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首页> 外文期刊>Biochemical Pharmacology >Site-specific DNA methylation and apoptosis: induction by diabetogenic streptozotocin.
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Site-specific DNA methylation and apoptosis: induction by diabetogenic streptozotocin.

机译：位点特异性DNA甲基化和凋亡：糖尿病性链脲佐菌素的诱导。

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摘要

Streptozotocin (STZ) is known to induce insulin-dependent diabetes mellitus via DNA damage in experimental animals. The mechanism of induction of DNA damage by STZ was investigated in vitro, using a human cell line and 32P-labeled DNA fragments isolated from human genes. STZ induced cellular DNA damage and apoptosis, and frequently initiated DNA modification at guanines, especially at the middle guanine in runs of three and at the guanine at the 3'-end of runs of two guanines, similar to N-methyl-N-nitrosourea, a typical methylating agent. Scavengers for reactive oxygen species or nitric oxide did not inhibit the induction of DNA damage by STZ. On the other hand, damage induction was inhibited by sodium acetate and sodium chloride, which can reduce the reactivity of methylating agents to DNA via the sodium cation. These results suggest that STZ induces DNA damage by methylation of guanines via methyl cations. This alkylation may be responsible for triggering apoptosis, and subsequently diabetes.
机译：已知链脲佐菌素（STZ）通过实验动物的DNA损伤诱导胰岛素依赖性糖尿病。使用人类细胞系和从人类基因分离的32P标记的DNA片段，体外研究了STZ诱导DNA损伤的机制。 STZ诱导细胞DNA损伤和细胞凋亡，并经常在鸟嘌呤中启动DNA修饰，特别是在三个运行的中间鸟嘌呤和两个鸟嘌呤的运行3'末端的鸟嘌呤，类似于N-甲基-N-亚硝基脲，一种典型的甲基化剂。活性氧或一氧化氮的清除剂不会抑制STZ对DNA损伤的诱导。另一方面，乙酸钠和氯化钠抑制了损伤诱导，这可以降低甲基化剂通过钠阳离子对DNA的反应性。这些结果表明STZ通过鸟嘌呤通过甲基阳离子的甲基化诱导DNA损伤。这种烷基化可能导致细胞凋亡，进而引发糖尿病。

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