Artigo Revisado por pares

VP-16-induced nucleotide pool changes and poly(ADP-ribose) synthesis: The role of VP-16 in interphase death

1989; Elsevier BV; Volume: 185; Issue: 1 Linguagem: Inglês

10.1016/0014-4827(89)90052-9

ISSN

1090-2422

Autores

Akihiko Tanizawa, Masaru Kubota, Hisako Hashimoto, Tsunehiro Shimizu, Tetsuya Takimoto, Toshiyuki Kitoh, Yuichi Akiyama, Harukí Mikawa,

Tópico(s)

Calcium signaling and nucleotide metabolism

Resumo

Exposure of human promyelocytic leukemia cell line (HL-60) to VP-16 resulted in accumulation of DNA strand breaks. Concomitantly, intracellular NAD levels fell at 1 h, followed by declines in ATP at 2 h and in GTP, CTP, and UTP at 3 h. Furthermore, marked morphological changes, such as loss of microvilli or bleb formation, appeared at 4 h and cell death by 8–10 h. The addition of an inhibitor of poly(ADP-ribose) polymerase, 3-aminobenzamide (5 mM), theophylline (2 mM), or thymidine (1 mM), prevented these sequential reductions of nucleotide pools and cell death. In fact, the activation of poly(ADP-ribose) synthesis was detectable within a few hours after treatment with VP-16, although it was smaller than that induced by N-methyl-N′-nitro-N-nitrosoguanidine. These results may suggest the possible role of activation of poly(ADP-ribosyl)ation in VP-16-induced nucleotide pool changes and subsequent interphase death.

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