Diet carotenoid lutein modulates the expression of genes related to oxygen transporters and decreases DNA damage and oxidative stress in mice

- The carotenoid lutein did not induce genotoxicity or oxidative stress in mice liver and kidney.
- Lutein ameliorated genotoxicity and oxidative stress induced by cisplatin in mice liver and kidney.
- Treatments with cisplatin alone or in combination with lutein reduced the expression of GPx2, APC, Nqo1 and CCs.
- Lutein increased the expression of the important oxygen transporters Hbq1a, Mb, Ngb, Vim e Xirp1.

Lutein (LT) is a carotenoid obtained by diet and despite its antioxidant activity had been biochemically reported, few studies are available concerning its influence on the expression of antioxidant genes. The expression of 84 genes implicated in antioxidant defense was quantified using quantitative reverse transcription polymerase chain reaction array. DNA damage was measured by comet assay and glutathione (GSH) and thiobarbituric acid reactive substances (TBARS) were quantified as biochemical parameters of oxidative stress in mouse kidney and liver. cDDP treatment reduced concentration of GSH and increased TBARS, parameters that were ameliorated in treatment associated with LT. cDDP altered the expression of 32 genes, increasing the expression of GPx2, APC, Nqo1 and CCs. LT changed the expression of 37 genes with an induction of 13 mainly oxygen transporters. In treatments associating cDDP and LT, 30 genes had their expression changed with a increase of the same genes of the cDDP treatment alone. These results suggest that LT might act scavenging reactive species and also inducing the expression of genes related to a better antioxidant response, highlighting the improvement of oxygen transport. This improved redox state of the cell through LT treatment could be related to the antigenotoxic and antioxidant effects observed.