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Apoptosis and oxidative stress induced by ochratoxin A in rat kidney.
Arch Toxicol. 2003 Dec; 77(12):685-93.AT

Abstract

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 as one of the aetiological agents involved in the development of endemic nephropathy. OTA-induced oxidative stress and apoptosis may play key roles in the development of chronic tubulointerstitial nephritis connected to the long-term exposure to this food contaminant. We studied the effects of low doses of OTA on kidney cells. Wistar rats were treated with 120 microg OTA/kg bodyweight daily, for 10, 30 or 60 days. Toxin concentration in kidney was proportional to the time of exposure, and amounted to 547.2, 752.5 and 930.3 ng OTA/g kidney tissue after 10, 30 and 60 days, respectively. OTA treatment caused an increased number of cells undergoing apoptosis in both proximal and distal epithelial kidney cells. The apoptotic cells were visualised using the TUNEL assay and staining with haematoxylin and eosin in situ. The number of apoptotic cells in rats treated for 10, 30 and 60 days increased by 5-, 6.4- and 12.7-fold, respectively, compared with the control cells. However, DNA electrophoresis did not show characteristic fragmentation (DNA laddering). The oxidative stress was evident via increased malondialdehyde formation. The concentration of lipid peroxides showed an increase (36%), but the activity of superoxide dismutase decreased (26%) in 60-day treated rats. In spite of the observed biochemical and morphological changes in the kidney cells, renal functional status was preserved to the end of experiment. This study demonstrates that a combination of morphologic and biochemical markers can be used to monitor early cell death in OTA-induced renal injury. We have shown that the exposure to the relatively low OTA concentrations has activated apoptotic processes and oxidative damage in kidney cells.

Authors+Show Affiliations

Department of Medical Biochemistry and Haematology, Faculty of Pharmacy and Biochemistry, University of Zagreb, Ante Kovacića 1, PO Box 156, 10000 Zagreb, Croatia, jpetrik@pharma.hrNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

13680094

Citation

Petrik, József, et al. "Apoptosis and Oxidative Stress Induced By Ochratoxin a in Rat Kidney." Archives of Toxicology, vol. 77, no. 12, 2003, pp. 685-93.
Petrik J, Zanić-Grubisić T, Barisić K, et al. Apoptosis and oxidative stress induced by ochratoxin A in rat kidney. Arch Toxicol. 2003;77(12):685-93.
Petrik, J., Zanić-Grubisić, T., Barisić, K., Pepeljnjak, S., Radić, B., Ferencić, Z., & Cepelak, I. (2003). Apoptosis and oxidative stress induced by ochratoxin A in rat kidney. Archives of Toxicology, 77(12), 685-93.
Petrik J, et al. Apoptosis and Oxidative Stress Induced By Ochratoxin a in Rat Kidney. Arch Toxicol. 2003;77(12):685-93. PubMed PMID: 13680094.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Apoptosis and oxidative stress induced by ochratoxin A in rat kidney. AU - Petrik,József, AU - Zanić-Grubisić,Tihana, AU - Barisić,Karmela, AU - Pepeljnjak,Stjepan, AU - Radić,Bozica, AU - Ferencić,Zeljko, AU - Cepelak,Ivana, Y1 - 2003/09/10/ PY - 2003/02/10/received PY - 2003/07/01/accepted PY - 2003/9/19/pubmed PY - 2004/10/27/medline PY - 2003/9/19/entrez SP - 685 EP - 93 JF - Archives of toxicology JO - Arch Toxicol VL - 77 IS - 12 N2 - 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 as one of the aetiological agents involved in the development of endemic nephropathy. OTA-induced oxidative stress and apoptosis may play key roles in the development of chronic tubulointerstitial nephritis connected to the long-term exposure to this food contaminant. We studied the effects of low doses of OTA on kidney cells. Wistar rats were treated with 120 microg OTA/kg bodyweight daily, for 10, 30 or 60 days. Toxin concentration in kidney was proportional to the time of exposure, and amounted to 547.2, 752.5 and 930.3 ng OTA/g kidney tissue after 10, 30 and 60 days, respectively. OTA treatment caused an increased number of cells undergoing apoptosis in both proximal and distal epithelial kidney cells. The apoptotic cells were visualised using the TUNEL assay and staining with haematoxylin and eosin in situ. The number of apoptotic cells in rats treated for 10, 30 and 60 days increased by 5-, 6.4- and 12.7-fold, respectively, compared with the control cells. However, DNA electrophoresis did not show characteristic fragmentation (DNA laddering). The oxidative stress was evident via increased malondialdehyde formation. The concentration of lipid peroxides showed an increase (36%), but the activity of superoxide dismutase decreased (26%) in 60-day treated rats. In spite of the observed biochemical and morphological changes in the kidney cells, renal functional status was preserved to the end of experiment. This study demonstrates that a combination of morphologic and biochemical markers can be used to monitor early cell death in OTA-induced renal injury. We have shown that the exposure to the relatively low OTA concentrations has activated apoptotic processes and oxidative damage in kidney cells. SN - 0340-5761 UR - https://www.unboundmedicine.com/medline/citation/13680094/Apoptosis_and_oxidative_stress_induced_by_ochratoxin_A_in_rat_kidney_ L2 - https://doi.org/10.1007/s00204-003-0501-8 DB - PRIME DP - Unbound Medicine ER -