Holliday R, Thompson K V
Gerontology. 1983;29(2):89-96. doi: 10.1159/000213098.
The level of heat-labile glucose-6-phosphate dehydrogenase (G6PD) has been measured in skin fibroblast cultures from premature ageing or DNA repair deficient genetic syndromes. The short in vitro longevity of Werner's syndrome, progeria, Cockayne's syndrome, ataxia telangiectasia, Fanconi's anaemia, and Bloom's syndrome cultures was correlated with the appearance of a significant fraction of heat-labile enzyme. Long-lived control cultures contain a low level of altered enzyme until they become senescent. The evidence that heat-labile G6PD molecules are derived from errors in synthesis, or from other causes, is critically assessed. It is shown that normal cells grown in medium containing the antibiotic, paromomycin, which is known to reduce the fidelity of ribosomal translation, produce a significant fraction of altered G6PD.
已对早衰或DNA修复缺陷遗传综合征患者皮肤成纤维细胞培养物中的热不稳定葡萄糖-6-磷酸脱氢酶（G6PD）水平进行了测定。沃纳综合征、早老症、科凯恩综合征、共济失调毛细血管扩张症、范可尼贫血和布卢姆综合征培养物在体外的短暂寿命与相当一部分热不稳定酶的出现相关。寿命较长的对照培养物在衰老之前含有低水平的改变酶。对热不稳定G6PD分子源自合成错误或其他原因的证据进行了严格评估。结果表明，在含有抗生素巴龙霉素的培养基中生长的正常细胞会产生相当一部分改变的G6PD，已知巴龙霉素会降低核糖体翻译的保真度。
