STUDY - Technical - New Dacian's Medicine
Disorders
in the Mechanism of Drugs
Translation Draft
I'll start with some classifications and functions related to microelements. The micro-elements category includes metals that are found in concentrations of less than one microgram per gram of liquid mass. Most are essential nutritional compounds in humans (Fe - Iron with specific biochemical function in oxygen transport, Zn - Zinc with function in the degradation of nucleic acids and proteins as well as in alcohol metabolism, Cu - Copper with function in hemoglobin synthesis, connective tissue metabolism and bone development, Co - Cobalt with function in methionine metabolism, Mn - Mangan with function in oxidative phosphorylation, metabolism of fatty acids, mucopolysaccharides and cholesterol, Mo - Molybdenum with function in the metabolism of xanthin, Se - Selenium with antioxidant function, Ni - Nickel with possible function in stabilizing the structure of RNA and Cr - Chromium with possible function in the binding of insulin at the cellular level as well as in glucose metabolism), others being essential for different species, but may also be necessary for humans (As - Arsenius , Sn - Staniul, V - Vanadi and Si - Silicium). Microelements, as well as metals found in higher concentrations in the body (Na - Natrium/ Sodium, K - Kaliul/ Potassium, Ca - Calcium, Mg - Magnesium), partly exercise their role due to their electrical charging, mobility and affinity for biological ligands. Sodium (Na) and potassium (K) form weak bonds with negatively charged ligands and easily cross cell membranes.
They play the role of transporters of electrical impulses transmitted along nerve fibers, etc. Other elements (Mg, Ca) form complexes with moderate stability with enzymes, nucleic acids and other ligands. They act as biochemical triggers (triggers), modifying and/ or controlling the functioning of these molecules (for example, That it is involved in muscle contraction and relaxation). The elements of group three (Fe, Cu, Zn, etc.) form strongly stable complexes, becoming functional enzymatic and protein constituents.
Let's move on to deficiency or metal poisoning! Metals cause disease through deficiency, imbalance or intoxication. Deficiency usually occurs when food intake is inadequate or when other pathogenic factors occur under the conditions of appropriate intake. Deficiency can occur in malabsorption from chronic diarrheal diseases, through surgical resections of the small intestine or through the formation of food complexes containing metals, which cannot be absorbed (e.g. combinations between fitates and Zn).
It may also occur in the case of increased losses by pancreatic secretions, urine, other exocrine secretions or metabolic imbalances due to antagonistic or synergistic interactions between metals. For example, increased amounts of Ca decrease the absorption of Zn and produce Zn deficiency. Excess Zn (10 times the recommended ration) leads to conditioned anemia by deficiency of Cu. Analog, Mo and Cu are mutually competitive (excess of Mo, in cattle, leads to Cu deficiency, manifested by diarrhea and fatigue). Until the use of total parenteral nutrition (TNP) it was thought that micro-element deficiency in humans was rare. Diagnostic criteria for deficiencies in microelements include decreased serum, blood, hair and/ or other accessible fluids/ tissues, changes in the activity of enzymes containing metals and characteristic signs and symptoms.
Toxic effects are dependent on the chemical form, the amount ingested, how they got into the body, the biological ligands, the tissue distribution, the concentration reached and the excretion rate. Mechanisms of toxicity include inhibition of enzyme activity, by binding to essential peptide radicals, alteration of the function and structure of nucleic acids, impairment of protein synthesis, alteration of membranary permeability, inhibition of phosphorylation, etc.
Metal toxicity in patients performing chronic hemodialysis for renal failure is a special problem, due to the frequency and seriousness of the problems generated and due to the large number of metals involved: Al, Zn, Cu, Ni, Sn. For example, even if there are only traces of Al in the dialysis fluid, it is rapidly absorbed and accumulates in the brain , bone, erythrocytic tissue, resulting in neurological, bone and haematological impairment. These changes include "sickness", memory loss, asteriskis, dementia, spasms and other manifestations, such as seizures and death, occurring in the context of metabolic encephalopathy. Vitamin D-resistant osteomalacia, fractures, muscle pain, weakness and anemia are possible manifestations. The diagnosis is made by highlighting the increased concentration of Al in plasma after administration of deferoxamine.
