Feeding 0.5% beta-carotene in the diet for life beginning at 29 days of age improved the average life span of C57BL/6J male mice by 5.0% but decreased the life span of mice started at 608 days of age by 11.5%. Neither difference, however, proved to be statistically significant. Feeding beta-carotene increased the concentration of beta-carotene in the serum by 60% but did not change the beta-carotene content of heart, liver or kidney. We conclude that singlet oxygen, which is very efficiently quenched by beta-carotene, is an important factor in senescence only if it is produced at organ sites not accessible to serum beta-carotene. Since we have found that beta-carotene feeding is not a useful means for increasing tissue concentrations of beta-carotene, other more sophisticated means must be developed for accomplishing this purpose. It is also clear that while dietary beta-carotene is not an effective means for prolonging life span, it is nontoxic when fed continuously at high concentrations.