自由基是造成老化和疾病的元兇?
你認為損害健康的物質可能是真正使你長壽的秘密
MyHealth Biosystems INC.翻譯
許多從事醫療與健康的專業人員都相信，人體在氧代謝過程中，所產生出的自由基是損害細胞、導致老化的元兇。然而，近來的許多關於自由基的研究文獻結果，可能要徹底顛覆這個理論了。
加拿大 McGill大學的研究人員於蛔蟲Caenorhabditis elegans的研究中發現，自由基（如氧化物）會促使細胞凋亡，並意外地延長生物壽命。
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| Image: Caenorhabditis elegans 線蟲 圖片來源McGill大學 |
細胞凋亡是損傷的細胞實施特定程序性地自殺計畫，以避免自體免疫疾病、避免細胞癌化，或是清除被病毒感染的細胞之自我防衛措施。這個分子調控機制在生物體內一向受到很完整的保藏與調控，直到在C. elegans蛔蟲內被發現。
加拿大 McGill大學的研究學者發現藉由自由基刺激細胞凋亡機制，可強化細胞的免疫力並增加其壽命。這個重大發現於2014年5月8日發表在國際知名期刊『細胞』期刊中。「一般人相信自由基會是有危害性的並導致老化，但自由基導致老化的理論是錯誤的。」 McGill大學生物學院的教授Siegfried Hekimi說，「實驗證實自由基事實上是與老化對抗，而非導致老化，所以在老化的過程中自由基會增加。在我們動物研究中，發現提高自由基的製造可顯著地延長壽命。」
這項發現是一顯著的轉淚點，「顯示自由基在實際的分子機制裡是具由延長壽命、正面影響的分子訊號」Hekimi教授說，「這同時也表示細胞凋亡的分子調控可以被用於延緩老化。細胞凋亡於人體免疫疾病及癌症疾病中都扮演很重要的角色，因此其在人體運作的機制已被深入研究探討，並廣泛地應用於藥理學中，但這不表示這是一條輕鬆簡單的路。」
Hekimi教授同時表示，誘發可延長壽命的細胞凋亡訊號應用於神經性退化疾病的治療需要特別嚴苛的處理方式。「比起其他種類的凋亡細胞，凋亡的神經細胞由於神經元連結的複雜性可能更難以被取代。因此，在大腦的細胞凋亡訊號調控中，可能較傾向於增加受損細胞對壓力的抵抗，而非誘發細胞凋亡。」
原文文章如下：
Unanticipated Link Found Between Cell Suicide and Long Life
By BiotechDaily International staff writersPosted on 28 May 2014
Many health professionals believe that free radicals, the occasionally toxic molecules generated by the body as it processes oxygen, are the cause behind aging. However, a number of studies recently have generated evidence that the contrary may be true.
Researchers from McGill University (Montreal, QC, Canada) have taken this finding further by showing how free radicals promote longevity in a research model organism, the roundworm Caenorhabditis elegans. Unexpectedly, the scientists discovered that free radicals (i.e., oxidants) act on a molecular mechanism that, in other surroundings, instructs a cell to kill itself.
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| Image: Caenorhabditis elegans nematode (roundworm) (Photo courtesy of McGill University). |
Apoptosis is a process by which injured cells commit suicide in a range of circumstances: to avoid inducing autoimmune disease, to avoid becoming cancerous, or to kill off viruses that have invaded the cell. The key molecular mechanism by which this occurs is well conserved in all animals, but was first discovered in C. elegans—a finding that earned a Nobel Prize.
The McGill University researchers discovered that this same mechanism, when stimulated in the correct manner by free radicals, in reality strengthens the cell’s defenses and increases its longevity. Their findings were published online May 8, 2014, in the journal Cell. “People believe that free radicals are damaging and cause aging, but the so-called ‘free radical theory of aging’ is incorrect,” said Siegfried Hekimi, a professor in McGill’s department of biology, and senior author of the study. “We have turned this theory on its head by proving that free radical production increases during aging because free radicals actually combat—not cause—aging. In fact, in our model organism we can elevate free radical generation and thus induce a substantially longer life.”
The findings have significant ramifications. “Showing the actual molecular mechanisms by which free radicals can have a pro-longevity effect provides strong new evidence of their beneficial effects as signaling molecules,” Prof. Hekimi said. “It also means that apoptosis signaling can be used to stimulate mechanisms that slow down aging. Since the mechanism of apoptosis has been extensively studied in people, because of its medical importance in immunity and in cancer, a lot of pharmacological tools already exist to manipulate apoptotic signaling. But that doesn’t mean it will be easy.”
Triggering pro-longevity apoptotic signaling could be especially critical in neurodegenerative disorders, according to Prof. Hekimi. “In the brain the apoptotic signaling might be particularly tilted toward increasing the stress resistance of damaged cells rather than killing them. That’s because it is harder to replace dead neurons than other kinds of cells, partly because of the complexity of the connections between neurons.”
