Iron supplementation does not aggravate impaired glucose tolerance and sugar overload-induced genotoxicity in rats.

High sugar intake is a major risk factor for metabolic disorders. Genotoxicity is an important factor in diabetes onset, and iron (Fe) may be an aggravating element. However, this relationship is still poorly established. Thus, this study evaluated whether Fe supplementation could aggravate obesity, impaired glucose tolerance, and sugar overload-induced genotoxicity in rats. A total of 24 rats were treated with different diets: standard diet (SD, n = 8), invert sugar overload (320 g/L, HSD, n = 8), or Fe plus invert sugar overload (2.56 mg/L of Fe 2+ , Fe-HSD, n = 8) for four months. After treatment, the Fe-HSD group showed no excessive weight gain or impaired glucose tolerance. DNA damage in blood, as assessed by comet assay, gradually increased in HSD during treatment (p < 0.001), whereas Fe-HSD showed a nonlinear increase in DNA damage. Moreover, Fe-HSD presented 0.6-fold more DNA damage compared with SD (p = 0.0055) in the 1st month of treatment. At months 2 and 3, results show a ≥ 1.4-fold increase in HSD and Fe-HSD DNA damage, respectively, compared with SD (p < 0.01). At the end of the experiment, only HSD DNA damage differed from SD (1.5-fold more, p = 0.0196). Fe supplementation did not aggravate the invert sugar-induced DNA damage (p > 0.05). In the pancreas, results showed no differences in DNA damage. Mutagenicity, evaluated by micronucleus testing, was not observed regardless of treatment (p = 0.428). Fe supplementation, in the evaluated concentration, did not aggravate weight gain, impaired glucose tolerance, and sugar overload-induced genotoxicity in rats.