Iron

Iron, Ferrum (Fe), a heavy metal belonging to Group VIII of Mendeleev's periodic system. Atomic weight 55.84 (0=16), with two known isotopes having atomic weights of 56 and 54. Pure iron has a silvery-white color; specific gravity 7.88; it is softer and more ductile than forged iron. It melts at about 1,520°. In dry air and in air-free, carbon dioxide-free water, iron does not change, but in moist air, especially in water containing air, it rapidly oxidizes, rusting and becoming covered with a layer of hydrated oxides. At high temperatures, iron oxidizes to form iron scale, consisting of a combination of ferrous oxide FeO with ferric oxide Fe₂O₃. Iron is attracted by a magnet. Hardened steel, when acted upon by a magnet, itself acquires the properties of the latter. Dilute acids—hydrochloric, sulfuric, acetic, etc.—easily dissolve iron, releasing hydrogen; very dilute nitric acid dissolves iron without releasing gases, forming ferrous iron salt Fe(NO₃)₂ and ammonium nitrate salt NH₄NO₃; concentrated nitric acid dissolves iron, especially when heated, with the release of nitrogen oxides and forming ferric iron salt Fe(NO₃)₃. Halogens, as well as sulfur, when heated, readily combine with iron. In its compounds, iron is hexa-, tri-, and divalent. Derivatives of the hexavalent oxide, which is acidic, are unstable and have no significance in medicine. The tri- and divalent oxides are basic and form a series of salts of both inorganic and organic acids. Compounds in which iron is divalent are called ferrous (ferro-); trivalent iron and its salts are called ferric (ferri-). Salts of ferrous oxide are usually white in the anhydrous state, and light or dark bluish-green in aqueous solution; salts of ferric oxide are yellowish-brown or reddish-brown in color. Two types of iron compounds are distinguished: 1) inorganic iron compounds, which dissociate with the release of iron ions, such as salts of both inorganic and organic acids, and 2) organic iron compounds, in which iron is in a hidden (non-dissociating) form, i.e., where it is bound to corresponding organic molecules, and cannot be detected by ordinary reagents. Iron is very widespread in nature. According to Mendeleev's hypothesis, it occurs in the deeper layers of the earth in a higher percentage content than in the earth's crust. In the latter, it occurs in the form of various ores containing iron oxides, and sometimes also its compounds with sulfur, carbon, silicon, etc. In small amounts, iron is contained in every soil. More or less pure iron is found in meteorites, where it is accompanied by other metals of the same group: nickel, cobalt, etc. Iron is an essential part of animal and plant protoplasm, being present mainly in the form of organic iron. Although its quantity in animal and plant tissues is generally small, and in some tissues very insignificant, its presence even in negligible amounts is necessary for every living cell. For plants, the presence of iron is necessary for the formation of chlorophyll, although the latter does not contain iron. In animal organisms, iron is found in greater quantities than in plants, with warm-blooded animals containing more than cold-blooded ones. In worms with red blood, iron is part of the hemoglobin dissolved in the blood that gives it its color. However, iron is usually an essential component of the blood even in lower animals where it is not red, and only in rare cases, copper or other heavy metals are found instead of iron, biologically replacing it. In the tissues of humans and higher animals, the blood is richest in iron content, where it is part of hemoglobin. When separated from heme during the physiological breakdown of red blood cells, the iron molecule undergoes a cycle in the intermediate iron metabolism, i.e., it is not excreted but again goes to the synthesis of heme-hemoglobin, resp. to the formation of new red blood cells. How and by what paths iron from the sites of red blood cell breakdown (spleen, liver) reaches the bone marrow, where the formation of new blood cells occurs, is not exactly known. It is believed that iron is transported there by macrophages. Despite the fact that 60-100 mg of iron are daily liberated during the physiological breakdown of red blood cells, it is either not found at all in tissues or is found only to a small degree microscopically. It becomes visible only in the pathological breakdown of blood (see below—deposition of iron). Besides blood, iron occurs