Let's move on to specific metabolic disorders! I'll start with the zinc. The daily zinc requirement varies with age and state of development, being about 800 microg/day at 1 month, 3-10 mg/ day between 1 and 10 years, and 10-15 mg/ day in the normal adult. During pregnancy, the need increases to 20-25 mg/day to ensure Zn necessary for the growth of the fetus. The intestinal absorption of Zn in the small intestine is diminished by dietary fibers, fitates, phosphates, Ca, Cu and is amplified by amino acids, glucose, peptides, iodochinol and other chelating agents.
Approximately 2-5 mg Zn are excreted daily through pancreatic and intestinal secretions. Losses also occur in the renal proximal tube (around 500-800 microg/day) and through the sweat glands (approximately 500 microg/day). 99% of the total zinc is intracellular, the rest being found in plasma and extracellular fluids. Plasma zinc concentrations are approximately 100 microg/ 100 ml, of which 70% is albumin-related and most of the rest is associated with alpha2-macroglobulin, although small amounts are related to uncharacteristic proteins.
Plasma zinc is the metal source for cellular needs and its levels are relatively noticeable, with small diurnal variations. More significant changes occur under certain circumstances. Zn decrease occurs in pregnancy and when oral contraceptives are used, when ingestion is reduced (regional enteritis) or when there is increased urinary loss (nephrotic syndrome, cirrhosis of the liver, other hypoalbuminic states, when administering peniclamamide or other chelating agents, in intensely catabolic states from trauma, burns, surgery, in hemolytic anemias and sickle cell). Plasma zinc also decreases in acute myocardial infarction, infections, neoplasia, hepatitis, etc.
This decrease may be due to redistribution from plasma to tissues such as the liver, probably mediated by ACTH, cortisol and/ or cytokines (interleukins 2 and 6). Hepatic take-over is associated with the concomitant entry of amino acids, iron and other metal ions. Zn functions in cells and tissues depend on those of the metalloproteins and enzymes with which it is associated (Zn-influenced systems include reproductive, neurological, immune, dermatological and gastrointestinal). Testicular zn is vital for normal spermatogenesis and sperm physiology (it ensures genomic integrity in sperm and stabilizes the attachment of sperm head to tail).
Zn function in mammalian eggs is little understood, but Zn is essential for embryological development. Deficits result in malformations of the brain, eyes, bones, heart and other organs. The survival of the embryo is at risk when zn intake is reduced, even over a period of days, especially in the first trimester. The action of steroid hormones is dependent on Zn because the receptors require Zn to bind to the genes they activate. In the brain, the largest amounts of Zn are in the hippocampus and cerebral cortex, especially in the giant cufflinks of the muscular system.
Zinc works in these areas by inhibiting the binding of peptides and other ligands to their neuroceptors (opioid, muscarinic, acetylcholine, teta-aminobutyric acid, N-methyl-D-aspartate) and influencing neurotransmission. Zn is essential for the formation and function of the immune system. With the deprivation of Zn, the thymus atrophies and no longer forms viable thymocytes. Activation of macrophages and T cells is altered. The result is the inability to respond to antigens or to defend the body against infections. Zn also plays a role in the sense of taste and wound healing.
Zn deficiency in humans was initially reported in adolescents who consumed a diet rich in fitic acid, totally avoiding an animal protein, and who ate soil (later described in patients receiving NPT without supplemental Zn and in patients with Wilson's disease after treatment with penicilamine). Some patients with chronic diarrheal disease and malabsorption, including cystic fibrosis, regional enteritis, celiac sprue and malabsorption of disaccharides, show signs and symptoms of Zn deficiency. In the recessive autosomal defect, enteropathic acrodermatitis, Zn deficiency may be a consequence of a defect in the absorption of Zn (symptoms often begin when an affected child is weaned and is fed with cow's milk and include psoriatic dermatitis with epidermal hyperplasia , parakeratosis, edema and focal necrosis; bodies with ovoid or lysosome-like rhomboids, with Paneth cells inside; hypoplastic thymus with decrease or absence of germinator centers in the lymph and spleen lymph nodes and immature plasmocytes in paracortical areas).
Zn-deficient cells no longer divide and differentiate, with impaired growth (tissues that do not have turn-over - rate of regeneration - increased, such as skin, gastrointestinal mucosa, chondrocytes, spermatogonias, thymocytes, are particularly affected). The possibility of a Zn deficiency is suggested by dermatological manifestations (hyperkeratosis, parakeratosis, acrodermatitis, alopecia). Usually, dermatological lesions are located in regions subject to traumatic demands (elbows, knees), but can occur in any other region. Keratosis lesions can turn into pustules or crusts, grouped into erythematous plaques. functional immunological defect of T lymphocytes is typical.
