Opstati ili umrijeti – regulacija stanične smrti Miletić, Marina; Murati, Teuta; Slavica, Anita ...
Hrvatski časopis za prehrambenu tehnologiju, biotehnologiju i nutricionizam,
06/2021, Volume:
16, Issue:
1-2
Journal Article
Open access
Stanično umiranje je temeljni biološki proces, koji je u fiziološkom smislu embrionalnoga razvoja i obnove tkiva, te kao patološki odgovor na ozljedu
stanica i infekciju patogenima, uključen u ...mehanizme koji kontroliraju razvoj, homeostazu i imunološku regulaciju višestaničnih organizama.
Stanice mogu umrijeti slučajnom (biološki nekontrolirani procesi) ili reguliranom (genetski kontrolirani molekularni procesi) staničnom smrću.
Stanična smrt odvija se različitim mehanizmima koji dovode do pojave različitih morfoloških promjena u stanicama zahvaćenim tim procesima.
Nedavna otkrića u tom području i detekcija sve većeg broja novih oblika regulirane stanične smrti, rezultirala su novom sustavnom klasifikacijom
i nomenklaturom različitih tipova stanične smrti. U ovom preglednom radu dan je uvid u sustav klasifikacije, mehanizme i obilježja glavnih tipova
stanične smrti: nekroze, apoptoze i autofagije.
Cell death is fundamental biological activity involved in mechanisms controlling the development, homeostasis and immune regulation of
multicellular organisms in the physiological context of embryonic development and tissue regeneration, as a pathological response to cell injury
and pathogen infection. Cells can die by accidental (biologically uncontrolled processes) or regulated (genetically controlled molecular processes)
cell death. Cell death occurs by different mechanisms leading to the development of specific morphologies. Recent discoveries in this field and
the increasing number of new forms of regulated cell death have resulted in a novel classification system and nomenclature of different cell death
modalities. This review provides an insight into the system of classification, mechanisms and characteristics of main cell death modalities: necrosis,
apoptosis and autophagy.
Noise and toluene can have significant adverse effects on different systems in the human body, but little is known about their combination. The aim of this study was to see how their combined action ...reflects on serum levels of inflammatory cytokines tumour necrosis factor alpha (TNF-α) and interleukin 1 beta (IL-1β), body weight, and pathological changes in the heart, lung, stomach, and spleen tissues. To do that we exposed New Zealand rabbits to 1000 mg/L toluene and 100 dB of white noise in a chamber specifically designed for the purpose over two consecutive weeks. Serum levels of TNF-α and IL-1β were measured with the enzyme-linked immunosorbent assay (ELISA), whereas Bax and Bcl-2 expressions in tissues were determined with real-time polymerase chain reaction (PCR). Noise and toluene changed TNF-α and IL-1β serum levels on different days following the end of exposure and significantly increased the Bax/Bcl-2 ratio in the lung and spleen. In addition, they induced different pathological changes in the heart, lung, spleen, and stomach tissues. This study has confirmed that exposure to noise and toluene can induce a range of toxicopathological changes, probably by inducing inflammatory pathways and apoptosis, but their combined effects look weaker than those of its components, although histopathological findings suggest the opposite.
This study investigated possible growth-inhibiting effects of bee venom applied alone or in combination with a cytotoxic drug bleomycin on HeLa and V79 cells in vitro based on clone formation, cell ...counting, and apoptosis. Melittin, the key component of bee venom, is a potent inhibitor of calmodulin activity, and also a potent inhibitor cell growth and clonogenicity. Intracellular accumulation of melittin correlates with the cytotoxicity of antitumour agents. Previous studies indicated that some calcium antagonists and calmodulin inhibitors enhanced intracellular levels of antitumor agents by inhibiting their outward transport. In this study, treatment of exponentially growing HeLa and V79 cells with bleomycin caused a dose-dependent decrease in cell survival due to DNA damage. This lethal effect was potentiated by adding a non-lethal dose of the bee venom. By preventing repair of damaged DNA, bee venom inhibited recovery from potentially lethal damage induced by bleomycin in V79 and HeLa cells. Apoptosis, necrosis, and lysis were presumed as possible mechanisms by which bee venom inhibited growth and clonogenicity of V79 cells. HeLa cells, on the other hand, showed greater resistance to bee venom. Our findings suggest that bee venom might find a therapeutic use in enhancing cytotoxicity of antitumour agent bleomycin.
