Retroviruses, Ascorbate, and Mutations, in the Evolution of Homo sapiens
- UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
- Ethan W Taylor, Senior Research Professor (Creator)
- Institution
- The University of North Carolina at Greensboro (UNCG )
- Web Site: http://library.uncg.edu/
Abstract: Mutations, induced by free radicals, provide a rich molecular palette that other evolutionary forces can select for or against. A recent hypothesis proposed that large numbers of free radicals were produced when, millions of years ago, Anthropoidea lost the ability to produce endogenous ascorbate, increasing the frequency of mutations and accelerating the evolution of higher primates. Recognizing that retroviruses have been active throughout the period of primate evolution, we suggest that an endogenous retrovirus or other retroviral-like element may have been involved in mutating the gene coding for gulonolactone oxidase (GLO), the terminal step in ascorbate synthesis, approximately 45 million years ago. This possibility is supported by the presence of Alu elements (a common primate retroelement) adjacent to the site of a missing segment of the nonfunctional GLO gene. Although Homo sapiens and other higher primates produce other endogenous antioxidants, including superoxide dismutase and uric acid, they do not quench the same radicals as ascorbate and cannot fully compensate for a lack of endogenous ascorbate. As a consequence, a retrovirus may have played a pivotal role in primate and H. sapiens evolution, and the absence of endogenous ascorbate may be continuing to accelerate the rate of H. sapiens and primate evolution.
Retroviruses, Ascorbate, and Mutations, in the Evolution of Homo sapiens
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Additional Information
- Publication
- Free Radical Biology and Medicine. Volume 25, Issue 1, 1 July 1998, Pages 130-132. https://doi.org/10.1016/S0891-5849(98)00034-3
- Language: English
- Date: 1998
- Keywords
- Ascorbate, Vitamin C, Free radicals, Evolution, Endogenous retroviruses, Gulonolactone oxidase, Alu, Reverse transcriptase