Pregled bibliografske jedinice broj: 157953
Apoptosis : a Crucial Event in the Development of Ota-induced Nephrotoxicity
Apoptosis : a Crucial Event in the Development of Ota-induced Nephrotoxicity // Congress of the Croatian Society of Biochemistry and Molecular Biology with International Participation : HDBMB2004 : Book of Abstracts / Dumić, Jerka (ur.).
Zagreb: Farmaceutsko-biokemijski fakultet Sveučilišta u Zagrebu, 2004. str. 59-59 (poster, domaća recenzija, sažetak, znanstveni)
CROSBI ID: 157953 Za ispravke kontaktirajte CROSBI podršku putem web obrasca
Naslov
Apoptosis : a Crucial Event in the Development of Ota-induced Nephrotoxicity
Autori
Barišić, Karmela ; Petrik, Jozsef ; Rumora, Lada ; Žanić-Grubišić, Tihana
Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni
Izvornik
Congress of the Croatian Society of Biochemistry and Molecular Biology with International Participation : HDBMB2004 : Book of Abstracts
/ Dumić, Jerka - Zagreb : Farmaceutsko-biokemijski fakultet Sveučilišta u Zagrebu, 2004, 59-59
ISBN
953-6256-44-4
Skup
Congress of the Croatian Society of Biochemistry and Molecular Biology with international participation
Mjesto i datum
HOC Bjelolasica, Hrvatska, 30.09.2004. - 02.10.2004
Vrsta sudjelovanja
Poster
Vrsta recenzije
Domaća recenzija
Ključne riječi
ochratoxin A; apoptosa; LDH; MAPKs; stress proteins
Sažetak
Ochratoxin A (OTA) is a widespread mycotoxin produced by several species of fungi. OTA induces a tubular-interstitial nephropathy in humans and in animals. It has been implicated in aetiology of Endemic nephropathy, the disease that has a silent onset, and appears in its overt form with the symptoms of renal insufficiency. We addressed the question of the involvement of apoptosis in the development of OTA-induced nephropathy. The LLC-PK1 kidney cells were used as our experimental model. The cells were treated with different concentrations of OTA simulating natural exposure to low and high doses of OTA. Cell undergoing apoptosis were identified by morphological changes (haematoxylin/eosin staining and TUNEL reaction) as well as by biochemical markers of apoptotic pathways (caspases, MAPKs, and Hsps). 5mM OTA treatment reduced cell viability for 30, 8% after 48 hours. We found that the same treatment induced apoptosis in 15% cells. However, we did not detect the activation of caspase-3. We observed short and transient activation of ERK and strong activation of JNK and p38 following 12 and 48 hours of treatment. The expression of Hsp72, an inhibitor of apoptotic pathway, was independent of exposure of the cells to OTA. It has been suggested that nephrotoxicity provoked by OTA develops through mechanisms that lead to necrosis of proximal tubules. However, based on our results we can conclude that apoptosis might be crucial event in the development of OTA-induced nephrotoxicity.
Izvorni jezik
Engleski
Znanstvena područja
Kliničke medicinske znanosti
POVEZANOST RADA
Projekti:
0006631
Ustanove:
Farmaceutsko-biokemijski fakultet, Zagreb
Profili:
Tihana Žanić-Grubišić
(autor)
Jozsef Petrik
(autor)
Lada Rumora
(autor)
Karmela Barišić
(autor)