U uvjetima in vitro istražen je inhibitorni u _inak p _elinjeg otrova, samog ili združenog s citostatikom bleomicinom, na rast stanica HeLa i V79. Rabljene su sljedeće metode: brojenje stanica, metoda klonskog rasta i apoptoza. Poznato je da neki antagonisti kalcija i kalmodulinski inhibitori povisuju unutarstani _nu razinu protutumorskih lijekova inhibirajući njihov prijenos iz stanice. Unutarstani _na akumulacija melitina izravno povećava citotoksi _ni u _inak protutumorskog lijeka. Obrada stanica HeLa i V79 u eksponencijalnoj fazi rasta bleomicinom uzrokuje oštećenje DNA ovisno o dozi te smanjenje broja živih stanica. Uo _eno je da se letalni u _inak bleomicina može poja _ati dodatkom neletalne doze p _elinjeg otrova. P _elinji otrov pritom inhibira popravak nastalih oštećenja u stanicama HeLa i V79 te sprje _ava oporavak stanica tretiranih bleomicinom. Apoptoza, nekroza i liza mogući su mehanizmi kojima p _elinji otrov inhibira rast i stvaranje kolonija stanica V79, dok HeLa-stanice pokazuju poja _anu otpornost na p _elinji otrov. Istraživanje također potvrđuje mogućnost uporabe p _elinjeg otrova u povećanju citotoksi _nosti bleomicina.
THE REAL TITLE: The role of galactosylceramide synthase (UGT8) and galactosiloceramic (GalCer) in response to cellular stress in the drug resistance of breast cancer cells
Polish summary in the ...Comment tab
In the electronic version, only a summary of the doctoral dissertation is available
POPRAWNY TYTUŁ ROZPRAWY: Rola syntazy galaktozyloceramidu (UGT8) i galaktozyloceramidu (GalCer) w odpowiedzi na stres komórkowy w lekooporności komórek raka gruczołu piersiowego
Streszczenie polskie w zakładce Komentarz
W wersji elektronicznej dostępne wyłącznie streszczenie rozprawy doktorskiej
Okratoksin A (OTA) posvuda je prisutan mikotoksin za koji se smatra da je potencijalno nefrotoksičan i karcinogen, a može uzrokovati i smrt stanice. OTA se smatra mogućim uzročnikom balkanske ...endemske nefropatije koju karakterizira povećani rizik od razvoja tumora mokraćnog sustava te različitih drugih vrsta intersticijskog nefritisa. Osjetljivost stanice naspram OTA ovisi ponajprije o koncentraciji mikotoksina, vremenu izloženosti i o unutarstaničnome molekularnom i genskom sklopu. OTA može djelovati na stanicu
tako što potiče ili inhibira određene signalne putove u stanici poput puta proteinskih kinaza aktiviranih mitogenima (MAPK). Tri glavne MAPK u sisavaca su proteinska kinaza regulirana izvanstaničnim
signalima (ERK), kinaza koja fosforilira N-kraj transkripcijskog faktora c-Jun (JNK) i p38 MAPK. Svi članovi porodice MAPK reguliraju različite stanične programe, s time da ERK najčešće stimuliraju preživljavanje stanica, dok JNK i p38 MAPK najčešće uzrokuju umiranje stanica apoptozom. U ovome smo preglednom članku prikazali na koji način stanice odgovaraju na aktivaciju MAPK koju potiče OTA.
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