2,8-Dihydroxyadenine

2,8-Dihydroxyadenine (60-240 µg/mL; 72 h) induces dose-dependent transcriptional changes in HK-2 cells, with upregulation of TNF-α, mTORC1, E2F targets, and G2M checkpoint pathways, and downregulation of EMT and oxidative phosphorylation, highlighting inflammation, metabolic stress, and cell cycle dysregulation^[3].

2,8-Dihydroxyadenine (50 μM) undergoes quasi-reversible oxidation at a glassy carbon electrode in pH 4.5 acetate buffer, forming an unstable oxidation product and, at high scan rates, detectable dimers^[2].
2,8-Dihydroxyadenine (50 μM) oxidation at a GCE is pH-dependent, occurring with a 2-electron transfer and forming a strongly adsorbing electroactive product P₂,₈-DHA, with maximum oxidation current at pH 4.5^[2].
2,8-Dihydroxyadenine reduction at a GCE is reversible in the absence of oxygen, but molecular oxygen interferes with the reductive electron transfer, shifting the reduction potential and increasing the reduction current^[2].
2,8-Dihydroxyadenine (DHA) (60-480 µg/mL; 72 h) reduces viability of HEK293, MDCK, and HK-2 cells in a dose-dependent manner, with HEK293 cells showing the greatest decrease to approximately 40% at 480 µg/mL^[3].
2,8-Dihydroxyadenine (120-480 µg/mL; 24 h) impairs wound closure in HEK293, MDCK, and HK-2 cells, with HEK293 cells treated with 480 µg/mL DHA achieving only ~50% closure at 72 h compared to full closure in controls, and HK-2 cells reaching ~70-80% closure at 72 h^[3].
2,8-Dihydroxyadenine (120-480 µg/mL; 72 h) upregulates CD44 gene expression in HK-2 cells, while HEK293 cells show increased CD44 gene expression at higher DHA concentrations, but MDCK cells do not show increased CD44 gene expression^[3].
2,8-Dihydroxyadenine (120-480 µg/mL; 72 h) increases CD44 protein expression in HEK293, MDCK, and HK-2 cells, with CD44 localized adjacent to DHA crystals^[3].