in humans and mammals in relatively large quantities in the liver, spleen, bone marrow, heart, lungs, and brain. Muscles contain little iron, with significantly more in myostromin, which forms the basis of anisotropic, rapidly contracting structures, than in myosin. According to Nencki (Nencki) and his students, iron in hemoglobin appears in the form of ferrous oxide. In other tissues, iron is chemically bound to tissue proteins—globulins or stromins—forming compounds of the histone type (Danilevsky). In some organs (liver, kidneys, spleen, bone marrow), in addition to tissue iron, it occurs in the form of residues of destroyed red blood cells, forming clumps of ferric compounds, where iron is easily detected by ordinary reagents (ammonium sulfide or ferrocyanide calcium). Finally, in some tissues, iron occurs in the form of reserve iron, for example, liver ferratin, serving as a reserve from which the organism draws iron when needed; here 78% of iron is in the form of an organic compound, apparently of the ferrous type. The total amount of iron in the body of a 70kg adult person, according to Bunge, is 3.1-5.2g, with 2.4-2.7g in the blood. In hemoglobin, it is approximately 0.336%. Here, as generally in the organism, iron is in the form of organic compounds; the presence of its inorganic salts is unlikely. All the iron in the organism cannot be attributed only to hemoglobin, since such tissues as the lens and epidermal formations also contain it, and besides, the animal body always contains more iron than is present only in hemoglobin. This non-hemoglobin part of iron is particularly large immediately after birth, but a large part of it soon goes to the formation of hemoglobin. Cell nuclei are generally richer in iron than protoplasm. Milk, eggs, and sperm also always contain iron, though in small amounts. Connective tissue is richer in it than nervous and muscular tissue. In the tissues of invertebrates, even those without an iron-containing blood pigment, it is constantly found. The question of iron content in the liver and spleen as sites of destruction and construction of blood pigment has been particularly studied. In the liver, its content varies from 0.0308 to 1.1835% depending on the animal species, with newborns always having more; it is then consumed by the organism as it grows. In leukemia, as well as in diabetes, particularly high iron content is observed in the liver (up to 3.607% of dry substance). The spleen in young animals is poorer in iron (0.08-0.6% of dry substance) than in old ones (2.1% of dry substance). Iron deposited in the liver in the form of organic compounds partly passes into the bile, where its content in humans is about 0.0065%. The unassimilated part of iron taken with food is excreted mainly with feces and to a lesser extent with urine. Here the daily amount varies about 1 mg, but in some diseases, such as diabetes, anemia, chlorosis, it reaches 8.3 mg. The absence of iron in food, along with a decrease in hemoglobin content in the blood, also leads to edema and other severe disorders, which are cured by the administration of iron salts. The latter, according to Warburg's theory, is that component of the respiratory enzyme which transports oxygen. This position is based on the following observations: 1) iron is found in all cells; 2) substances reacting with iron (HCN, H₂S, etc.) stop oxidation when taken in amounts necessary for the stoichiometric reaction with the amount of iron in the cells; 3) the addition of the latter to cells or coal gives oxidation a certain speed, but such action can be paralyzed by hydrocyanic acid even in the case of coal; 4) many autoxidation processes have proved to be typical catalyses with the participation of iron. Warburg and Brefeld established that activation of iron is possible only with nitrogen-containing coals; in this case, the catalytically acting and hydrocyanic acid-sensitive complex consists of |N|. Each atom of divalent iron (Fe) reacts with one molecule of oxygen (O₂); in this case, an extremely unstable and unextractable compound FeO₂ is formed, where iron is tetravalent; it easily gives up oxygen to organic substances, thereby oxidizing it, and iron again becomes divalent. Of the |Fe| systems found in the animal organism, the blood pigment is known: hemoglobin has an extremely high ability to activate oxygen, which is noted, for example, in the autoxidation of glutathione, unsaturated fatty acids, hydroxylamine, etc.