The ability to generate an immune response in the presence of parasites is reduced. Fungal or bacterial overinfections are common. Toxicity occurs when inhaling Zn vapours (weld), by ingestion per bone or by intravenous administration. Inhalation of vapours with high zinc oxide content produces acute intoxication known as "smoke fever" or "alloy gout", which is manifested by fever, gout, hypersalivation, headache, cough and leukocytosis. Dialysis fluids can be contaminated with Zn from adhesive patches applied to the dialysis spiral or from galvanized ducts. Toxic syndrome associated with hemodialysis is characterized by anemia, fever and damage to the central nervous system. Zn in toxic amounts decreases chemotaxia, phagocytosis, pinocytosis and platelet aggregation.
Now about copper (Cu). The liver, kidney, heart and brain contain the highest amounts of Cu. Over 90% of Plasma Cu is bound to ceruloplasmin and 60% of Erythrocytic Cu is coupled with superoxide dismutase. The main path of excretion is the ball. The serum concentration of Cu is normally constant. it increases in patients with acute myocardial infarction, leukemia, solid tumors, infections, cirrhosis of the liver, hemochromatosis, thyrotoxicosis and connective tissue disorders. The consequences of increasing The Cu are not known. Decrease Dus is found in nephrotic syndrome, Kwashirkor syndrome, hepato-lenticular degeneration (Wilson's disease), severe diarrheal diseases accompanied by malabsorptions and other conditions associated with increased excretion or reduction of ceruloplasmin synthesis.
Premature babies fed with deficient preparations in Cu exhibit low serum levels of ceruloplasmin and Cu, anemia, osteopenia, skin and hair depigmentation, psychomotor retardation. Cu deficiency in patients receiving total parenteral nutrition causes anemia and neutropenia. A complex change in Cu metabolism occurs in Menke's disease, a recessive autosomal condition transmitted to X-linked. Intestinal absorption of Cu is normal, but With tissue varies (in the intestine, kidneys, skin - fibroblasts - copper has normal or elevated values, while in serum, liver, brain and - possibly - vascular cells is reduced). The content in ceruloplasmin and the activity of enzymes that have In-U (such as aminoxidases in connective tissue) are low.
The clinical picture is identical to that produced by Cu deficiency in animals, with the exception of anaemia, which does not occur. Patients have brittle hair and decrease in the amount of mature collagen and elastin, which leads to dissecting aneurysms, cardiac rupture, emphysema, osteoporosis. Death usually occurs in the first 5 years of life. Excessive oral intake of Cu or carrying out hemodialysis with Water Contaminated with Cu are toxic. Acute symptomatology consists of hemolytic anaemia, nausea, vomiting, diarrhea. Cu toxicity is typical in Wilson's disease, when renal and hepatic failure and central nervous system damage occur.
Now about cobalt (Co) that forms part of vitamin B12, its deficiency generating symptoms that are associated with vitamin deficiency. Co administered in pharmacological quantities induces erythropoiesis. Chronic administration blocks the capture of iodine by the thyroid, leading to the appearance of goiter. Cardiomyopathy, congestive heart failure with pericardial fluid, polycytemia, increased thyroid volume and neurological abnormalities have been reported in beer-in-drinking patients to whom Co has been added for foam stabilization. Co accumulates at the heart level, forms complexes with lipoic acid and interacts with decarboxylation reactions, which are critical for the proper conduct of pyruvate metabolism and fatty acids.
Manganese (Mn) acts both as an enzyme activator and as a component of metaloenzymes. Mn deficiency in animals causes damage to the skeleton, central nervous system and gonads. In humans, a normal diet provides enough Mn, so the deficiency syndrome is exceptional. There has been an increase in prothrombin time and no response to vitamin K. In serum, Mn is bound transmanganin. Mn is excreted mainly through bile and pancreatic juice. Serum Mn increases in patients with acute myocardial infarction and diminishes in children with convulsive manifestations. Miners, who inhale increased amounts of Mn through dust for long periods, develop asthenia, anorexia, apathy, headache, impotence, limb cramps, speech disorders, sometimes more serious symptoms.
