THE PEPTIDOGLYCAN FRACTION ENRICHED WITH MURAMYL PENTAPEPTIDE FROM Lactobacillus bulgaricus INHIBITS GLIOBLASTOMA U373MG CELL MIGRATION CAPABILITY AND UPREGULATES PARP1 AND NF-kB LEVELS

Nedzvetsky, V. S.; Ağca, Can Ali; Baydaş, Gıyasettin

doi:10.15407/biotech13.02.065

Cited by 4 publications

(2 citation statements)

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“…Виявлені зміни вмісту GFAP в мозку риб експериментальних груп можуть бути опосередковані великим числом різних механізмів в гліальних клітинах, включаючи експресію та метаболізм цитоскелетних білків [8,10]. Отримані результати свідчать про наявність у клітинах мозку риб складного механізму впливу різних доз міді на регуляцію GFAP.…”

Section: рис 2 відносний вміст Nf-kb у мозку райдужної форелі контрол...unclassified

Molecular markers of cytotoxicity induced with copper-contained pesticides

Nedzvetsky

Масюк

2022

ahsu

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The applying copper sulphate is a cheap, however it leads to global the environment contamination. Especially, the contamination of the water sources is crucial for fish harvesting and farming. The copper contamination in some areas are caused by decades. The impact of copper ions is dependent on the inhibition of invasive aquatic plants, many microorganisms and protozoa. The family of copper-contained chemicals is frequently used as algaecides in swimming pools. Despite the copper ions are well known as a high toxic for fish in freshwater ponds, the copper sulphate remains one of the prevalent pesticides in fish farming everywhere. High cytotoxicity and accumulation of the copper ions in the sediments require studying and calculation of the optimal dosage to use it as an antiseptic agent that should prevent the detrimental effect in various tissue types of aquatic organisms. The main depicted mechanism, which is associated with cytotoxicity is the generation of oxidative stress. Neural tissue cells are extremely susceptible to oxidative damages. Neural damaging is important cause of the CNS disfunction as well as is the critic to the organism vitality. Glial cells maintain the structure and many vital functions of neuronal cells. Glial fibrillary acidic protein (GFAP), transcriptional nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) and poly(ADP-ribose) polymerase (PARP) are critic regulators in a cell response to the environment toxicity. Based on this fact, it could be applied as the boimarkers of heavy metal toxicity. In presented study, we investigated the effects of copper ions on PARP, NF-kB, and GFAP expression in the rainbow trout (Oncorhynchus mykiss) brain tissue. For 96 hours the fishes were exposed to the copper sulphate sublethal concentrations 380 µg/L, estimated as 1/4 of the LC50 value. Western blot analysis of GFAP, NF-kB and PARP was used to assess further effects in the brain tissue. The modulatory effect of copper ions on the expression of GFAP was detected in fish brain. Reciprocal changes were observed in respect with 24 hours exposure in compare to both 48 hours and 96 hours treatment. Obtained results demonstrated meaningful disturbance in the expression of transcriptional factor NF-kB in the brain of fish group exposed to copper in compare to control group. Furthermore, the time-depended effect in a range 24 – 96 hours was detected. However, the short time exposure to copper ions initiated no effect in fish group treated 24 hours while in compare to both 48 hours and 96 hours treatment. The similar changes of PARP content in the brain of fish were determined as well. It deserves to be mentioned that all of aforementioned changes of GFAP, NF-kB and PARP expression were accompanied by increasing in reactive oxygen species content. Thus, copper ions cytotoxic effect could be initiated with oxidative injury in a brain tissue. On the other hand, the observed effect of copper in the fish brain evidences the unspecific toxicity of this ion in brain tissue cells. The results showed that copper ions could induce astroglial response accompanied by modulations of NF-kB and PARP-1 expression. Obtained in presented study data suggest that copper sulphate has significant effect on astrogliosis and DNA damage in the fish brain.

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Section: рис 2 відносний вміст Nf-kb у мозку райдужної форелі контрол...unclassified

Molecular markers of cytotoxicity induced with copper-contained pesticides

Nedzvetsky

Масюк

2022

ahsu

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“…Культура гліобластоми U373MG була отримана від АТСС (American Type Culture Collection, Manassas, USA). Використовували клітини гліомних ліній, які походять від астроцитів, і широко застосовуються у токсикологічних дослідженнях як їх адекватна модель [35,42].…”

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Influence of cadmium contamination on brain glial cells: consequences and bioindication possibilities

Nedzvetsky

Gasso

Hahut

et al. 2020

vsllr

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Cadmium (Cd) is a heavy metal that currently presents in almost all components of the environment. Cd is a ubiquitous pollutant that is constantly entering the environment from industry and agriculture, mining, forest fires and many more sources. Some occupational diseases have aftereffects associated with Cd cytotoxicity. Despite long-term studies of the toxic effects of Cd, its cytotoxicity of low doses and the chronic effects on the nerve tissue cells remain undiscovered. The results of determining the Cd neurotoxicity indicate a disturbance of the permeability of the blood-brain barrier, the accumulation of Cd in the brain and the deterioration of the functional activity of the central nervous system. One of the main cellular targets for Cd in the brain are astrocytes. Astrocytes provide nutrition and functional activity of neurons, as well as recovery of physical and metabolic damage. The cytoskeleton of astrocytes is built of glial fibrillary acidic protein (GFAP). GFAP participates in important functions of astrocytes and its condition reflects the astrocytes reactivity. The molecular mechanisms of the neurotoxic effects of Cd on the glial cytoskeleton remain unknown. Glioblastomas are widely used to study the cytotoxic mechanisms of various compounds, including heavy metals, as cellular models of astrocytes. Taking into account the role of oxidative stress in a cell damage, as well as the reactive response of glial cells, we study the influence of low doses of Cd on oxidative stress and expression of GFAP and glucose-6-phosphate dehydrogenase (G6PD) in U373GM cells. Doses of 2-10 μM Cd induced a dose-dependent increase in reactive oxygen species and lipid peroxidation products. The same doses inhibited the expression of the cytoskeletal marker of astrocytes (GFAP) and metabolic marker of glucose utilization (G6PD). The obtained results indicate a pronounced cytotoxic effect of low doses of Cd in the astrocytic cell model U373GM. In addition, the astroglial cytotoxicity of Cd may be mediated by oxidative damage, inhibition of glial intermediate filament expression, and glucose utilization disorders. These parameters can be promising biomarkers of toxic effects both for the assessment of human and animal health and for determining the state of the environment as a whole.

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