In these cases, hematoporphyrin (which, as is known, does not contain Iron) proves ineffective. The body constantly loses Iron in all secretions and excretions, as well as in the loss of hair, epidermis, etc. On average, the loss of Iron by an adult person on a diet not containing Iron is about 10 mg per day. These losses with a normal diet are covered by the iron in food, where it is present in the form of organic compounds. Among the varieties of food particularly rich in iron, one can name eggs, spinach, beets; milk is very poor in Iron, and if the growing body of a breast-fed infant does not suffer from a lack of Iron, it is because it was abundantly supplied with reserves of Iron during intrauterine development. Schmidt (M. V. Schmidt) experimentally established that if this last factor is absent, i.e., if the animal is born from anemic producers with insufficient Iron reserves and after birth is fed milk, then after some time a noticeable anemia develops in it, expressed in oligocytosis and impoverishment of red blood cells of hemoglobin. If such an animal is continued to be fed with Iron-poor food, the anemia can be brought to high degrees. The offspring of such a generation are born weak and markedly anemic, and the next generation (the fourth) is already non-viable and perishes. Timely administration of normal, i.e., containing the usual amount of Iron, food or Iron preparations (which is completely equivalent) not only stops the further development of anemia but also leads to a complete restoration of the blood. Thus, these experiments vividly illustrate the enormous importance of Iron introduced with food and prove its participation in blood formation. The therapeutic value of Iron. The benefit of using various Iron preparations in diseases associated with an abnormal content of hemoglobin in the blood, such as chlorosis, anemia after blood loss, etc., has been empirically established for a long time. In view of the fact that Iron constitutes an essential part of hemoglobin, being present in it in greater quantity than in any of the substances that make up the body, the benefit from the use of Iron was naturally explained by the delivery to the body of the material necessary for the formation of hemoglobin. If such an explanation for the value of dietary and generally organic Iron, whose absorption could not be doubted, did not encounter difficulties, it was considerably more difficult to apply the same considerations to the therapeutic value of inorganic Iron, whose absorption in the intestine for a long time caused great doubts. The reason for the latter was the fact of a negligible increase in the excretion of Iron in the urine (only by 1 mg) when large doses of Iron are administered per os and the finding in the feces of almost all the inorganic Iron introduced in this way, as shown by the research of Kobert, Kletzinsky, Hamburger and others in those cases when Iron salts are administered per os in concentrations that do not damage (cauterize) the mucous membranes.-Denying the possibility of absorption of inorganic Iron, Bunge explains the benefit of its use by the fact that inorganic Iron is able to combine in the intestine with sulfur of hydrogen sulfide (and sulfur alkalis) and thereby protect dietary Iron from the action of H₂S, thanks to which dietary Iron is preserved in the form of assimilable compounds, not passing into the non-assimilable ferrous sulfide. The very suffering in chlorosis, according to this theory, depends to a large extent on the lack of assimilation of the dietary Iron introduced due to abnormal fermentation processes in the intestine with great development of hydrogen sulfide and sulfur alkalis. This theory proved untenable firstly because other substances that bind hydrogen sulfide (e.g., bismuth) do not help in chlorosis, and then in the latter Iron helps in the form of ferrous Iron, the non-assimilability of which is the basic proposition of the theory.-According to Schmiedeberg, who, like Kobert and Bunge, does not recognize the possibility of absorption of inorganic Iron salts, unless they cause changes in the epithelium of the mucous membranes of the digestive tract, special importance in the exchange of Iron is played by ferratin, containing 6% Iron, with the latter being connected here with proteins of an acidic nature, 'organically', without forming a salt-like compound. Ferratin is incapable of dissociation with the release of an Iron ion. It is found in particularly large quantities in the liver, containing in it a reserve Iron, expended by the body as needed. At the same time, ferratin is easily assimilated; when taken per os only about ¹/₁₃ of the introduced amount appears in the feces. In explaining the benefit brought by the administration of inorganic Iron, Schmiedeberg joins Bunge's theory, which, however, as has already been pointed out, is refuted by essential data. Subsequent research on the absorption of inorganic Iron showed that the latter is absorbed to one degree or another, in favor of which the following facts speak. If an adult animal, kept on an Iron-poor diet, is brought to anemia by bloodletting, then with the addition to the diet of preparations of organic or inorganic Iron, the animal soon recovers, and the amount of hemoglobin and the number of red blood cells return to normal. Similar results were obtained when both types of Iron preparations were used on young growing animals without bloodletting, but kept only on an Iron-poor diet (milk). At the same time, in the chemical analysis of both the liver and the whole body of animals (excluding intestinal contents) in which anemia was artificially induced, a significantly greater content of Iron could be found in the experiments with the addition of Iron preparations to the diet than in the control animals. Moreover, the absorption of inorganic Iron was also proved by the direct treatment with ammonium sulfide of sections of the intestines of experimental animals, in the epithelial intestinal villi of which in microscopic examinations inclusions of ferrous Iron were found. On the basis of these data, it can be concluded that inorganic Iron is absorbed