Anehus S, Pohjanpelto P, Baldetorp B, Långström E, Heby O
Mol Cell Biol. 1984 May;4(5):915-22. doi: 10.1128/mcb.4.5.915-922.1984.
This study analyzes the effects of polyamine starvation on cell cycle traverse of an arginase-deficient CHO cell variant (CHO-A7). These cells grow well in serum-free medium, provided that it contains ornithine or polyamines or both. In the absence of ornithine or polyamines or both, the CHO-A7 cells develop severe polyamine deficiency and, as a consequence, grow more slowly. When grown to a stationary phase in the presence of ornithine or putrescine or both, the CHO-A7 cells became arrested in G0/early G1. However, when starved for ornithine and polyamines, they accumulated in the S and G2 phases. Ornithine and polyamine starvation of CHO-A7 cells causes an increase in ornithine decarboxylase activity. When this increase was prevented by treatment with DL-alpha-difluoromethylornithine, an enzyme-activated irreversible inhibitor of ornithine decarboxylase, growth was further suppressed, and a greater fraction of cells were found in the S and G2 phases of the cell cycle.
本研究分析了多胺饥饿对精氨酸酶缺陷型CHO细胞变体(CHO-A7)细胞周期进程的影响。这些细胞在无血清培养基中生长良好,前提是该培养基含有鸟氨酸或多胺或两者都有。在缺乏鸟氨酸或多胺或两者都缺乏的情况下,CHO-A7细胞会出现严重的多胺缺乏,结果生长得更慢。当在存在鸟氨酸或腐胺或两者都存在的情况下生长至稳定期时,CHO-A7细胞停滞在G0/早期G1期。然而,当缺乏鸟氨酸和多胺时,它们会在S期和G2期积累。CHO-A7细胞的鸟氨酸和多胺饥饿会导致鸟氨酸脱羧酶活性增加。当用DL-α-二氟甲基鸟氨酸(鸟氨酸脱羧酶的一种酶激活不可逆抑制剂)处理来阻止这种增加时,生长会进一步受到抑制,并且在细胞周期的S期和G2期发现更大比例的细胞。