In the present study, we investigated the cooperative role of the TRX/GSH system during the systemic iron accumulation in mouse kidney tissue. Iron accumulation was induced in mice and the total iron content of mouse kidney tissue was determined by spectroscopic method. The expression of Fth1, Fpn1, and Hamp genes were analyzed using qPCR. The results obtained show that the iron overload model is formed. Subsequently, the impact of iron toxicity on Trx system members (Trx1, TrxR1, and Txnip) was examined at the gene and protein expression level, and enzyme activity. Iron toxicity unaffected the Trx system at the gene expression level, but activation of the Trx system was observed at the protein expression level and enzyme activity. Additionally, MDA level, TAS, TOS, and OSI were measured in mouse kidney tissue where oxidative stress was induced by iron toxicity. Finally, the effect of iron supplementation on the activities of GSH system enzymes (GPx, GR, GST) and other enzymatic antioxidants (SOD, CAT) was determined by spectroscopic method. This study demonstrated that SOD and CAT, in particular, protect mouse kidney tissue from iron overload by cooperating with the TRX system against iron toxicity. The effect of iron toxicity on kidney tissue has been shown to differ from that observed in heart and liver tissues in previous studies.
Aydın et al. (Tue,) studied this question.