in the upper parts of the intestine (duodenum) and is excreted in the lower parts, where it is also found in the villi. From the villi of the duodenum, Iron enters the lymphatic pathways and mesenteric glands, from where it is already carried by the blood to the spleen and then to the liver, where it is partly deposited. Iron introduced directly into the blood is also largely deposited in the liver. In this process of absorption of Iron from the intestine and its excretion in the latter, macrophages also participate. The absorbability of inorganic Iron in the upper parts of the intestine was also confirmed by the study of intestinal contents in patients with ileal fistula. In the intestinal contents obtained through the latter, a deficiency of Iron was observed compared to the amount introduced per os, but when examining the fecal masses excreted in the normal way, it is in most cases almost impossible to establish. The latter is easily explained by the excretion in the lower parts of the intestine of Iron absorbed above. If the absorption of inorganic iron in the intestine is now a firmly established fact, it is not possible to determine the degree of this absorption in view of its excretion in the lower part of the intestine. In any case, this absorbability of inorganic Iron is probably significantly lower than that of organic Iron and its compounds such as ferratin. From this it does not follow that in the therapeutic sense inorganic Iron is inferior to organic Iron. Abderhalden points out that while when adding to an Iron-poor diet of young animals needing Iron, both inorganic and organic Iron is absorbed and serves as material for the construction of hemoglobin, both,-with a normal diet, the use of both types of Iron gives very different results, in that inorganic Iron compared to organic Iron leads to a more rapid increase in Hb and weight of the animals. Such a result leads one to assume that in addition to delivering material for the blood, Iron stimulates the activity of blood-forming organs (anemic). In accordance with this, after treatment with Iron, the number of nucleated red blood cells and the number of hematoblasts in the stage of karyokinesis in the bone marrow increases in artificially anemic animals. The difference in effect when giving organic and inorganic Iron indicates that only Iron compounds capable of detaching the latter in the form of a free ion have the said stimulating effect on blood formation. It should be noted that, according to many authors, among inorganic compounds, ferrous and ferric Iron compounds are by no means equivalent. In chlorosis, the former are supposedly much more effective. According to Heubner's theory, this is explained by the fact that in chlorosis the body is unable to convert the ferric Iron of food into the ferrous Iron of the blood. According to the experiments of Amatzu, the restoration of the normal composition of the blood and the content of ferratin in the liver in artificially anemic animals occurs much more energetically under the influence of ferrous Iron than ferric Iron.

According to the latest research by Starkenstein, the difference between ferrous and ferric salts of iron consists, firstly, in the fact that ferrous salts, similar to complex compounds of the type of ferritartrate oxalate salts of tartaric, lactic, or malic acid, do not precipitate proteins and, contrary to the opinion of previous researchers, may exhibit toxic effects when administered per os. The absorption of ferrous salts occurs most vigorously in the lower parts of the intestine, while complex salts are absorbed uniformly throughout the intestine. In contrast to the aforementioned compounds, ferric salts of iron, although also absorbed by the intestine, do not cause poisoning. A further difference between ferrous and ferric salts is that only the former have the ability to act as catalysts and activate vital processes in tissues, whereas ferric salts are always inactive and can only serve as reserve material for plastic purposes of the body. The fate of ferrous and ferric iron compounds absorbed by the intestine is also different. Ferric compounds are partly rapidly captured by the spleen, deposited there, and then excreted, and partly converted in the liver into inactive ferrous compounds used for the construction of hemoglobin. Although active ferrous compounds are gradually oxidized in the body to ferric compounds, the latter differ sharply from the usual ferric salts administered per os. They are not captured by the spleen, circulate in the blood for a long time, and are only later captured by the liver, where they are converted into inactive ferrous compounds. The sooner and in what percentage iron from a given preparation is deposited in the spleen and liver, the less its toxic and therapeutic significance. It is very probable that, in addition to stimulating hematopoietic organs, iron to some extent exerts a stimulating effect on the growth and vital activity of other tissues. In the treatment with iron, an increase in body weight is observed, but of course there is no certainty that the latter is not a secondary effect in this case. In any case, in artificial anemia (by removing iron from food), Schmidt obtained a marked retardation in growth in mice. When such animals were given iron preparations, they evened out in their development and almost caught up in this respect with the control animals. It is curious that in iron deficiency, the thyroid gland atrophies particularly sharply. No general resorptive effects of iron are observed in humans with short-term use in therapeutic doses; when administered to animals per os in the form of ferrous salts, according to Starkenstein, the phenomena resemble the narcotic action of magnesium and are expressed by symptoms of paralysis of the central nervous system. The paralysis may pass, but with large doses, after a temporary improvement in the animal's condition, a second phase sets in - convulsive, ending in death. With even larger doses, the latter may occur directly after the first phase (paralysis). With long-term therapeutic use of iron, some authors attribute the following