engleski

Effects of citrinin treatment on oxidative stress in rat kidney

Citrinin (CTN) is nephrotoxic mycotoxin, secondary product of Penicillium, Aspergillus and Monascus moulds that contaminate cereals. The mechanism of CTN toxicity has been studied mostly on cell cultures while studies on laboratory animals are rare and inconclusive. In this study parameters of oxidative stress were measured in adult male rats treated orally either with CTN (20 mg/kg b.w. daily for 2 days) or vehicle (Na2CO3) and sacrificed 24 h after the second treatment. In urine collected in metabolic cages 24 h before the beginning of treatment and 3 and 6 h afterwards the concentration malondialdehyde (MDA) as a parameter of lipid peroxidation was measured. The concentration of glutathione (GSH) and MDA were measured in plasma, kidney and liver. The presence of oxidative DNA damage in kidney and liver cells was evaluated using hOGG1 modified single cell gel electrophoresis (comet assay). CTN treatment caused the decrease of GSH concentration in plasma (19.8±2.9 and 13.9±2.5
mol/L in controls and treated animals, respectively), liver (0.17±0.01 and 0.15±0.01
mol/g tissue) and kidney (0.21±0.06 and 0.19±0.04
mol/g tissue), while MDAconcentration in organs was not changed. The analysis ofMDA concentration in urine showed very similar pattern in control and treated animals indicating the importance of external stress on animals in metabolic cages. Comet assay revealed the significant increase of tail intensity in kidney cells of CTN- treated animals. The comet tail intensity of control rats was 0.72±1.02 and 1.65±0.32 in CTN treated animals (P < 0.05). In liver the CTN treatment did not affect these parameters. The results of specific oxidative DNA lesions caused by

citrinin; oxidative stress; rat kidney

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