918 publications from this institution
standard is high.The main problem is that almost all the material in this book is already in the literature somewhere or other, and there is no attempt to report or summarize the discussions at the conference.The book is of some use because it is so comprehensive and reminds one who is doing what in the field, but I am one of the many scientists who question the point of publishing conference proceedings at all in book form. B. Halliwell
It seems that Superoxide dismutase plays the key role in protecting aerobes against O2 toxicity, but there is a whole range of ancillary mechanisms; enzymes to remove H202 (catalase, peroxidases) and hence to control formation of ·OH from 02, which requires H202; antioxidants (ascorbate, GSH, α-tocopherol, carotenoids), which also react with singlet oxygen and/or ·OH and often inhibit lipid peroxidation and last, but not least in animals, glutathione peroxidase, which controls the rate of lipid peroxidation. These mechanisms cope well at normal 02 concentrations but are insufficient at higher levels.
Abstract Statistical techniques have been developed and refined to help detect the causes of human disease. Since these techniques were first applied to infectious diseases, this medical discipline is called epidemiology, a term originally referring to its application to epidemic diseases such as smallpox, plague, and so on. Epidemiology attempts to relate the occurrence of disease in a given population to some common factor. Early examples include the relation of cholera to consumption of infected drinking water, and the association of some forms of lung cancer with cigarette smoking. Most epidemiological studies are either retrospective or prospective. In the former, patients with a particular disease are studied to identify aspects of their lifestyle that may be common to them all. By contrast, prospective studies examine a population and see what happens to the individuals with time. An example would be measuring the level of selenium in the blood of 5000 patients and then following them to see which developed cancer or heart disease.
Humans are exposed to many carcinogens, but the most significant may be the reactive species derived from metabolism of oxygen and nitrogen. Nitric oxide seems unlikely to damage DNA directly, but nitrous acid produces deamination and peroxynitrite leads to both deamination and nitration. Scavenging of reactive nitrogen species generated in the stomach may be an important role of flavonoids, flavonoids and other plant-derived phenolic compounds. Different reactive oxygen species produce different patterns of damage to DNA bases, e.g., such patterns have been used to implicate hydroxyl radical as the ultimate agent in H2O2-induced DNA damage. Levels of steady-state DNA damage in vivo are consistent with the concept that such damage is a major contributor to the age-related development of cancer and so such damage can be used as a biomarker to study the effects of diet or dietary supplements on risk of cancer development, provided that reliable assays are available. Methodological questions addressed in this article include the validity of measuring 8-hydroxydeoxyguanosine (8OHdG) in cellular DNA or in urine as a biomarker of DNA damage, the extent of artifact formation during analysis of oxidative DNA damage by gas chromatography-mass spectrometry and the levels of oxidative damage in mitochondrial DNA.
Conference Article| September 01 1973 The Role of Formate in Photorespiration BARRY HALLIWELL BARRY HALLIWELL 1Botany School, University of Oxford, South Parks Road, Oxford OX1 3RA, U.K. Search for other works by this author on: This Site PubMed Google Scholar Biochem Soc Trans (1973) 1 (5): 1147–1150. https://doi.org/10.1042/bst0011147 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation BARRY HALLIWELL; The Role of Formate in Photorespiration. Biochem Soc Trans 1 September 1973; 1 (5): 1147–1150. doi: https://doi.org/10.1042/bst0011147 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Society Transactions Search Advanced Search This content is only available as a PDF. © 1973 Biochemical Society1973 Article PDF first page preview Close Modal You do not currently have access to this content.
The term ‘antioxidant paradox’ is often used to refer to the observation that oxygen radicals and other reactive oxygen species are involved in several human diseases, but giving large doses of dietary antioxidant supplements to human subjects has, in most studies, demonstrated little or no preventative or therapeutic effect. Why should this be? First, the role of reactive oxygen species in the origin and/or progression of most human diseases is unclear, although they are probably important in cancer, neurodegenerative diseases and perhaps some others. Second, the endogenous antioxidant defences in the human body are complex, interlocking and carefully regulated. The body's ‘total antioxidant capacity’ seems unresponsive to high doses of dietary antioxidants, so that the amount of oxidative damage to key biomolecules is rarely changed. Indeed, manipulation of endogenous antioxidant levels (e.g. by supplying weak pro‐oxidants) may be a more useful approach to treatment and prevention of diseases in which reactive oxygen species are important than is consumption of large doses of dietary antioxidants.
Measurement of nitrotyrosine in biological fluids and tissues is increasingly being used to monitor the production of reactive nitrogen species in vivo. The detection of nitrotyrosine in vivo has been reported with the use of a variety of methods including immunoassay, HPLC and GLC/MS. The validity of HPLC and immunoassays have been questioned with regard to their selectivity and sensitivity limits. In principle, the measurement of nitrotyrosine by GLC/MS permits a highly specific, highly sensitive and fully quantitative assay. The nitration of tyrosine under acidic conditions in the presence of nitrite is well documented. Derivatization for the full quantification of nitrotyrosine by using GLC/MS can lead to the artifactual nitration of tyrosine if performed under acidic conditions in the presence of nitrite. We describe a novel alkaline method for the hydrolysis and derivatization of nitrotyrosine and tyrosine, and demonstrate its applicability to the measurement of plasma concentrations of both free and protein-bound nitrotyrosine and tyrosine. A detection limit of 1 pg for nitrotyrosine and 100 pg for tyrosine has been achieved. Our method allows, for the first time, the analysis of free and protein-bound nitrotyrosine and tyrosine in biological samples. The plasma concentrations (means+/-S.E.M.) of free tyrosine and nitrotyrosine in eight normal subjects were 12+/-0.6 microg/ml and 14+/-0.7 ng/ml respectively. Plasma proteins contained tyrosine and nitrotyrosine at 60.7+/-1.7 microg/mg and 2.7+/-0.4 ng/mg respectively.
Significance: During my long career in the field of redox biology, I met many inspiring people, especially Lester Packer. Recent Advances: This special issue of Antioxidants & Redox Signaling is dedicated to Lester Packer. Critical Issues: In this short review, I explore how Lester and other pioneers helped to develop the redox biology field and how I interacted with them. Future Directions: In our research to advance the field of redox biology, we stand on the shoulders of giants, including Lester Packer. Antioxid. Redox Signal. 38, 792–802.
THE mechanism of nigral cell death in Parkinson's disease (PD) remains unknown, but it is increasingly proposed that free radical reactions are important in the disease pathology. One of the most striking features of PD is an approximate 40% decrease in the levels of reduced glutathione (GSH) which occurs early in the development of the disease. We describe a possible mechanism of GSH depletion which results from the reaction of L-DOPA and dopamine with the superoxide free radical (O2-) and leads to a very rapid loss of GSH.
Potentially damaging species (reactive oxygen, nitrogen and chlorine species) arise as by-products of metabolism and as physiological mediators and signalling molecules. Levels of these species are controlled by the antioxidant defence system. Several components of this system are micronutrients (e.g. vitamins C and E) or are dependent upon dietary micronutrients (e.g. CuZn and Mn superoxide dismutase). The antioxidant defences act as a coordinated system where deficiencies in one component may affect the efficiency of the others. Oxidative stress may be an important factor in infection if micronutrients are deficient.
