Oxidative damage and cellular defense mechanisms in sea urchin models of aging.

Oxidative damage and cellular defense mechanisms in sea urchin models of aging.
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DOI:
10.1016/j.freeradbiomed.2013.05.023
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发表时间:
2013-10
影响因子:
7.4
通讯作者:
Bodnar, Andrea
Bodnar, Andrea
中科院分区:
医学1区
文献类型:
--
作者:
Du, Colin;Anderson, Arielle;Lortie, Mae;Parsons, Rachel;Bodnar, Andrea

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衰老的自由基或氧化应激理论提出,氧化细胞损伤的积累是衰老过程的主要贡献者,也是物种寿命的关键决定因素。本研究探讨了氧化应激理论在一个新的模型老化研究,海胆。海胆为研究衰老提供了一个独特的模型,因为存在着自然寿命差异巨大的物种,包括一些具有非凡寿命和可忽略衰老的物种。细胞氧化损伤,抗氧化能力和蛋白酶体酶的活性进行了测量,在三个海胆物种的组织:短寿命的Lytechinus variegatus,长寿的Strongylocentrotus franciscanus和Strongylocentrotus purpuratus,具有中间寿命。在组织(肌肉、神经、食管、性腺、体腔细胞、壶腹)中测量的蛋白质羰基和4-羟基壬烯醛(HNE)水平以及在无细胞体腔液中测量的8-羟基-2 '-脱氧鸟苷(8-OHdG)水平未显示出随年龄的普遍增加。在肌肉、神经和食管中测得的荧光年龄色素脂褐素随年龄增加而增加,但似乎主要是细胞外的。抗氧化机制(总抗氧化能力,超氧化物歧化酶)和蛋白酶体酶活性保持与年龄。在某些情况下,与短寿命物种相比,长寿物种的细胞或组织中的氧化损伤水平较低,抗氧化活性较高,但需要进一步研究以确定这些动物中氧化损伤与寿命之间的关系。与衰老的氧化应激理论的预测相一致,结果表明,可忽略的衰老是伴随着缺乏积累的细胞氧化损伤与年龄和维护的抗氧化能力和蛋白酶体酶的活性可能是重要的机制,以减轻损害。
The free radical or oxidative stress theory of aging proposes that the accumulation of oxidative cellular damage is a major contributor to the aging process and a key determinant of species longevity. This study investigates the oxidative stress theory in a novel model for aging research, the sea urchin. Sea urchins present a unique model for the study of aging due to the existence of species with tremendously different natural life spans including some species with extraordinary longevity and negligible senescence. Cellular oxidative damage, antioxidant capacity and proteasome enzyme activities were measured in the tissues of three sea urchin species: short-lived Lytechinus variegatus, long-lived Strongylocentrotus franciscanus and Strongylocentrotus purpuratus which has an intermediate lifespan. Levels of protein carbonyls and 4-hydroxynonenal (HNE) measured in tissues (muscle, nerve, esophagus, gonad, coelomocytes, ampullae) and 8-hydroxy-2’-deoxyguanosine (8-OHdG) measured in cell-free coelomic fluid showed no general increase with age. The fluorescent age-pigment lipofuscin measured in muscle, nerve and esophagus, increased with age however it appeared to be predominantly extracellular. Antioxidant mechanisms (total antioxidant capacity, superoxide dismutase) and proteasome enzyme activities were maintained with age. In some instances, levels of oxidative damage were lower and antioxidant activity higher in cells or tissues of the long-lived species compared to the short-lived species, however further studies are required to determine the relationship between oxidative damage and longevity in these animals. Consistent with the predictions of the oxidative stress theory of aging, the results suggest that negligible senescence is accompanied by a lack of accumulation of cellular oxidative damage with age and maintenance of antioxidant capacity and proteasome enzyme activities may be important mechanisms to mitigate damage.
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