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Pregled bibliografske jedinice broj: 203144

Ochratoxin A inhibits metabolic activity of renal cells and induces apoptotic and necrotic cell death


Žlender, Vilim; Fuchs, Radovan; Domijan, Ana-Marija; Lucić Vrdoljak, Ana; Peraica, Maja; Radić, Božica
Ochratoxin A inhibits metabolic activity of renal cells and induces apoptotic and necrotic cell death // Toxicology Letters / Elsevier (ur.).
Amsterdam: Elsevier, 2005. str. 228-228 (poster, međunarodna recenzija, sažetak, znanstveni)


CROSBI ID: 203144 Za ispravke kontaktirajte CROSBI podršku putem web obrasca

Naslov
Ochratoxin A inhibits metabolic activity of renal cells and induces apoptotic and necrotic cell death

Autori
Žlender, Vilim ; Fuchs, Radovan ; Domijan, Ana-Marija ; Lucić Vrdoljak, Ana ; Peraica, Maja ; Radić, Božica

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
Toxicology Letters / Elsevier - Amsterdam : Elsevier, 2005, 228-228

Skup
42nd Congress of the European Societies of toxicology, Eurotox 2005

Mjesto i datum
Kraków, Poljska, 11.09.2005. - 14.09.2005

Vrsta sudjelovanja
Poster

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
Ochratoxin A; Kidney desease; Cytotoxicity; Apoptosis

Sažetak
Ochratoxin A (OTA) is a mycotoxin produced by several Aspergillus and Penicillium species. It is known as a worldwide common food contaminant. This toxin has received considerable attention because of its deleterious effects on human and animal health. It has immunotoxic, hepatotoxic, teratogenic, neurotoxic and carcinogenic properties in different experimental animals, with the kidney being its main target organ. The role of OTA as a possible causative agent involved in the etiology of human Endemic nephropathy has still not been ruled out. To study adverse effects of OTA on cellular level, three renal cell lines (CV-1, Hek293, LLC-PK1) were cultivated and exposed to the different OTA concentrations, ranging from 0.1 to 50 μ M, respectively. Metabolic activity was measured by using thiazolyl-tetrazolium bromide mitochondrial dehydrogenase activity test (MTT) over 72 hours. Remaining cell viability after treatment with 20 μ M OTA amounted to 18.2 % for CV-1 and 64.9 % for LLC-PK1. The same OTA concentration induced cell death of almost 43 % Hek293 cell population. Induction of apoptotic and necrotic cell death was measured by anexin V cell labeling and flow cytometry analysis after being exposed to treatment in the same OTA concentration range over 24 hours. Results suggest to apoptosis and necrosis induction in OTA dose dependent manner. Ochratoxin A (OTA) is a mycotoxin produced by several Aspergillus and Penicillium species. It is known as a worldwide common food contaminant. This toxin has received considerable attention because of its deleterious effects on human and animal health. It has immunotoxic, hepatotoxic, teratogenic, neurotoxic and carcinogenic properties in different experimental animals, with the kidney being its main target organ. The role of OTA as a possible causative agent involved in the etiology of human Endemic nephropathy has still not been ruled out. To study adverse effects of OTA on cellular level, three renal cell lines (CV-1, Hek293, LLC-PK1) were cultivated and exposed to the different OTA concentrations, ranging from 0.1 to 50 μ M, respectively. Metabolic activity was measured by using thiazolyl-tetrazolium bromide mitochondrial dehydrogenase activity test (MTT) over 72 hours. Remaining cell viability after treatment with 20 μ M OTA amounted to 18.2 % for CV-1 and 64.9 % for LLC-PK1. The same OTA concentration induced cell death of almost 43 % Hek293 cell population. Induction of apoptotic and necrotic cell death was measured by anexin V cell labeling and flow cytometry analysis after being exposed to treatment in the same OTA concentration range over 24 hours. Results suggest to apoptosis and necrosis induction in OTA dose dependent manner.

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti



POVEZANOST RADA


Projekti:
0022018
0022015

Ustanove:
Institut za medicinska istraživanja i medicinu rada, Zagreb


Citiraj ovu publikaciju:

Žlender, Vilim; Fuchs, Radovan; Domijan, Ana-Marija; Lucić Vrdoljak, Ana; Peraica, Maja; Radić, Božica
Ochratoxin A inhibits metabolic activity of renal cells and induces apoptotic and necrotic cell death // Toxicology Letters / Elsevier (ur.).
Amsterdam: Elsevier, 2005. str. 228-228 (poster, međunarodna recenzija, sažetak, znanstveni)
Žlender, V., Fuchs, R., Domijan, A., Lucić Vrdoljak, A., Peraica, M. & Radić, B. (2005) Ochratoxin A inhibits metabolic activity of renal cells and induces apoptotic and necrotic cell death. U: Elsevier (ur.)Toxicology Letters.
@article{article, author = {\v{Z}lender, Vilim and Fuchs, Radovan and Domijan, Ana-Marija and Luci\'{c} Vrdoljak, Ana and Peraica, Maja and Radi\'{c}, Bo\v{z}ica}, year = {2005}, pages = {228-228}, keywords = {Ochratoxin A, Kidney desease, Cytotoxicity, Apoptosis}, title = {Ochratoxin A inhibits metabolic activity of renal cells and induces apoptotic and necrotic cell death}, keyword = {Ochratoxin A, Kidney desease, Cytotoxicity, Apoptosis}, publisher = {Elsevier}, publisherplace = {Krak\'{o}w, Poljska} }
@article{article, author = {\v{Z}lender, Vilim and Fuchs, Radovan and Domijan, Ana-Marija and Luci\'{c} Vrdoljak, Ana and Peraica, Maja and Radi\'{c}, Bo\v{z}ica}, year = {2005}, pages = {228-228}, keywords = {Ochratoxin A, Kidney desease, Cytotoxicity, Apoptosis}, title = {Ochratoxin A inhibits metabolic activity of renal cells and induces apoptotic and necrotic cell death}, keyword = {Ochratoxin A, Kidney desease, Cytotoxicity, Apoptosis}, publisher = {Elsevier}, publisherplace = {Krak\'{o}w, Poljska} }




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