Autofluorescence as a noninvasive biomarker of senescence and advanced glycation end products in Caenorhabditis elegans.

IF 5.4 Q1 GERIATRICS & GERONTOLOGY NPJ Aging and Mechanisms of Disease Pub Date : 2021-06-07 DOI:10.1038/s41514-021-00061-y
Tomomi Komura, Mikihiro Yamanaka, Kohji Nishimura, Keita Hara, Yoshikazu Nishikawa
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Abstract

To assess the utility of autofluorescence as a noninvasive biomarker of senescence in Caenorhabditis elegans, we measured the autofluorescence of individual nematodes using spectrofluorometry. The fluorescence of each worm increased with age. Animals with lower fluorescence intensity exhibited longer life expectancy. When proteins extracted from worms were incubated with sugars, the fluorescence intensity and the concentration of advanced glycation end products (AGEs) increased over time. Ribose enhanced these changes not only in vitro but also in vivo. The glycation blocker rifampicin suppressed this rise in fluorescence. High-resolution mass spectrometry revealed that vitellogenins accumulated in old worms, and glycated vitellogenins emitted six-fold higher fluorescence than naive vitellogenins. The increase in fluorescence with ageing originates from glycated substances, and therefore could serve as a useful noninvasive biomarker of AGEs. C. elegans can serve as a new model to look for anti-AGE factors and to study the relationship between AGEs and senescence.

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自发荧光作为草履虫衰老和高级糖化终产物的非侵入性生物标记。
为了评估自发荧光作为线虫衰老的非侵入性生物标志物的实用性,我们使用分光荧光测定法测量了单个线虫的自发荧光。每条线虫的荧光随着年龄的增长而增加。荧光强度越低的线虫寿命越长。将从蠕虫体内提取的蛋白质与糖类一起培养,随着时间的推移,荧光强度和高级糖化终产物(AGEs)的浓度都会增加。核糖不仅在体外而且在体内都增强了这些变化。糖化阻滞剂利福平抑制了荧光的上升。高分辨率质谱分析表明,卵黄原蛋白在老蚕体内积累,糖化的卵黄原蛋白发出的荧光比未糖化的卵黄原蛋白高六倍。随着年龄的增长,荧光的增加源于糖化物质,因此可以作为 AGEs 的一种有用的非侵入性生物标志物。elegans 可以作为寻找抗衰老因子和研究 AGEs 与衰老之间关系的新模型。
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NPJ Aging and Mechanisms of Disease
NPJ Aging and Mechanisms of Disease Medicine-Geriatrics and Gerontology
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8 weeks
期刊介绍: npj Aging and Mechanisms of Disease is an online open access journal that provides a forum for the world’s most important research in the fields of aging and aging-related disease. The journal publishes papers from all relevant disciplines, encouraging those that shed light on the mechanisms behind aging and the associated diseases. The journal’s scope includes, but is not restricted to, the following areas (not listed in order of preference): • cellular and molecular mechanisms of aging and aging-related diseases • interventions to affect the process of aging and longevity • homeostatic regulation and aging • age-associated complications • translational research into prevention and treatment of aging-related diseases • mechanistic bases for epidemiological aspects of aging-related disease.
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