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德纳姆哈曼（1916年2月14日- 2014年11月25号），医学博士，FACP，FAAA biogerontologist，是教授 名誉在内布拉斯加大学医学中心。[1] [2] [3]博士 哈曼被广泛称为“父亲的的自由基理论的老化”。[2] [3] [4]
出生在旧金山，[5]他获得了学士和博士学位 在1943年，从化学学院在加州大学伯克利分校和他的博士从斯坦福大学，完成他的实习于1954年。
随即他获得博士学位，1943年后，哈曼参加了反应动力学系壳牌石油公司在埃默里维尔，加利福尼亚州。他工作了6年的壳牌研究化学家，部分研究自由基反应的石油产品。在此期间，他获得了35 项专利，一个是在胶条用来杀人的化合物苍蝇（“壳牌无病虫害条”）。
哈曼迷上的现象老龄化，其原因和可能的治疗。为了帮助他了解这个问题，他去医学院在斯坦福大学。哈曼成为了椅子的心血管研究在医学内布拉斯加大学大学于1958年。
哈曼嫁给了同一个女人大多数他的生活，一个新闻学生的人，他 ??在会见联谊会舞蹈，而在加州大学。夫妇有四个孩子和四个孙辈。哈曼保持健康的生活方式，在他的生活。他从不抽烟和饮酒要适量。他跑两英里一天，直到他是82，他辞职是因为背伤，但他继续采取定期散步，以帮助他保持140磅重，他身高5英尺10帧。
哈曼死在内布拉斯加州奥马哈市，于2014年11月25日，从短的疾病，年龄在98 [6]
1954年，他的实习和居住在内科，哈曼成为了一个研究助理的唐纳实验室医学物理在加州大学伯克利分校，[2] 在那里他能够追求的拼图老化的原因。经过四个月的挫折，他想出的主意自由基，以被称为“大分子造成损坏的原因老化 ”。虽然最初其他科学 ??家不愿意接受他的理论，他终于能够把它发表在什么现在是一个广为引用的文章老年学杂志。[7]
哈曼试图检测自由基与联想酶的 过氧化氢 ??酶，但没有成功。他试图做寿命研究与短命菌株的小鼠受到辐射和给定的辐射防护化合物2-MEA（2-巯基乙胺 ），并且是能够显示在增加了30％的平均寿命。他能够显示出延长寿命与许多抗氧化剂。
1961年，哈曼发表的一项研究显示，程度多不饱和脂肪对产生巨大影响的癌症率在老鼠。最高度多不饱和脂肪的饮食被发现是最致癌。
1968年，哈曼发表了一份饮食抗氧化剂研究报告显示，食品防腐剂BHT喂过一辈子给小鼠产生寿命增加了45％。哈曼成为了关注的是，尽管他的许多研究显示增加平均寿命抗氧化剂，没有显示增加最长寿命。
经过多年的挫折在他无法增加与抗氧化补充剂最大寿命，哈曼来到该结论线粒体受损的自由基被生产以及，但外源性抗氧化剂，不进入线粒体。而且，这是线粒体确定寿命。他发表了关于他所谓的“他的想法衰老的线粒体理论在1972年4月出版的美国老年医学会杂志上。”[2] [8]
1969年，哈曼成为了关注的是，一些参与的老年学是研究生物的各个方面老化，少仍然在发现老龄事业的严重关注。1970年，他成为了一个创始人美国老化协会（AGE）创建的科学家的社会专注于老龄化研究和宣传老龄化研究。1985年，他成为了创办生物医学老年学协会（IABG）。
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Denham Harman (February 14, 1916 – November 25, 2014), MD, PhD, FACP, FAAA biogerontologist, was Professor emeritus at the University of Nebraska Medical Center.[1][2][3] Dr. Harman is widely known as the "father of the free radical theory ofaging".[2][3][4]
Born in San Francisco,[5] he earned his BS and Ph.D. in 1943 from the College of Chemistry at the University of California, Berkeley and his M.D. from Stanford University, finishing his internship in 1954.
Immediately after earning his Ph.D., in 1943, Harman joined the reaction kineticsdepartment of Shell Oil in Emeryville, California. He worked for six years as a Shell research chemist, in part studying free radical reactions in petroleum products. During that period he was granted 35 patents, one for a compound used in plastic strips to killflies ("Shell No Pest Strip").
Harman became fascinated with the phenomenon of aging, its cause and possible cure. To assist him in understanding this problem, he went to medical school at Stanford University. Harman became chair of cardiovascular research at the University of Nebraska College of Medicine in 1958.
Harman was married to the same woman for most of his life, a journalism student whom he met at a fraternity dance while at the University of California. The couple had four children and four grandchildren. Harman maintained a healthy lifestyle throughout his life. He neversmoked and drank alcohol in moderation. He ran two miles a day until he was 82. He quit because of a back injury, but he continued to take regular walks to help him maintain a weight of 140 pounds on his 5-foot-10 frame.
Harman died in Omaha, Nebraska, on November 25, 2014, from a short illness, aged 98.[6]
In 1954, between his internship and residency in internal medicine, Harman became a research associate at the Donner Laboratory of Medical Physics at UC Berkeley,[2] where he was able to pursue the puzzle of the cause of aging. After four months of frustration he hit upon the idea of free radicals as cause of the damage to macromolecules known as "aging". Although initially other scientists were reluctant to accept his theory, he was finally able to get it published in what is now a much-cited article in the Journal of Gerontology.[7]
Harman attempted to detect free radicals in association with the enzyme catalase, but without success. He attempted to do life span studies with short-lived strains of micesubject to radiation and given the radiation protection compound 2-MEA (2-mercaptoethylamine), and was able to show a 30% increase in average life expectancy. He was able to show extension of life expectancy with a number of antioxidants.
In 1961, Harman published a study showing that the degree of polyunsaturation in fats had a dramatic effect on cancer rates in mice. The most highly polyunsaturated dietary fats were found to be the most carcinogenic.
In 1968 Harman published a dietary antioxidant study showing that the food preservative BHTfed over a lifetime to mice produced a 45% increase in life span. Harman became concerned that although many of his studies showed an increase in average lifespan by antioxidants, none showed an increase in maximum life span.
After years of frustration over his inability to increase maximum lifespan with antioxidant supplements, Harman came to the conclusion that mitochondria were producing as well as being damaged by free radicals, but that exogenous antioxidants don‘t enter the mitochondria. And that it is mitochondria that determine lifespan. He published his ideas on what he called the "mitochondrial theory of aging" in the April 1972 issue of the Journal of the American Geriatrics Society.[2][8]
In 1969 Harman became concerned that few of those involved in gerontology were studying thebiological aspects of aging, and fewer still had a serious interest in discovering the cause of aging. In 1970 he became a founder of the American Aging Association (AGE) to create a society of scientists focused on aging research and advocacy of aging research. In 1985 he became a founder of the International Association of Biomedical Gerontology(IABG).[2]
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原文地址：http://www.cnblogs.com/biopy/p/4793752.html
