone level and an increase in serum follicle stimulating hormone and luteinizing hormone. 3.5 The study of zinc and nephrotic syndrome found that the serum zinc concentration was parallel to the serum albumin and globulin content, showing a significant positive correlation. In serum, 30%-40% zinc is firmly bound to α2 macroglobulin, and 60%-70% zinc is loosely bound to albumin. It is suggested that the loss of protein, especially albumin, in patients with glomerular diseases is the main reason for the decrease of serum zinc value, and it is also related to the decrease of appetite, zinc intake, intestinal absorption and clinical application of diuretics and antihypertensive drugs. Jin Zhijuan et al. compared the serum zinc concentration of children with 3 1 nephrotic syndrome before and after treatment. Results The serum zinc concentration after treatment was significantly higher than that before treatment, which indicated that the protein loss in urine was obviously controlled and the appetite was obviously increased after taking adrenocortical hormone in children with nephrotic syndrome. Gastrointestinal absorption is the main reason for the increase of serum zinc. 3.6 The content of zinc in the complex of retina and choroid of visually impaired eyes is the highest, and the levels of several zinc-containing enzymes, including carbonic anhydrase and retinol dehydrogenase, are very high, and the latter can oxidize retinol into retinol aldehyde, that is, the form of vitamin A in rod cells. Night vision depends on providing appropriate amount of retinaldehyde to rod cells to form rhodopsin. Zinc deficiency leads to weakened dark adaptation, decreased vision, myopia, hyperopia and astigmatism. 3.7 Zinc and neuropsychiatric disorders Zinc plays an important role in brain development. Some foreign scholars have determined the zinc content in eight areas of rat brain, and found that the zinc content in hippocampus is the highest, and the other places with high zinc content are brain, striatum and cerebellum in turn. Zinc deficiency has a great influence on brain function and neuropsychiatry. Zinc deficiency can cause the brain of young rats to become smaller, the number of brain cells to decrease and the nuclear-cytoplasmic ratio to increase. Severe zinc deficiency can cause fetal central nervous system malformation, such as anencephaly and spina bifida. In addition, zinc deficiency may also change the ultrastructure of the brain, such as the decrease of granulosa cells in mice, the abnormality of Purkinje cells, and the decrease of dendrite branches and synaptic connections. Flow cytometry also found that the cell proliferation index and the percentage of G+M cells in zinc deficiency group were significantly lower than those in control group. The percentage of G0/G 1 cell was significantly higher than that of the control group. The model of zinc-deficient young rats established from weaning or lactation period found that the contents of DNA and RNA in brain tissue, DNA content in hippocampal pyramidal cells, maze learning ability and active avoidance response acquisition ability of young rats in zinc-deficient group were significantly lower than those in normal control group. Electron microscopic observation also showed that zinc deficiency in synaptic vesicles of hippocampal neurons was significantly reduced. The research of Kong et al. shows that zinc water can obviously improve the learning and memory ability of rats, accompanied by changes in brain ultrastructure; However, long-term low zinc diet can lead to the decrease of zinc content, DNA synthesis, induction rate of long-term enhancement effect and learning and memory ability in the brain. 3.8 Zinc and Skin Diseases In the early studies of zinc deficiency in rats and mice, hair loss and visible skin damage have been observed. When people are seriously deficient in zinc, they will also show skin damage. Common ones are oral ulcer, angular stomatitis, atrophic glossitis, symmetrical erosion, blisters or pustules around eyes, mouth, anus, limbs, elbows and knees, forearms, hyperkeratotic scars and so on. Histological observation showed psoriasis-like dermatitis, epidermal hyperplasia, dyskeratosis and sporadic dyskeratotic cells. Hair is fluffy, brittle, dull and alopecia; Repeated oral ulcers, poor wound healing, etc. 3.9 Zinc and decreased immune function. At present, a large number of documents show that the immune function of zinc deficiency patients is impaired, and zinc deficiency patients are prone to repeated infections, mainly manifested as hypoplasia or atrophy of thymus, lymph nodes, spleen and tonsil, weakened or negative skin delayed allergic reaction, and decreased lymphocyte transformation rate.