4.7 Article

Protective effect of selenomethionine on kidney injury induced by ochratoxin A in rabbits

Journal

ENVIRONMENTAL SCIENCE AND POLLUTION RESEARCH
Volume 30, Issue 11, Pages 29874-29887

Publisher

SPRINGER HEIDELBERG
DOI: 10.1007/s11356-022-24297-7

Keywords

Ochratoxin A (OTA); Selenomethionine (SeMet); Kidney injury; Nrf2/HO-1; Oxidative stress; Inflammatory response

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The study investigated the protective effect and mechanism of selenomethionine (SeMet) on ochratoxin A (OTA)-induced nephrotoxicity in rabbits. The results showed that SeMet supplementation improved blood physiological indices, renal function decline, and pathological kidney injury caused by OTA poisoning in the rabbits. SeMet also increased antioxidant capacity, decreased oxidative stress and inflammation, and activated the Nrf2 signaling pathway.
The purpose of this study was to investigate the protective effect and mechanism of selenomethionine (SeMet) on ochratoxin A (OTA)-induced nephrotoxicity in rabbits. In total, sixty Ira rabbits were randomly divided into 5 groups (the control group, OTA group, 0. 2 mg/kg SeMet + OTA group, 0. 4 mg/kg SeMet + OTA group, and 0. 6 mg/kg SeMet + OTA group). The rabbits were fed diets supplemented with different doses of SeMet for 21 days and given 0. 2 mg/kg OTA starting on day 15 for a week. The results showed that the SeMet supplementation could improve the changes in blood physiological indices and renal function decline caused by OTA poisoning, and alleviate pathological kidney injury in the rabbits. SeMet also increased the activities of total antioxidant capacity, superoxide dismutase, and glutathione peroxidase, and decreased the contents of malondialdehyde and reactive oxygen species and the expression of interleukin-1 beta, interleukin-6, and tumor necrosis factor-a in the damaged kidneys of the rabbits. In addition, the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream gene heme oxygenase 1 (HO-1) was also inhibited after OTA poisoning, while SeMet activated the Nrf2 signaling pathway and enhanced the expression of Nrf2 and the downstream gene HO-1. In conclusion, SeMet protected against kidney injury caused by OTA in rabbits, and the mechanism may be the activation of the Nrf2 signaling pathway.

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