Dietary Bioactive Components
Objectives : Dietary fat has been shown to enhance oxidative stress and adipose tissue (AT) accrual, further exacerbating redox imbalance. Lycopene is a potent lipophilic antioxidant with singlet oxygen quenching abilities. Thus, lycopene may mediate excess levels of oxidative stress imposed by a high fat diet. The purpose of this study was to evaluate systemic and AT redox balance in Sprague-Dawley rats fed lycopene-supplemented diets meeting and exceeding recommendations for fat intake in humans.
Methods : Male Sprague-Dawley rats (n=18) at four weeks of age were fed 30% fat (control) or 60% fat purified diet (HFD) supplemented with 100mg lycopene/d. Three rats in each diet group were euthanized at weeks 3, 7, and 10, respectively, with body weight and visceral AT weight recorded. Redox markers assessed included serum and AT lipid peroxides by the thiobarbituric acid-reactive substances (TBARS) assay and antioxidant capacity (AC) by the oxygen radical absorbance capacity assay. All statistical models were adjusted for dietary intake.
Results : At weeks 3 and 7, there were no significant differences in serum or AT redox markers or AT mass between the two groups; however, body weight was significantly lower in the HFD group at both time points (p=0.016 and p=0.008, respectively). At week 10, AT was significantly higher (p=0.028) in the HFD group, yet there were no significant differences in lipid peroxides between the two groups. Of interest, AT in the HFD group exhibited significantly greater lipophilic AC (p=0.031). Significant correlations between serum and AT TBARS (p=0.036, r=0.841) and serum and AT lycopene (p=0.021, r=0.879) were only observed at week 10.
Conclusions : Despite a 30% greater provision of dietary fat to the HFD group with subsequent AT accrual, no significant differences in systemic and AT oxidative stress measures were observed between the two groups at study completion; however, the HFD group exhibited increased lipophilic AC. Results suggest that lycopene may modulate systemic redox balance through the attenuation of AT oxidative stress.
Funding Sources : University of Alabama Pilot Grant