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Zinc in medicine and treatment

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Zinc is an essential and the second most abundant trace element in humans. It is critical for the growth, development and differentiation of cells, as well as for RNA transcription, DNA synthesis, cell division and cell activation. Zinc deficiency affects mainly functions of the immune system, but other consequences include inferior sperm activity, skin lesions, growth retardation, impaired wound healing, anemia and gastrointestinal disorders. Zinc supplementation protects against the hepatotoxic effects of alcohol, enhances the transport of water and electrolytes across the intestinal mucosa and improves immune and anti-inflammatory responses. Zinc is also known as an essential mineral for normal mobilization of vitamin A from the liver to the plasma. Besides, it increases the promoter response to 1,25-dihydroxyvitamin D in osteoblasts. On the other hand, excessive amounts of free zinc in tissues are toxic and accelerated zinc accumulation of zinc is a potent killer of neurons and glial cells. Over 300 signaling molecules and transcription factors contain zinc as a cofactor. Free zinc in immune and tumor cells is regulated by 14 distinct zinc importers (ZIP) and transporters. An elevated amount of zinc transporters LIV-1, a subfamily of ZIP zinc transporters, appears in estrogen receptor–positive breast cancer and has been used as a reliable breast cancer marker. However, the fact that malignant cells are unable to accumulate zinc is an important factor in the development and progression of malignancy of prostate cancer.
Mycoplasma bovis is the smallest known bacterium that does not have a cell wall. It is therefore resistant to some antibiotics that inhibit the synthesis of the cell structure. Little is known about the mechanisms of antibiotic resistance in M. bovis, since it has no plasmids and there are insufficient data about the role of the biofilm formation by these bacteria. Previous studies have shown that the development of antibiotic resistance is due to gene mutations. Antibiotics generally considered as effective against M. bovis infection are macrolides, fluoroquinolones, tetracyclines, lincosamides, aminoglycosides, and chloramphenicol. Several recent studies, however, indicate that the efficacy of tetracyclines, macrolides, and lincosamides has diminished. Increased resistance to erythromycin, spectinomycin, and tilmicosin, antibiotics commonly used in the treatment of M. bovis infections, has also been reported. Among field strains of M. bovis no resistance or rare resistance has only been observed for enrofloxacin, florfenicol, tylosin, and tulathromycin. Considering the rapidly growing antibiotic resistance of the isolated strains of M. bovis, it is necessary to search for alternative compounds that could effectively inhibit these bacteria.
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Biochemistry of magnesium

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Magnesium is essential for biochemical functions of cells. Since Mg2+ has a relatively low ionic radius in proportion to the size of the nucleus (0.86 versus 1.14 f A for Ca2+), it shows exceptional biochemical activity. Due to its physicochemical properties, intracellular magnesium can bind to the nucleus, ribosomes, cell membranes or macromolecules occurring in the cell’s cytosol. It is indispensable for the nucleus to function as a whole and for the maintenance of physical stability as well as aggregation of rybosomes into polysomes able to initiate protein synthesis. Mg2+ can also act as a cofactor for ribonucleic acid enzymes (ribozymes) capable of specifically recognizing and cleaving the target mRNA. As an essential cofactor in NER, BER, MMR processes, Mg2+ is required for the removal of DNA damage. An activator of over 300 different enzymes, magnesium participates in many metabolic processes, such as glycolysis, Krebs cycle, β-oxidation or ion transport across cell membranes. Mg2+ plays a key role in the regulation of functions of mitochondria, including the control of their volume, composition of ions and ATP production.
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