engleski

Ochratoxin A induced apoptosis in rat tubular kidney tissue

Nephrotoxic mycotoxin ochratoxin A (OTA), probably involved in the etiology of endemic nephropathy (EN), increases lipid peroxidation and produces oxygen reactive metabolites which may cause apoptosis. In our work, adult female Wistar rats were treated i.p. with multiple doses of OTA (500 mg OTA/kg b.w./day/3 times a week for up to 4 weeks). Animals were sacrificed 24 h after 1, 3, 6 and 12 treatments, as well as 1 and 3 weeks after the 12th treatment, respectively. The number of apoptotic cells was counted in a section of the rat whole kidney, 4 mm thick, paraffin embedded. The number of apoptotic cells increased progressively from the 1st up to the 6th treatment. Necrosis was not seen. Apoptotic cells were not seen in controls. The activities of alkaline phosphatase (AP), lactate dehydrogenase (LDH), leucine amino-peptidase (LAP) and isocitrate dehydrogenase (ICDH) were measured in urine collected for a 24 h period after 1st, 3rd, 6th, 9th, and 12th treatments and 3 weeks after the last treatment, respectively, and in control animals. In OTA treated rats, the enzyme excretion rate of AP and LDH increased progressively up to the 3rd treatment, while LAP and ICDH increased up to the 9th treatment.

ochratoxin A; apoptosis; rat; kidney; tubular tissue

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