Beryllium (Be)
Bone Destroyer
Beryllium belongs to toxic ultra-trace elements. The physiological role of beryllium in the human body is not well studied, however, it is known that beryllium may participate in the regulation of phosphorus-calcium metabolism and support the immune status of the body.
The daily requirement for the human body is not precisely established, but there are data suggesting that the optimal average daily intake of beryllium is 10–20 µg.
Beryllium can enter the human body both through food and via the lungs. When introduced in a soluble form into the gastrointestinal tract, beryllium interacts with phosphates and forms poorly soluble Be3(PO4)2 or binds with proteins of epithelial cells into stable proteinates. Therefore, the absorption of beryllium in the gastrointestinal tract is low, ranging from 4 to 10% of the amount ingested. It should be noted that this indicator also depends on the acidity of gastric juice.
The total amount of beryllium in the body of an adult varies (according to different sources) from 0.4 to 40 µg. Beryllium is constantly present in the blood, bone, and muscle tissues (0.001–0.003 µg/g) and other organs. It has been established that beryllium can be deposited in the lungs, liver, lymph nodes, bones, and myocardium.
Beryllium is primarily excreted from the body through urine (over 90%).
Biological role in the human body. Primarily, beryllium participates in the metabolism of magnesium and phosphorus in tissues. It has been established that the activity of beryllium compounds is distinctly manifested in various biochemical transformations associated with the involvement of inorganic phosphates.
The effects of beryllium on the body are multifaceted. To date, its toxic (including cytotoxic), sensitizing, embryotoxic, and carcinogenic effects have been proven. The latter has been established in experiments on certain animal species and is discussed in relation to humans. Beryllium and its compounds have the ability to penetrate all organs, cells, and their nuclei, as well as cellular organelles, particularly mitochondria. It damages cell membranes, including their lipid components, disrupting microviscosity. Beryllium inhibits the activity of ATP-ase of the sarcoplasmic reticulum by inhibiting the transport of magnesium and calcium.
By penetrating the nuclei of cells, beryllium reduces the activity of DNA synthesis enzymes, particularly DNA polymerase, and there are indications regarding the significance of disturbances in DNA synthesis for the emergence of abnormal proteins that play the role of autoantigens.
The cytotoxic effect of beryllium compounds has been studied on phagocytes. In particular, the introduction of beryllium sulfate and citrate causes blockade of mononuclear phagocyte system cells and reduces the phagocytosis index by 65–75%. The introduction of beryllium phosphate suppresses the inflammatory reaction.
Upon intratracheal administration of beryllium compounds, there is an increased output of macrophages and polymorphonuclear cells into the alveolar lumen. However, the mobility of macrophages decreases, their organelles are damaged, and DNA synthesis is reduced.
It has been shown that inhalation of soluble beryllium salts leads to the proliferation of connective tissue primarily in the perivascular and peribronchial zones. Fibrosis develops in response to the penetration of beryllium into the lungs, and this process has the highest rate during the first month after the intratracheal administration of beryllium hydroxide. Lung tissue sclerosis is usually associated with the formation of peculiar granulomas. Recent electron microscopy and histochemical studies have shown their similarity to allergic granulomas. It has been proven that in the lymphocytes of granulomas, the number of organelles is increased. This fact and the presence of a large number of free ribosomes indicate their active state. Epithelioid cells of granulomas arise from mononuclear and lymphocyte cells. Already in the first months after inhalation of soluble beryllium compounds, granuloma-like nodules develop, consisting of lymphoid-histiocytic elements. In the center of such nodules, decaying macrophages and cellular debris are found. This is interpreted as a result of the release of beryllium upon the death of macrophages that have engulfed it.
Synergists and antagonists of beryllium. The antagonist of beryllium is
magnesium. Magnesium in the body is primarily found inside cells, where it forms compounds with proteins and nucleic acids containing Mg–N and Mg–O bonds. The similarity of the physicochemical characteristics of Be
2+ and Mg
2+ ions accounts for their ability to mutually replace each other in such compounds. This explains, in particular, the inhibition of magnesium-dependent enzymes when beryllium enters the body.
Signs of beryllium deficiency. Scientific data is lacking.
Increased beryllium content in food contributes to the formation of beryllium phosphate. By systematically “taking away” phosphates from the most important part of bones – calcium phosphate, beryllium weakens and destroys bone tissue. It is known that the introduction of this element to animals causes “beryllium” rickets. It has been established that even a small amount of beryllium in the composition of bones leads to their softening.
At the sites of parenteral administration of beryllium, destruction of surrounding tissues occurs, from which beryllium is excreted very slowly. Eventually, beryllium is deposited in the skeleton and liver.
According to modern views, beryllium is a toxic, carcinogenic, and mutagenic element. The pathogenic action of beryllium is observed when inhaled at concentrations exceeding the permissible limits by 2 or more times. Beryllium salts at a concentration of 1 µmol/L specifically inhibit the activity of alkaline phosphatase and have an inhibitory effect on other enzymes. The immunotoxic properties of beryllium are well studied.
In pathology, acute and chronic beryllium poisoning are distinguished. It is known, for example, that the elimination of beryllium compounds from the body (especially from the lymphoid system organs, where they accumulate) occurs extremely slowly, over more than 10 years. Elevated levels of beryllium are found in families of workers who come into contact with this element in production.
Main manifestations of beryllium excess: lung tissue damage (fibrosis, sarcoidosis), skin damage – eczema, erythema, dermatosis (upon contact of beryllium compounds with the skin), berylliosis, foundry fever (irritation of the mucous membranes of the eyes and respiratory tract); erosions of the mucous membranes of the gastrointestinal tract, disruption of myocardial and liver functions, development of autoimmune processes, tumors.
Beryllium is necessary: in ancient times, beryl (a silicate of aluminum and beryllium) was used to treat a large number of women’s diseases. It was believed that beryl powder could prevent uterine prolapse, dental and headache, and that beryllium bracelets protect against diseases of the ovaries and bladder. Modern lithotherapists recommend wearing beryl in cases of nervous system disorders and chronic respiratory diseases.
Dietary sources of beryllium: the intake of beryllium through food and water is negligible; significant concentrations of this element can be accumulated by
tomatoes and
lettuce.
The primary route of beryllium entry into the body is inhalation (via the respiratory tract). In individuals working in environments with a risk of inhaling dust containing beryllium or its compounds, a specific occupational disease may develop —
berylliosis (beryllium or chemical pneumonia).