Selenium (Se) is part of glutaion peroxidase, in this capacity having a critical role in the control of oxygen metabolism, especially in the catalysing of the degradation of oxygenated water (H2O2), It is necessary for the growth of human fibroblasts and other tissue cultures. It prevents or cures Keshan disease, an endemic syndrome (in the Chinese province of Keshan), in which the soil appears to be deficient in Se. This disease is characterized by multifocal myocardial necrosis, accompanied by the reduction of serum content in Se. Clinical severity varies from severe arrhythmias and cardiogenic shock to medium forms, in which cardiomegaly is asymptomatic.
Muscle degeneration can lead to peripheral myopathy. Children and women of the age of procreation are the most susceptible population categories. It plays a role against carcinogens and viruses in animals. It binds Cd, Hg and other metals, decreasing their toxic effect, even if their tissue level remains elevated. Intoxication with It is due to ingestion of contaminated water.
There's something else to mention about other microelements. Silica is found in bones and skin and seems to play a role in the cross-linking of collagen. Deficiency in animals leads to impaired growth, abnormal bone development and epiphysis content (and epiphysis plateaus) low in hexozamine. The deficiency of man has not been described. Inhalation of fine silicon dioxide particles (SiO2) produces granulomas and pulmonary fibrosis (silicosis). Fluoride (F) is part of the teeth and bones. In adequate amounts prevents the appearance of caries, and its use in patients with osteoporosis leads to increased bone mineralization. The complications of its long-term administration in these patients consist in calcification of ligaments and tendons.
Chronic fluoride consumption also produces fluorosis, characterized by weakness, weight loss, anemia, bone friability and yellowing of teeth (if administered during the period of malt formation). Acute ingestion of toxic amounts (e.g. insect venom) causes severe abdominal pain, nausea, vomiting, diarrhea and hypocalcemia. Tetanus and cardiorespiratory arrest may occur. Deficiency of arsen, nickel, tin or vanadium causes pathological manifestations in plants and in some vertebrates. Their role in maintaining health in humans is still undefined.
I was able to complete this post... Next time I take on the effects of drugs (in terms of classical medicine, allopaths)...
I'll start with some classifications and functions related to microelements. The micro-elements category includes metals that are found in concentrations of less than one microgram per gram of liquid mass. Most are essential nutritional compounds in humans (Fe - Iron with specific biochemical function in oxygen transport, Zn - Zinc with function in the degradation of nucleic acids and proteins as well as in alcohol metabolism, Cu - Copper with function in hemoglobin synthesis, connective tissue metabolism and bone development, Co - Cobalt with function in methionine metabolism, Mn - Mangan with function in oxidative phosphorylation, metabolism of fatty acids, mucopolysaccharides and cholesterol, Mo - Molybdenum with function in the metabolism of xanthin, Se - Selenium with antioxidant function, Ni - Nickel with possible function in stabilizing the structure of RNA and Cr - Chromium with possible function in the binding of insulin at the cellular level as well as in glucose metabolism), others being essential for different species, but may also be necessary for humans (As - Arsenius , Sn - Staniul, V - Vanadi and Si - Silicium). Microelements, as well as metals found in higher concentrations in the body (Na - Natrium/ Sodium, K - Kaliul/ Potassium, Ca - Calcium, Mg - Magnesium), partly exercise their role due to their electrical charging, mobility and affinity for biological ligands. Sodium (Na) and potassium (K) form weak bonds with negatively charged ligands and easily cross cell membranes.
They play the role of transporters of electrical impulses transmitted along nerve fibers, etc. Other elements (Mg, Ca) form complexes with moderate stability with enzymes, nucleic acids and other ligands. They act as biochemical triggers (triggers), modifying and/ or controlling the functioning of these molecules (for example, That it is involved in muscle contraction and relaxation). The elements of group three (Fe, Cu, Zn, etc.) form strongly stable complexes, becoming functional enzymatic and protein constituents.
Let's move on to deficiency or metal poisoning! Metals cause disease through deficiency, imbalance or intoxication. Deficiency usually occurs when food intake is inadequate or when other pathogenic factors occur under the conditions of appropriate intake. Deficiency can occur in malabsorption from chronic diarrheal diseases, through surgical resections of the small intestine or through the formation of food complexes containing metals, which cannot be absorbed (e.g. combinations between fitates and Zn).
