engleski

Sterigmatocystin induces oxidative stress in male Wistar rats

Sterigmatocystin (STC) is a polyketide mycotoxin with a bifuran ring structurally similar to aflatoxin. It is a precursor in aflatoxin biosynthesis in some Aspergillus species from the section Flavi and the final product in a number of Aspergilli from the section Versicolores. STC has been detected in various foodstuffs as well as indoor environments such as damp, moldy dwellings, carpets, and grain dust. In acute oral exposure it targets the liver and the kidneys. Its oral LD50 in male rats is about 160 mg kg-1 b.w. Similar to aflatoxin, STC's mechanism of action has been linked to the formation of exo- epoxide, which readily forms DNA adducts. Considering that aflatoxin toxicity has also been associated with oxidative stress, the aim of this study was to check whether the same is true for STC toxicity. With that in mind, we treated male Wistar rats with single oral STC doses of 1/4, 1/8, and 1/16 of LD50 (40, 20, and 10 mg kg-1 b.w., respectively) and measured superoxide dismutase (SOD) activity in plasma on a plate reader using a commercial kit. We also measured glutathione (GSH) and malondialdehyde (MDA) in plasma, kidney, and liver tissue using a spectrophotometer and HPLC, respectively. To assess oxidative DNA damage in the liver and kidneys we used comet tail intensity (i. e. DNA % in tail) obtained with the hOGG1-modified comet assay. STC did not affect GSH concentrations. SOD activity in plasma dropped significantly only in rats treated with 1/8 of LD50 (9.26±0.26 vs. 10.08±0.82 U mL-1 in control). All doses significantly increased MDA concentrations in plasma and kidney, but not in the liver. Oxidative DNA damage showed up in the liver and kidney cells, and was more pronounced in the kidneys, particularly at 1/8 of LD50. Our findings suggest that acute oral exposure to STC causes greater oxidative stress in the kidneys than the liver. This work has been fully supported by the Croatian Science Foundation under the project MycotoxA (HRZZ-IP- 09-2014-5982).

DNA damage, glutathione, malondialdehyde, sterigmatocystin, superoxide dismutase

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