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Ochratoxin A Induces Apoptosis in LLC-PK1 Cells via JNK and p38 MAPK Activation

Karmela Barišić
Lada Rumora
József Petrik
Ivana Čepelak
Tihana Žanić-Grubišić

Puni tekst: engleski, pdf (250 KB) str. 385-392 preuzimanja: 350* citiraj
APA 6th Edition
Barišić, K., Rumora, L., Petrik, J., Čepelak, I. i Žanić-Grubišić, T. (2005). Ochratoxin A Induces Apoptosis in LLC-PK1 Cells via JNK and p38 MAPK Activation. Croatica Chemica Acta, 78 (3), 385-392. Preuzeto s https://hrcak.srce.hr/47
MLA 8th Edition
Barišić, Karmela, et al. "Ochratoxin A Induces Apoptosis in LLC-PK1 Cells via JNK and p38 MAPK Activation." Croatica Chemica Acta, vol. 78, br. 3, 2005, str. 385-392. https://hrcak.srce.hr/47. Citirano 16.09.2019.
Chicago 17th Edition
Barišić, Karmela, Lada Rumora, József Petrik, Ivana Čepelak i Tihana Žanić-Grubišić. "Ochratoxin A Induces Apoptosis in LLC-PK1 Cells via JNK and p38 MAPK Activation." Croatica Chemica Acta 78, br. 3 (2005): 385-392. https://hrcak.srce.hr/47
Harvard
Barišić, K., et al. (2005). 'Ochratoxin A Induces Apoptosis in LLC-PK1 Cells via JNK and p38 MAPK Activation', Croatica Chemica Acta, 78(3), str. 385-392. Preuzeto s: https://hrcak.srce.hr/47 (Datum pristupa: 16.09.2019.)
Vancouver
Barišić K, Rumora L, Petrik J, Čepelak I, Žanić-Grubišić T. Ochratoxin A Induces Apoptosis in LLC-PK1 Cells via JNK and p38 MAPK Activation. Croatica Chemica Acta [Internet]. 2005 [pristupljeno 16.09.2019.];78(3):385-392. Dostupno na: https://hrcak.srce.hr/47
IEEE
K. Barišić, L. Rumora, J. Petrik, I. Čepelak i T. Žanić-Grubišić, "Ochratoxin A Induces Apoptosis in LLC-PK1 Cells via JNK and p38 MAPK Activation", Croatica Chemica Acta, vol.78, br. 3, str. 385-392, 2005. [Online]. Dostupno na: https://hrcak.srce.hr/47. [Citirano: 16.09.2019.]

Sažetak
Ochratoxin A (OTA) is a potential inducer of a tubular-interstitial nephropathy in humans and animals. In our study we addressed the question of involvement of apoptosis in the development of OTA-provoked nephrotoxicity. LLC-PK1 kidney cells were treated with nanomolar and micromolar concentrations of OTA for different lengths of time. The apoptotic process was estimated by morphological (haematoxylin/eosin staining, fluorescent staining of DNA free ends – TUNEL assay) and biochemical (MAPKs and Hsps) changes of cells. Forty-eight hours of treatment with 5  10–6 M OTA significantly decreased cell viability and induced apoptosis in 30.7 % of cells. In addition, a transient activation of ERK was observed as well as a strong and prolonged activation of stress kinases, JNK and p38 MAPK, after 12 and 48 hours of treatment. Expression of Hsp72 and Hsp27 was not affected by OTA. The results suggest that apoptosis mediated by activation of JNK and p38 MAPK might play an important role in OTA-induced nephrotoxicity in LLC-PK1 cells.

Ključne riječi
OTA; LLC-PK1 cells; apoptosis; MAPKs; Hsps

Hrčak ID: 47

URI
https://hrcak.srce.hr/47

[hrvatski]

Posjeta: 675 *