Antioxidant supplementation & age-associated lesion incidence

We studied the potential for augmented antioxidant consumption started during middle-age to alter lesion incidence. One hundred sixty-eight male C57BL/6 mice aged 18 months were fed modified AIN76 (C), or C supplemented with one of the following: 470 ppm vitamin E, 0.5% glutathione, 470 ppm vitamin E + 0.5% glutathione. 11 ppm melatonin, or 1 % strawberry extract. Mice had ad libitum access to food and water. Those surviving to 24 months of age were sacrificed, and samples of heart, lung, liver, spleen, kidney, and testes were evaluated for lesions using standard histologic methods. At 24 months of age, there were no differences between diet groups in body weight, 45.92±8.0 g, or in the average number of lesions observed per mouse. Antioxidant supplementation started during middle-age appears to he an ineffective means to alter age-associated lesion patterns in older mice. The mice in this study were significantly heavier than a reference population (RP) of male C57BL/6 mice fed a grain-based diet (34.48±4.4 g, p=0.0006). Fatty liver was observed in 73% of the mice in this study, significantly more than in the RP (p=0.04). Additionally, the severity of fatty liver was much more profound in this study. Focal kidney atrophy was observed significantly more frequently in this study than in the RP (p=0.0009). Further, the kidneys from 87% of the mice in this study were observed to contain proteinaceous casts which were seen in no RP mice. These observations suggest this semi-synthetic diet formulation is inappropriate for long-term study of older mice.