phenomena to its resorptive action: 1) a general stimulating effect on the central nervous system, expressed as insomnia and some increase in nervous excitability; 2) an effect on the vessels - probably through the center - manifested by rushes of blood to the head and increased tendency to bleeding; 3) a stimulating effect on the temperature-regulating center, the consequence of which is an increase in temperature. It is difficult to say with certainty at present whether all these phenomena represent a direct effect of the iron ion or, conversely, whether they are only a secondary consequence of iron administration methods, for example, a vascular reflex to local irritation of the digestive tract. When iron compounds that precipitate proteins are introduced into the blood, phenomena of thrombosis and embolism are observed due to the formation of insoluble albuminates and clotting of the blood; however, if compounds that do not give albuminates are introduced, such as double salts of iron and compounds such as Ferrum albuminatum, phenomena of poisoning are observed, similar to the action of other heavy metals and especially arsenic, namely: a fall in blood pressure, diarrhea, and inflammatory phenomena from the stomach and intestines, often accompanied by hemorrhages. The probable cause is the peripheral effect of iron on the vessels. Furthermore, kidney damage is observed and finally a general depressing effect on the central nervous system, which is partly, and perhaps entirely, to be explained as a secondary phenomenon, depending on the fall in blood pressure. The heart suffers relatively little. It should be noted that when introduced into the blood, Amatzu observed twice the toxicity of ferrous tartrate compared to the corresponding ferric salt. The local action of iron is based on its property, like other heavy metals, to precipitate proteins, forming with them compounds - albuminates. According to Starkenstein, the main significance here is the hydrolytic cleavage of iron salts, determining the degree of acidity of the solution, and not the degree of electrical dissociation of the salts, as is usually stated in textbooks. Depending on the speed of protein precipitation, iron salts can have an astringent and cauterizing effect on mucous membranes and wound and ulcer surfaces. When taken per os, even small doses of weak concentrations have a certain constipating effect; the latter is explained, firstly, by the astringent action on the mucous membranes of the digestive tract and, secondly, by the binding of hydrogen sulfide, which stimulates intestinal peristalsis. High concentrations and high doses of iron preparations can cause vomiting and diarrhea. "Iron is used outside the body in the form of ferrous sulfate as a weak disinfectant, the action of which is also based on the coagulation of bacterial proteins, and especially as a deodorant because iron salts bind hydrogen sulfide and ammonium sulfide formed during the decomposition of organic substances, and perhaps also because, serving as carriers of O₂, they can promote the oxidation and thus destruction of organic substances. - Locally, iron is used as a hemostatic (formation of insoluble albuminates and clotting of the blood) in the form of solutions of ferric chloride (perchloride of iron) or in the form of wool, previously treated with a solution of this salt. An excess of ferric chloride dissolves the formed albuminate, from which bleeding may resume. Another disadvantage of such use of iron salts is the danger of embolism as a result of the transport by the blood flow of the formed blood clots. In stomach bleeding, ferric chloride acts weakly; in intestinal bleeding it does not act at all, just as in hemorrhages from the lungs and kidneys, because iron reaches these organs already in the form of albuminates. As an astringent, solutions of the same ferric chloride (not exceeding 1%; constricting vessels) are used, while stronger solutions of the same substance have a cauterizing effect. - Per os, iron is prescribed especially in chlorosis and other forms of anemia, with inorganic compounds of ferrous iron apparently having an advantage over others. A drawback is the irritating effect of these compounds on the digestive tract, especially on the stomach, which is why sometimes compounds such as Liquor Ferri albuminati, which only slowly release the iron ion and do not have an irritating effect, are preferred. The resorptive significance of iron administration has been discussed above. The success of iron treatment in chlorosis usually occurs after 1-2 weeks and is so certain that if there is a negative effect, other causes of the disease must be sought. In other forms of anemia, the positive effect is by no means as certain, however, iron preparations are often successfully used in prolonged febrile diseases, chronic diarrhea, bronchitis, malarial cachexia, scrofula, and rickets, if these diseases are accompanied by anemia. It has also been proposed to give iron to children when they are artificially fed with cow's milk, which is much poorer in iron compared to maternal milk. Finally, freshly prepared hydrated oxide is an essential part of Antidotum arsenici. Contraindications to the prescription of iron are usually considered: 1) diseases of the heart and blood vessels with a tendency to bleed, especially in pulmonary tuberculosis; some authors, however, believe that the contraindication to iron therapy in this case is based more on theoretical considerations than on clinical observation; 2) febrile condition; 3) abnormal condition of the digestive tract, when even small concentrations of iron can cause undesirable consequences. If in chlorosis dyspeptic phenomena are observed, it is recommended to take measures to eliminate or cure them before starting iron treatment. For the constipation often observed with iron administration, laxatives are prescribed. When using iron, especially in the form of mineral waters, a light diet is recommended, usually prohibiting the intake of substances containing tannin (such as tea) 1 hour before and after taking iron due to the formation of insoluble compounds with iron (ink).

