Aging is associated with the accumulation of cellular toxins and damage.

Aging is associated with the accumulation of cellular toxins and damage. Declines in cellular detoxification mechanisms and impairments in antioxidant protection are consistently
observed in aging models and likely contribute to ageassociated accumulation of cellular damage. The master regulator, Nuclear factor erythroid 2-related factor 2 (Nrf2), is a transcription factor that regulates the basal and inducible expression of a large battery of genes encoding for
cytoprotective factors including those that defend against electrophilic stressors and oxidative insults. The Nrf2/electrophile response element (EpRE) Antioxidant Protection and Phase II Detoxification pathways are impaired with aging due to age-related changes in gene expression (2). A key example is the reduction in glutathione (GSH) levels in all tissues with age due primarily to declines in glutamatecysteine ligase and glutathione synthase expression (1). Opposing these changes in gene expression may delay or attenuate the aging process. Most anti-aging intervention strategies to date, have tested single ingredients and have focused solely on an individual gene, in an isolated tissue. A more comprehensive strategy is to examine changes in the expression patterns of multiple genes or pathways in specific tissues and then to identify a
blend of phytochemicals that opposes those age-related changes. It seems prudent to examine changes that occur during middle age rather than waiting until old age when an intervention may not be as impactful. Accordingly, the purpose of this study was to test a blend of natural
compounds in middle-aged mice, compared to young mice, for the ability to oppose age-related changes in the expression of Nrf2-regulated genes involved in the detoxification of xenobiotics and xenobiotic metabolites and in the synthesis and regulation of intrinsic antioxidants and
antioxidant enzymes.

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