کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
1910492 | 1046773 | 2008 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Oxidative stress and chronological aging in glycogen-phosphorylase-deleted yeast
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کلمات کلیدی
YPdpKaRT-PCRROS - ROSApoptosis - خزان یاختهایStandard error of measurement - خطای استاندارد اندازه گیریFree radicals - رادیکال آزادAging - سالخوردگیSaccharomyces cerevisiae - ساکارومایسس سرویزیهSOD - سدSuperoxide dismutase - سوکسوکس دیسموتازChronological life span - طول عمر طولانی مدتYeast extract peptone dextrose medium - عصاره گیاه پپتون دی کرتروزCarbohydrate metabolism - متابولیسم کربوهیدراتSEM - مدل معادلات ساختاری / میکروسکوپ الکترونی روبشیsynthetic complete medium - مصنوعی کامل رسانهwild type - نوع وحشیreverse transcription–polymerase chain reaction - واکنش زنجیره ای رونویسی-پلیمراز معکوسprotein kinase A - پروتئین کیناز AGlycogen phosphorylase - گلیکوژن فسفریلاسReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Chronological aging in yeast resembles aging in mammalian, postmitotic tissues. Such chronological aging begins with entrance into the stationary phase after the nutrients are exhausted. Many changes in metabolism take place at this moment, and survival in this phase strongly depends on oxidative-stress resistance. In this study, hypo- and hyperglycogenic phenotypes of Saccharomyces cerevisiae strains with deletions of carbohydrate-metabolism enzymes were selected, and a comparison of their chronological longevities was made. Stress sensitivity, ROS, and apoptosis markers during aging were analyzed in the emerged candidates. Among the strains that accumulated greater amounts of glycogen, the deletion of glycogen phosphorylase, gph1Î, was unique in showing a shortened life span, stress intolerance, and higher levels of ROS during its survival. The transcription of superoxide dismutase genes during survival was three- to fourfold lower in gph1Î. Extra copies of SOD1/2 counteracted the stress sensitivity and the accelerated aging of gph1Î. In conclusion, the lack of gph1 produced a rapidly aging strain, which could be attributed, at least in part, to the weakened stress resistance associated with the decreased expression of both SODs. Gph1p seems to be a candidate in a scenario that could link early metabolic changes with other targets of the stress response during stationary-phase survival.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 45, Issue 10, 15 November 2008, Pages 1446-1456
Journal: Free Radical Biology and Medicine - Volume 45, Issue 10, 15 November 2008, Pages 1446-1456
نویسندگان
Cristián Favre, Pablo S. Aguilar, MarÃa C. Carrillo,