It may also occur in the case of increased losses by pancreatic secretions, urine, other exocrine secretions or metabolic imbalances due to antagonistic or synergistic interactions between metals. For example, increased amounts of Ca decrease the absorption of Zn and produce Zn deficiency. Excess Zn (10 times the recommended ration) leads to conditioned anemia by deficiency of Cu. Analog, Mo and Cu are mutually competitive (excess of Mo, in cattle, leads to Cu deficiency, manifested by diarrhea and fatigue). Until the use of total parenteral nutrition (TNP) it was thought that micro-element deficiency in humans was rare. Diagnostic criteria for deficiencies in microelements include decreased serum, blood, hair and/ or other accessible fluids/ tissues, changes in the activity of enzymes containing metals and characteristic signs and symptoms.
Toxic effects are dependent on the chemical form, the amount ingested, how they got into the body, the biological ligands, the tissue distribution, the concentration reached and the excretion rate. Mechanisms of toxicity include inhibition of enzyme activity, by binding to essential peptide radicals, alteration of the function and structure of nucleic acids, impairment of protein synthesis, alteration of membranary permeability, inhibition of phosphorylation, etc.
Metal toxicity in patients performing chronic hemodialysis for renal failure is a special problem, due to the frequency and seriousness of the problems generated and due to the large number of metals involved: Al, Zn, Cu, Ni, Sn. For example, even if there are only traces of Al in the dialysis fluid, it is rapidly absorbed and accumulates in the brain , bone, erythrocytic tissue, resulting in neurological, bone and haematological impairment. These changes include "sickness", memory loss, asteriskis, dementia, spasms and other manifestations, such as seizures and death, occurring in the context of metabolic encephalopathy. Vitamin D-resistant osteomalacia, fractures, muscle pain, weakness and anemia are possible manifestations. The diagnosis is made by highlighting the increased concentration of Al in plasma after administration of deferoxamine.
Let's move on to specific metabolic disorders! I'll start with the zinc. The daily zinc requirement varies with age and state of development, being about 800 microg/day at 1 month, 3-10 mg/ day between 1 and 10 years, and 10-15 mg/ day in the normal adult. During pregnancy, the need increases to 20-25 mg/day to ensure Zn necessary for the growth of the fetus. The intestinal absorption of Zn in the small intestine is diminished by dietary fibers, fitates, phosphates, Ca, Cu and is amplified by amino acids, glucose, peptides, iodochinol and other chelating agents.
Approximately 2-5 mg Zn are excreted daily through pancreatic and intestinal secretions. Losses also occur in the renal proximal tube (around 500-800 microg/day) and through the sweat glands (approximately 500 microg/day). 99% of the total zinc is intracellular, the rest being found in plasma and extracellular fluids. Plasma zinc concentrations are approximately 100 microg/ 100 ml, of which 70% is albumin-related and most of the rest is associated with alpha2-macroglobulin, although small amounts are related to uncharacteristic proteins.
Plasma zinc is the metal source for cellular needs and its levels are relatively noticeable, with small diurnal variations. More significant changes occur under certain circumstances. Zn decrease occurs in pregnancy and when oral contraceptives are used, when ingestion is reduced (regional enteritis) or when there is increased urinary loss (nephrotic syndrome, cirrhosis of the liver, other hypoalbuminic states, when administering peniclamamide or other chelating agents, in intensely catabolic states from trauma, burns, surgery, in hemolytic anemias and sickle cell). Plasma zinc also decreases in acute myocardial infarction, infections, neoplasia, hepatitis, etc.
This decrease may be due to redistribution from plasma to tissues such as the liver, probably mediated by ACTH, cortisol and/ or cytokines (interleukins 2 and 6). Hepatic take-over is associated with the concomitant entry of amino acids, iron and other metal ions. Zn functions in cells and tissues depend on those of the metalloproteins and enzymes with which it is associated (Zn-influenced systems include reproductive, neurological, immune, dermatological and gastrointestinal). Testicular zn is vital for normal spermatogenesis and sperm physiology (it ensures genomic integrity in sperm and stabilizes the attachment of sperm head to tail).
Zn function in mammalian eggs is little understood, but Zn is essential for embryological development. Deficits result in malformations of the brain, eyes, bones, heart and other organs. The survival of the embryo is at risk when zn intake is reduced, even over a period of days, especially in the first trimester. The action of steroid hormones is dependent on Zn because the receptors require Zn to bind to the genes they activate. In the brain, the largest amounts of Zn are in the hippocampus and cerebral cortex, especially in the giant cufflinks of the muscular system.
