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Involvement of lipid peroxidation and apoptosis in acute toxicity of ochratoxin A

Ochratoxin A (OTA) is the nephrotoxic product of moulds that contaminate food and feed at all climatic conditions. It is supposed to be involved in the mechanism of endemic nephropathy, disease known also to occur in our country. The mechanism of OTA toxicity is not yet understood. The proposed mechanisms of OTA toxicity are the inhibition of t-RNA phenylalanine syntethase, inhibition of phosphoenolpyruvate carboxykinase and the enhancement of lipid peroxidation. Biological marker of lipid peroxidation is malondialdehyde (MDA), the final product of lipid peroxidation. Apoptosis is the type of active cell death caused by intrinsic factors. It occurs in physiological and pathological conditions. It was observed in some tumors as well as the consequence of exposure to some toxic compounds. The aim of the study was to check whether the single dose of OTA causes apoptosis in kidney tissue and changes of lipid peroxidation in kidney and urine. In female rats given single OTA dose (1.0 mg/kg.b.w., i.p.) and sacrificed 1, 2, 6 and 9 days afterwards, the number of apoptotic cells in kidney (mean&plusmn ; ; ; SD) was 19&plusmn ; ; ; 23, 13&plusmn ; ; ; 19, 0 and 0, respectively. The same was not seen in kidney tissue of control rats (given vehicle only). The OTA concentration in kidney, urine and plasma of treated animals was the highest at the first time point and afterwards decreased gradually. However, the concentration of MDA in kidney and urine of treated animals did not differ from that in control animals. The appearance of apoptotic cells in kidney of OTA-treated animals seems to be in correlation with OTA concentration. The lack of changes in MDA concentration in OTA-treated animals indicates that MDA is not involved in the induction of apoptotic cells in experimental animals.

apoptosis; ochratoxin A; lipid peroxidation

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