When taking Iron, especially in solution, it is recommended to keep the mouth in special cleanliness and rinse it after taking Iron to avoid darkening of the teeth, which is a consequence of the deposition of iron sulfide in them, formed from the effect of hydrogen sulfide—a product of decay in the oral cavity. Darkening of the teeth can, however, also occur from the formation of dark-colored compounds of Iron with tannin in food substances. Iron Preparations Metallic iron. Ferrum reductum (ФУП) - reduced by hydrogen from oxide of Iron. Finest dark gray matte powder, containing 90% Iron, soluble in gastric juice with conversion to chloride salt. Dose in powders and tablets 0.05-0.3 several times a day.-Ferrum pulveratum, Limatura Ferri, finest iron powder, gray in color, soluble in diluted acids; contains about 98% Fe.- Electroferrol, solution of colloidal iron (0.5% Fe). Used subcutaneously, intramuscularly and intravenously 0.5-1 cm³ and per os 3-4 cm³. With intravenous use, side effects were observed (headache, chills). Compounds of ferrous Iron. Ferrum carbonicum saccharatum (Ph. VII), carbonate of ferrous iron with sugar (10-15% Fe), greenish amorphous powder, insoluble in water, sweet and slightly astringent taste. In the stomach, carbonate Iron gradually passes into chloride, with the release of CO₂. Dose 1.0 several times a day.-Ferrum sulfuricum oxy-dulatum purum siccum (Ph. VII), pure dry ferrous sulfate: FeSO₄·H₂O. Fine greenish-white powder, containing approx. 30% Iron. Slowly but completely soluble in water. Per os 0.05-0.3 several times a day in pills and powders.-Pilulae Blaudii are prepared from a mixture of Ferri sulfur. and Ka-lii carbonici according to different prescriptions (see Blaudii pilulae), with the sulfate passing into carbonate. Excess alkali reduces the astringent and cauterizing effect of Iron, which is why this iron preparation is one of the best. Sometimes prescribe and 79Г> with 0.005 Aloes for each pill (Pilulae Blaudii cum Aloe).-Ferrum lactas (Ph. VII), lactic acid Iron, Fe(CH₃CHOH.COO)₂ + 3H₂O, greenish-white, sweetish with a metallic taste crystalline powder, containing 19.5% Iron. Soluble in water, giving a weakly acidic reaction; stored in a well-closed jar in a place protected from light. Dose 0.1-0.5 several times a day in pills and powders. Well tolerated by the stomach.-Ferrum jodatum ex tempore paratum, light yellow crystals, containing 4 particles of water. Soluble in water. Dose 0.05-0.3 in pills and solution.-Sirupus Ferri jodati (Ph. VII), syrup containing 5% anhydrous iodide of Iron, almost colorless, transparent, has an astringent taste. In pediatric practice - in drops (10-15) or teaspoons. Compounds of ferric Iron. Ferrum oxydatum saccharatum solubile, soluble oxide of Iron with sugar (2.8% Iron), red-brown powder. Dose for adults 1.5-3.0 several times a day. For children, it is prescribed in decigrams.--Extract. Ferri pomati, extract of malic acid Iron (5-8% Fe), greenish-black thick mass, soluble in water, obtained by evaporating on a water bath iron powder with apple juice. Dose 0.2-0.5 several times a day in pills.-T-ra Ferri pomati (0.5-1% iron), solution of 1 part of the previous preparation in 9 parts of alcoholic cinnamon water. Liquid of black-brown color, astringent taste, easily tolerated by the stomach. Dose 10-20 drops several times a day.-Bleggite citricum oxydatum, citric acid Iron. Red water-soluble scales. Dose 0.2-0.5 two to three times a day in powders and pills-Ferrum pyrophosphor, cum ammonio citrico, pyrophosphoric acid Iron with ammonium citrate. Yellowish-green scales, containing 14-14.8% Iron. Soluble in water. Dose 0.3-1.0 several times a day in powders and pills.