報(bào)告題目：硒在老化過(guò)程中的有益及悖論角色
報(bào) 告 人 ：鄭文興教授
報(bào)告時(shí)間：2018年6月28日下午16:00
報(bào)告地點(diǎn)：化學(xué)樓二樓一號(hào)會(huì)議室
邀 請(qǐng) 人 ：周軍教授
報(bào)告人簡(jiǎn)介：
鄭文興博士現(xiàn)任美國(guó)密西西比州立大學(xué)食品科學(xué)，營(yíng)養(yǎng)和健康促進(jìn)系副教授。主要研究方向是硒，腸道微生物群以及老化相關(guān)的失調(diào)等。鄭博士在過(guò)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(yīng)中的機(jī)制2）硒對(duì)癌癥，老化，糖尿病的影響。鄭博士在美國(guó)康奈爾大學(xué)獲得碩士及博士文憑。隨后在2001年至2007年間任美國(guó)國(guó)立衛(wèi)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(xué)的助理教授。鄭博士獲得過(guò)多項(xiàng)重要的研究獎(jiǎng)項(xiàng)，畢業(yè)了6.5名博士，先后在Aging Cell, PNAS, Nucleic Acids Research, Free Radical Biology and Medicine等國(guó)際一流雜志發(fā)表論文發(fā)表了80余篇同行評(píng)議論文和章節(jié)。現(xiàn)任營(yíng)養(yǎng)領(lǐng)域領(lǐng)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(bào)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.
