Abstract:
BACKGROUND/AIM:We have shown that either chronic nicotine (NIC) exposure or 5-aza-cytidine (AZA) augments oxidative stress-dependent injury through stimulating p66shc in renal cells. Hence, NIC could exacerbate adverse effects of AZA while antioxidants such as resveratrol (RES) could prevent it. MATERIALS AND METHODS:Renal proximal tubule cells (NRK52E) were treated with 20 μM RES prior to 200 μM NIC plus 100 nM AZA and cell injury (LDH release) was determined. Reporter luciferase assays determined p66shc activation and RES-induced antioxidant responses. Genetic manipulations identified the mechanism of RES action. RESULTS:NIC exacerbated AZA-dependent injury via augmenting p66shc transcription. While RES suppressed NIC+AZA-mediated injury, -surprisingly-it further enhanced activity of the p66shc promoter. RES protected cells via the cytoplasmic p66shc/Nrf2/heme oxygenase-1 (HO-1) axis. CONCLUSION:RES can protect the kidney from adverse effects of NIC in patients undergoing anticancer therapy.
journal_name
Anticancer Resjournal_title
Anticancer researchauthors
Arany I,Hall S,Faisal A,Dixit Mdoi
10.21873/anticanres.11793subject
Has Abstractpub_date
2017-08-01 00:00:00pages
4075-4079issue
8eissn
0250-7005issn
1791-7530pii
37/8/4075journal_volume
37pub_type
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