-T-ra Ferri chlorati aetherea, s. Liquor anodynus martialis, s. T-ra tonico-ner-vina Bestuschevi, Bestuzhev drops, alcoholic-ether solution of chloride of Iron (1.6%). Consists of 1 part of a solution of ferric chloride and 12 parts of Spir. aetherei. Transparent yellow liquid, astringent taste, ether smell. Dose 10-15 drops per dose.-Ferrum trichloratum solutum, s. Liquor Ferri sesquichlorati (Ph. VII), aqueous solution of ferric (ferric) Iron, FeCl₃ +6H₂O, transparent yellow-brown liquid, sp. gr. 1.28-1.29, contains 10% Iron. Used as a local astringent, cauterizing and hemostatic (per se and 1:1 and 1:2).-Ferro-kali tartaricum, tartaric acid Iron and potassium. There are 2 preparations: 1) crudum-greenish-black powder, browning over time. Used for baths, with 30.0-120.0 boiled in 100 cm³ water and added to the bath, and 2) purum-thin, almost black flakes, translucent reddish-brown; internally 0.3-0.6 several times a day; better in solution (for example in carbonated water). Compound with chlorophyll. Chlo-rosan Btirgi, tablets containing 0.02 chlorophyll and 0.005 Fe each. Recommended for anemias and in the initial stages of tuberculosis. Dose 2 tablets three times a day. Protein compounds. Liquor Ferri albuminat.i, s. Natrium Ferri-albuminicum solutum, aqueous solution of sodium ferric albuminate (4% Fe); transparent red-brown liquid of weakly alkaline reaction with a weak smell and taste of cinnamon. Dose for children 5-30 drops, for adults V,-1 teaspoon.-Ferrum peptonatum siccum. Peptonate of Iron, yellow-brown powder. Contains 5% Fe; internally 0.1-0.5 several times a day.-Ferratin, iron-albuminic acid (6% Fe), brown, amorphous, tasteless and odorless powder, in water gives a solution that does not change the color of litmus paper. Dose 0.5-1.5 three times a day.-Natrium ferratinicum, sodium compound of ferratin, brownish liquid, having an alkaline reaction, contains 0.4% Iron. Dose 10.0-15.0.-Triferrin, paranucleic acid Iron, red-yellow powder, containing about 14% Fe and 2.5% phosphorus. Dose 0.3-0.5 three times a day.-Carniferrin, phosphoric-malic acid iron (30% Fe), powder, soluble in weak alkalis. Dose 0.3-0.5.-Metaferrin, colloidal phosphate of protein compound of Iron (10% Fe and 10% phosphoric acid); internally three times a day 1-2 tablets of 0.25 each. Preparations obtained from blood and containing iron in forms close to food Iron, and therefore hardly can have the same significance as the previously listed preparations.-Liquor sanguinis-fresh defibrinated calf blood, 2 tablespoons three times a day.-Haemoglobinum, dose 1-2 teaspoons.-Haematogen, dose 0.3-1.0.-Haemogallolum, dose 0.05-0.3.-Haemol, dose 0.1-0.5. Arsenic compounds. Ferrum kakodylicum [(CH₃)₂AsO.O]₃Fe, kakodylate of Iron, greenish-yellow amorphous powder, easily soluble in water, almost insoluble in alcohol. Internally 0.02-0.1 three times a day, subcutaneously 0.03-0.1 pro die in solution 0.3:10.0 Aq. dest.-Arsenferratin, arsenferratin, in tablets of 0.25 with 6% Fe and 0.06% As.-Arsenferratose (Sirupus Ferratini arseniati), contains 0.3% Fe and 0.003% As, organically bound with protein, brown liquid of pleasant taste.-Arsentriferrin, contains 23% oxide of Iron, 0.1% As and 2.5% P; internally 1, 2 and 3 tablets of 0.3 each. Compound with antipyrine. Fer-ripyrin, compound of ferric Iron with antipyrine, yellow-red powder, soluble in water 1:5; internally 0.03-0.1 several times a day in gastric bleeding, also in chlorosis and anemia, especially in cases complicated by headaches and neuralgias.-Finally, Iron is taken in the form of mineral waters.