Zinc works in these areas by inhibiting the binding of peptides and other ligands to their neuroceptors (opioid, muscarinic, acetylcholine, teta-aminobutyric acid, N-methyl-D-aspartate) and influencing neurotransmission. Zn is essential for the formation and function of the immune system. With the deprivation of Zn, the thymus atrophies and no longer forms viable thymocytes. Activation of macrophages and T cells is altered. The result is the inability to respond to antigens or to defend the body against infections. Zn also plays a role in the sense of taste and wound healing.
Zn deficiency in humans was initially reported in adolescents who consumed a diet rich in fitic acid, totally avoiding an animal protein, and who ate soil (later described in patients receiving NPT without supplemental Zn and in patients with Wilson's disease after treatment with penicilamine). Some patients with chronic diarrheal disease and malabsorption, including cystic fibrosis, regional enteritis, celiac sprue and malabsorption of disaccharides, show signs and symptoms of Zn deficiency. In the recessive autosomal defect, enteropathic acrodermatitis, Zn deficiency may be a consequence of a defect in the absorption of Zn (symptoms often begin when an affected child is weaned and is fed with cow's milk and include psoriatic dermatitis with epidermal hyperplasia , parakeratosis, edema and focal necrosis; bodies with ovoid or lysosome-like rhomboids, with Paneth cells inside; hypoplastic thymus with decrease or absence of germinator centers in the lymph and spleen lymph nodes and immature plasmocytes in paracortical areas).
Zn-deficient cells no longer divide and differentiate, with impaired growth (tissues that do not have turn-over - rate of regeneration - increased, such as skin, gastrointestinal mucosa, chondrocytes, spermatogonias, thymocytes, are particularly affected). The possibility of a Zn deficiency is suggested by dermatological manifestations (hyperkeratosis, parakeratosis, acrodermatitis, alopecia). Usually, dermatological lesions are located in regions subject to traumatic demands (elbows, knees), but can occur in any other region. Keratosis lesions can turn into pustules or crusts, grouped into erythematous plaques. functional immunological defect of T lymphocytes is typical.
The ability to generate an immune response in the presence of parasites is reduced. Fungal or bacterial overinfections are common. Toxicity occurs when inhaling Zn vapours (weld), by ingestion per bone or by intravenous administration. Inhalation of vapours with high zinc oxide content produces acute intoxication known as "smoke fever" or "alloy gout", which is manifested by fever, gout, hypersalivation, headache, cough and leukocytosis. Dialysis fluids can be contaminated with Zn from adhesive patches applied to the dialysis spiral or from galvanized ducts. Toxic syndrome associated with hemodialysis is characterized by anemia, fever and damage to the central nervous system. Zn in toxic amounts decreases chemotaxia, phagocytosis, pinocytosis and platelet aggregation.
Now about copper (Cu). The liver, kidney, heart and brain contain the highest amounts of Cu. Over 90% of Plasma Cu is bound to ceruloplasmin and 60% of Erythrocytic Cu is coupled with superoxide dismutase. The main path of excretion is the ball. The serum concentration of Cu is normally constant. it increases in patients with acute myocardial infarction, leukemia, solid tumors, infections, cirrhosis of the liver, hemochromatosis, thyrotoxicosis and connective tissue disorders. The consequences of increasing The Cu are not known. Decrease Dus is found in nephrotic syndrome, Kwashirkor syndrome, hepato-lenticular degeneration (Wilson's disease), severe diarrheal diseases accompanied by malabsorptions and other conditions associated with increased excretion or reduction of ceruloplasmin synthesis.
Premature babies fed with deficient preparations in Cu exhibit low serum levels of ceruloplasmin and Cu, anemia, osteopenia, skin and hair depigmentation, psychomotor retardation. Cu deficiency in patients receiving total parenteral nutrition causes anemia and neutropenia. A complex change in Cu metabolism occurs in Menke's disease, a recessive autosomal condition transmitted to X-linked. Intestinal absorption of Cu is normal, but With tissue varies (in the intestine, kidneys, skin - fibroblasts - copper has normal or elevated values, while in serum, liver, brain and - possibly - vascular cells is reduced). The content in ceruloplasmin and the activity of enzymes that have In-U (such as aminoxidases in connective tissue) are low.
