報告題目：硒在老化過程中的有益及悖論角色
報 告 人 ：鄭文興教授
報告時間：2018年6月28日下午16:00
報告地點：化學樓二樓一號會議室
邀 請 人 ：周軍教授
報告人簡介：
鄭文興博士現任美國密西西比州立大學食品科學，營養和健康促進系副教授。主要研究方向是硒，腸道微生物群以及老化相關的失調等。鄭博士在過去十年的主要研究成果包括1）闡明了硒在腸道微生物群及DNA損傷反應中的機制2）硒對癌癥，老化，糖尿病的影響。鄭博士在美國康奈爾大學獲得碩士及博士文憑。隨后在2001年至2007年間任美國國立衛生研究院老化研究所的研究員，在2007年至2013年間任馬里蘭大學的助理教授。鄭博士獲得過多項重要的研究獎項，畢業了6.5名博士，先后在Aging Cell, PNAS, Nucleic Acids Research, Free Radical Biology and Medicine等國際一流雜志發表論文發表了80余篇同行評議論文和章節。現任營養領域領先期刊Journal of Nutrition及 Biological Trace Element and Research的編輯委員, 并且是Food Science & Nutrition 的副主編。
報告摘要：
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.
