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2 Wiadomości Chemiczne

2 2019

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Czynniki wirulencji bakterii - białkowe fosfatazy tyrozynowe : jako cel terapeutyczny w odpowiedzi na rozwijającą się antybiotykooporność

Kostrzewa Tomasz, Styszko Joanna, Przychodzeń Paulina, Kamm Anna, Górska-Ponikowska Magdalena, Kuban-Jankowska Alicja

Wiadomości Chemiczne

2019

[Z] 73, 11-12

679--699

Microbial virulence is the ability of pathogen to penetrate, replicate, multiplícate and, as a consequence, damage the cells of the infected organism. In recent years, rapid progress in bacterial genome sequencing has led to the discovery and characterization of many new virulence factors. One of the many mechanisms of bacterial virulence is the activity of bacterial kinases and phosphatases. These enzymes phosphorylate and dephosphorylate various amino acid residues in proteins, most commonly serine, tyrosine and threonine. Reversible phosphorylation and dephosphorylation can control the activity of target proteins, either directly, by inducing conformational changes in proteins, or indirectly, by regulating protein-protein interactions. Due to the increasing antibiotic resistance, new substances that could be used to treat diseases caused by resistant bacterial strains are sought. One of the possibilities seems to be the inhibition of bacterial tyrosine phosphatases. Phosphorylation of proteins containing tyrosine residues is a key post-translational modification that controls the numerous cellular functions in bacteria. So far, many tyrosine phosphatases have been found to be responsible for the virulence of various bacterial strains. Many bacterial species use protein tyrosine phosphatases activity in host-pathogen interaction, by affecting signalling pathways and subsequent induction of the infection process. Many studies are devoted to the search for tyrosine phosphatases inhibitors in the context of possible support of the current antibacterial treatment. This article presents a review of reports on bacterial virulence factors-protein tyrosine phosphatases as potential therapeutic targets.

Biologia i chemia nowotworu płuca

Musiał Claudia, Zaucha Renata, Kuban-Jankowska Alicja, Kamm Anna, Górska-Ponikowska Magdalena

Wiadomości Chemiczne

2019

[Z] 73, 7-8

505--522

Lung cancer is the most common fatal cancer disease in the world. A characteristic feature of lung cancer is genetic diversity. In the overwhelming majority of cases, smoking is the most important etiopathogenic factor. Lung cancer is a cancer with a very bad prognosis regarding long-term survival. The risk of lung cancer depends primarily on active or passive exposure to the carcinogenic components of tobacco smoke. According to available data, the development of lung cancer in addition to active and passive smoking is directly affected by environmental pollution such as smog and fumes, ionizing radiation, mycotoxins and long-term exposure to asbestos (occupational exposure). Research on the pharmacoprevention of lung cancer began over 30 years ago. The first nutrient that the researchers said could inhibit the development of lung cancer was beta carotene. Unfortunately, long-term regular supplementation with high doses of antioxidant in the form of beta-carotene brought the opposite effect. An increase in the incidence of lung cancer was found in people who received beta carotene in the form of a synthetic food supplement. The other component tested was N-acetylcysteine. It is a sulfur compound and a powerful antioxidant that supports the synthesis of glutathione and cysteine, with destructive effects on carcinogenic substances. N-acetyl-cysteine, used in the form of NAC adduct and epigallocatechin-3-gallate, showed efficacy in inhibiting the development of lung cancer only in animal models. In the pharmacoprevention of lung cancer, the use of vitamin E was also tested in the form of tocotrienol and tocopherol. The following work also shows the existence of a high concentration correlation which belongs to the steroid hormone, mainly estrogen, in the blood and the development of lung cancer in women. An increased risk of lung cancer has been observed in women undergoing long-term hormone replacement therapy. The results show that 2-methoxyestradiol, the endogenous metabolite of 17ß-estradiol, shows positive results that inhibit the growth of lung cancer cell lines. The aim of the work was to present the correlation between tobacco abuse and passive smoking and lung cancer, pharmacoprevention of lung cancer and the association of elevated estrogen concentration in women with an increased risk of lung cancer.