报告题目：硒在老化过程中的有益及悖论角色

报 告 人 ：郑文兴教授

报告时间：2018年6月28日下午16:00

报告地点：化学楼二楼一号会议室

邀 请 人 ：周军教授

报告人简介：

郑文兴博士现任美国密西西比州立大学食品科学，营养和健康促进系副教授。主要研究方向是硒，肠道微生物群以及老化相关的失调等。郑博士在过去十年的主要研究成果包括1）阐明了硒在肠道微生物群及DNA损伤反应中的机制2）硒对癌症，老化，糖尿病的影响。郑博士在美国康奈尔大学获得硕士及博士文凭。随后在2001年至2007年间任美国国立卫生研究院老化研究所的研究员，在2007年至2013年间任马里兰大学的助理教授。郑博士获得过多项重要的研究奖项，毕业了6.5名博士，先后在Aging Cell, PNAS, Nucleic Acids Research, Free Radical Biology and Medicine等国际一流杂志发表论文发表了80余篇同行评议论文和章节。现任营养领域领先期刊Journal of Nutrition及 Biological Trace Element and Research的编辑委员, 并且是Food Science & Nutrition 的副主编。

报告摘要：

Accumulation of genome and macromolecule damage is a hallmark of aging, age-associated degeneration, and genome instability syndromes. Although processes of aging are irreversible, they can be modulated by genome maintenance pathways and environmental factors such as diet. Selenium (Se) confers its physiological functions mainly through selenoproteins, but Se compounds and other proteins that incorporate Se nonspecifically also impact optimal health. Bruce Ames proposed that the aging process could be mitigated by a subset of low-hierarchy selenoproteins whose levels are preferentially reduced in response to Se deficiency. Consistent with this notion, results from two selenotranscriptomic studies collectively implicate three low-hierarchy selenoproteins in age or senescence. Experimental evidence generally supports beneficial roles of selenoproteins in the protection against damage accumulation and redox imbalance, but some selenoproteins have also been reported to unexpectedly display harmful functions under sporadic conditions. While longevity and healthspan are usually thought to be projected in parallel, emerging evidence suggests a trade-off between longevity promotion and healthspan deterioration with damage accumulation. We propose that longevity promotion under conditions of Se deficiency may be attributed to 1) stress-response hormesis, an advantageous event of resistance to toxic chemicals at low doses; 2) reduced expression of selenoproteins with paradoxical functions to a lesser extent. In particular, selenoprotein H is an evolutionally conserved nuclear selenoprotein postulated to confer Se functions in redox regulation, genome maintenance, and senescence. Altogether, there is a need to pinpoint roles of specific selenoproteins and Se compounds in healthspan and lifespan for a better understanding of Se contribution at nutritional levels of intake to healthy aging.