The clinical picture is identical to that produced by Cu deficiency in animals, with the exception of anaemia, which does not occur. Patients have brittle hair and decrease in the amount of mature collagen and elastin, which leads to dissecting aneurysms, cardiac rupture, emphysema, osteoporosis. Death usually occurs in the first 5 years of life. Excessive oral intake of Cu or carrying out hemodialysis with Water Contaminated with Cu are toxic. Acute symptomatology consists of hemolytic anaemia, nausea, vomiting, diarrhea. Cu toxicity is typical in Wilson's disease, when renal and hepatic failure and central nervous system damage occur.
Now about cobalt (Co) that forms part of vitamin B12, its deficiency generating symptoms that are associated with vitamin deficiency. Co administered in pharmacological quantities induces erythropoiesis. Chronic administration blocks the capture of iodine by the thyroid, leading to the appearance of goiter. Cardiomyopathy, congestive heart failure with pericardial fluid, polycytemia, increased thyroid volume and neurological abnormalities have been reported in beer-in-drinking patients to whom Co has been added for foam stabilization. Co accumulates at the heart level, forms complexes with lipoic acid and interacts with decarboxylation reactions, which are critical for the proper conduct of pyruvate metabolism and fatty acids.
Manganese (Mn) acts both as an enzyme activator and as a component of metaloenzymes. Mn deficiency in animals causes damage to the skeleton, central nervous system and gonads. In humans, a normal diet provides enough Mn, so the deficiency syndrome is exceptional. There has been an increase in prothrombin time and no response to vitamin K. In serum, Mn is bound transmanganin. Mn is excreted mainly through bile and pancreatic juice. Serum Mn increases in patients with acute myocardial infarction and diminishes in children with convulsive manifestations. Miners, who inhale increased amounts of Mn through dust for long periods, develop asthenia, anorexia, apathy, headache, impotence, limb cramps, speech disorders, sometimes more serious symptoms.
Selenium (Se) is part of glutaion peroxidase, in this capacity having a critical role in the control of oxygen metabolism, especially in the catalysing of the degradation of oxygenated water (H2O2), It is necessary for the growth of human fibroblasts and other tissue cultures. It prevents or cures Keshan disease, an endemic syndrome (in the Chinese province of Keshan), in which the soil appears to be deficient in Se. This disease is characterized by multifocal myocardial necrosis, accompanied by the reduction of serum content in Se. Clinical severity varies from severe arrhythmias and cardiogenic shock to medium forms, in which cardiomegaly is asymptomatic.
Muscle degeneration can lead to peripheral myopathy. Children and women of the age of procreation are the most susceptible population categories. It plays a role against carcinogens and viruses in animals. It binds Cd, Hg and other metals, decreasing their toxic effect, even if their tissue level remains elevated. Intoxication with It is due to ingestion of contaminated water.
There's something else to mention about other microelements. Silica is found in bones and skin and seems to play a role in the cross-linking of collagen. Deficiency in animals leads to impaired growth, abnormal bone development and epiphysis content (and epiphysis plateaus) low in hexozamine. The deficiency of man has not been described. Inhalation of fine silicon dioxide particles (SiO2) produces granulomas and pulmonary fibrosis (silicosis). Fluoride (F) is part of the teeth and bones. In adequate amounts prevents the appearance of caries, and its use in patients with osteoporosis leads to increased bone mineralization. The complications of its long-term administration in these patients consist in calcification of ligaments and tendons.
Chronic fluoride consumption also produces fluorosis, characterized by weakness, weight loss, anemia, bone friability and yellowing of teeth (if administered during the period of malt formation). Acute ingestion of toxic amounts (e.g. insect venom) causes severe abdominal pain, nausea, vomiting, diarrhea and hypocalcemia. Tetanus and cardiorespiratory arrest may occur. Deficiency of arsen, nickel, tin or vanadium causes pathological manifestations in plants and in some vertebrates. Their role in maintaining health in humans is still undefined.
I was able to complete this post... Next time I take on the effects of drugs (in terms of classical medicine, allopaths)...
Love, Gratitude and
Understanding!!! Don't forget that tomorrow is St. Andrew, Saint
of Romania! And the day after tomorrow is Romania's day!!!
Dorin, Merticaru