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

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.

Ochratoxin A; Kidney desease; Cytotoxicity; Apoptosis

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