A. Likhachev. Iron deposition occurs in the tissues of the animal organism in the form of a pigment detectable by the naked or aided eye, giving a positive reaction to iron or possessing at least the physical and chemical properties inherent to iron. Reactions used for determining iron: the Perls reaction, in which the pigment, upon exposure to a 2% solution of yellow blood salt and 1% hydrochloric acid, acquires the blue color of Prussian blue; the Quincke reaction, which with the aid of ammonium sulfide converts the pigment into iron sulfide; and the Turnbull reaction, in which the pigment, previously treated with a fresh solution of ammonium sulfide, acquires the violet color of Turnbull's blue upon the subsequent addition of 2% red blood salt and 1% hydrochloric acid. So-called masked iron, i.e., iron that is in combination with some organic substance and is invisible even upon microscopic examination, gives negative reactions to these tests. Deposited iron can 1) have various morphological forms and chemical composition, 2) vary in localization and distribution, and 3) be of different origins. Most frequently, iron is deposited in tissues in the form of small grains and large masses of yellow-brown hemosiderin (see). If the latter is located along the course of the gastrointestinal tract, under the influence of hydrogen sulfide, always present in the intestine, it can be converted into black iron sulfide. Less frequently, iron is encountered (mainly in the spleen) in the form of greenish-yellow homogeneous plates of iron phosphate, which, according to Kraus, is easily recognized by the fact that when ammonium molybdate and nitric acid are added to the section, typical yellow four-sided crystals of molybdic phosphate precipitate in it under the microscope. Iron is often encountered in colloidal form. In this case, it either diffusely impregnates the cell protoplasm and even bone substance, or is selectively absorbed by elastic and reticular tissue. Thus, the entire elastic framework of the lung, elastic membranes of arteries, the reticular stroma and trabeculae of the spleen, and the reticulum of lymph glands can become 'ossified' with iron. As a complex ion in combination with proteins or lipoids, iron is deposited only as an exception. Iron deposition can be found in any tissue of the body, in the stroma and parenchyma of any organ, in the reticulo-endothelial system and throughout the entire macrophage apparatus, with localization and distribution depending entirely on the origin of the iron. The main source of iron deposition is hemoglobin. Since the iron molecule is split off from hemoglobin with every breakdown of red blood cells, every hemorrhage can lead to focal deposition of iron anywhere in the body (in infarcts, scars, the brain in apoplexy, siderofibrous nodules of the spleen, etc.). Every prolonged active or passive hyperemia (in chronic inflammations, cardiac stagnations), which is accompanied by the exit of blood cells from the vascular bed, will also inevitably lead to pigment deposition in the entire organ or part of it. If pathological intravascular blood breakdown is present (in pernicious anemia, malaria, cancerous cachexia, pedatrophy, poisoning with hemolytic poisons: hydrogen arsenide, tolylene diamines) and the freed iron circulates in the bloodstream, it will inevitably be deposited either in the reticulo-endothelial apparatus of individual organs or in the entire macrophage system (and sometimes in the parenchyma of organs), thereby causing the picture of hemosiderosis and the characteristic 'rusty' appearance of organs, mainly the spleen, liver, and lymph glands. A prototype of hemosiderosis can be reproduced experimentally by poisoning an animal with hemolytic poisons. A picture similar to hemosiderosis is obtained upon intravenous administration of preparations of colloidal iron (colargol, electargol, Ferrum oxyd. saccharat., etc.). But not only the hemoglobin metamorphosis can serve as a source of deposited iron. The latter can also be deposited in tissues as a result of disturbed intermediate metabolism, i.e., due to a discrepancy between the absorption by cells of iron freed during the physiological breakdown of red blood cells and its assimilation and excretion. In such cases, literally all organs and tissues of the body can be saturated with iron, as for example in hemochromatosis (see). Once deposited, iron is not subject to resorption. If its amount is small, it can be carried away by the lymph current or macrophages to the nearest lymph glands and deposited there; in the opposite case, and all the more so with increasing intake of iron, it remains in place of deposition. Being a foreign body for the given location, it causes a reaction from the surrounding tissue, expressed in the development of connective tissue, which in turn causes indurative processes in organs (brown induration of the lungs, pigmentary cirrhosis of the liver, etc.). In conclusion, it should be noted that iron deposition is sometimes observed together with lime deposition in necrotic areas, elastic membranes of arteries, etc.

e. Gertsenberg.