Journal
MOLECULAR AND CELLULAR BIOLOGY
Volume 23, Issue 23, Pages 8786-8794Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.23.23.8786-8794.2003
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Funding
- NCI NIH HHS [R01 CA094076, R01 CA039416, CA94076, CA39416] Funding Source: Medline
- NIEHS NIH HHS [ES03819, P30 ES003819] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA094076, R01CA039416] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [P30ES003819] Funding Source: NIH RePORTER
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Proteasomes degrade damaged proteins formed during oxidative stress, thereby promoting cell survival. Neurodegenerative and other age-related disorders are associated with reduced proteasome activity. We show herein that expression of most subunits of 20S and 19S proteasomes, which collectively assemble the 26S proteasome, was enhanced up to threefold in livers of mice following treatment with dithiolethiones, which act as indirect antioxidants. Subunit protein levels and proteasome activity were coordinately increased. No induction was seen in mice where the transcription factor Nrf2 was disrupted. Promoter activity of the PSMB5 subunit of the 20S proteasome increased with either Nrf2 overexpression or treatment with antioxidants in mouse embryonic fibroblasts. Tandem antioxidant response elements in the proximal promoter of PSMB5 that controlled these responses were identified. We propose that induction of the 26S proteasome through the Nrf2 pathway represents an important indirect action of these antioxidants that can contribute to their protective effects against chronic diseases.
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