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Reduced scytonemin isolated from Nostoc commune induces autophagic cell death in human T-lymphoid cell line Jurkat cells

Itoh, Tomohiro, Tsuzuki, Ryosuke, Tanaka, Toshiomi, Ninomiya, Masayuki, Yamaguchi, Yuji, Takenaka, Hiroyuki, Ando, Masashi, Tsukamasa, Yasuyuki, Koketsu, Mamoru
Food and chemical toxicology 2013 v.60 pp. 76-82
DNA fragmentation, Nostoc commune, acetylcysteine, apoptosis, aquatic environment, autophagy, cell growth, growth retardation, humans, reactive oxygen species, soil, vacuoles
Nostoc commune is a terrestrial benthic blue-green alga that often forms an extended mucilaginous layer on the soil, accumulates on stones and mud in aquatic environments. Reduced-scytonemin (R-scy), isolated from N. commune Vaucher, has been shown to suppress the human T-lymphoid Jurkat cell growth. To reveal the mechanisms underlying the R-scy-mediated inhibition of Jurkat cell growth, we examined cell morphology, DNA fragmentation, and microtubule-associated protein light chain 3 (LC3) modification in these cells. We observed multiple vacuoles as well as the conversion of LC3-I to LC3-II in R-scy-treated cells. These results suggest that the R-scy induced Jurkat cell growth inhibition is attributable to the induction of type II programmed cell death (PCD II; autophagic cell death or autophagy). We further examined the mechanisms underlying R-scy-induced PCDII. The cells treated with R-scy produced large amounts of reactive oxygen species (ROS), leading to the induction of mitochondrial dysfunction. However, the elimination of R-scy-induced ROS by treatment with N-acetyl-l-cysteine (NAC) markedly opposed R-scy-induced PCDII. Based on these results, we conclude that ROS formation plays a critical role in R-scy-induced PCDII.