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Free radicals, uric acid, and human disease
Free Radical Biology
0891-5849(95)02155-8
ELSEVIER
+
& Medicine, Vol. 20, No. 5, pp. 761-762, 1996 Copyright 0 1996 Elsevier Science Inc. Printed in the USA. All rights reserved 0891-5849/96 $15.00 + .OO
Letters to the Editors FREE
RADICALS,
URIC
ACID,
Shamsi and Hadi ’ report that uric acid in the presence of copper oxidatively cleaves DNA. This reaction apparently involves superoxide and is augmented by light. There is an older literature supporting this work. For example, decades ago2 we reported that urate similarly promotes the free radical-mediated autooxidation of epinephrine. The possible role of transition-series metals in this reaction was suggested, but not examined. Nor was the radical species identified. This followed a still earlier suggestion that the reducing properties of uric acid might explain its physiological and evolutionary role-e.g., as a substitute for ascorbate,3 another “antioxidant,” which also has occasional prooxidant properties.
Peter H. Proctor 4126 SW Freeway, suite 1616 Houston, TX 77027, USA
We also noted2 that free radical mechanisms might figure in the etiology of such hyperuricemic syndromes as Gouty arthritis and the Lesch-Nyhan Syndrome. Similarly, because of common symptomology with other putative free radical diseases such as manganism, I furthur suggested a potential role for radical processes in other diseases such as, e.g., homocystinuria and alcaptonuria. Like the Lesch-Nyhan syndrome, such diseases are associated with the chronic presence of autooxidation-catalyzing charge-transfer agents. Thus, for example, the role of homocysteine-derived active oxygen species in homocystinuria and atherosclerotic disease was also recently independently rediscovered. Further, electronically activated mechanisms likely also explain certain aspects of the Hyperuricemic Syndrome in Dalmatian dogs.4,5 These include skin hyperpigmentation and “bronzing” as well as a clinical re-
TO THE LETTER
DISEASE
sponse to ectopic superoxide dismutase in its veterinary form 0rgotein4 These skin pigmentary changes were predicted’ on the basis that putative free radical diseases are often associated with skin pigmentation abnormalities, presumably secondary to some pigment-cell response to electronically activated species. They are particularly relevant to Shamsi and Hadi’s demonstration of the photoproduction of oxygen radicals in the presence of uric acid.’ Likewise, a response to SODase treatment implies a role for superoxide in this animal disease. This early work was followed up in several review articles.6’7 It is good to see that this question has now been revived.
To the Editors:
REPLY
AND HUMAN
REFERENCES
1. Shamsi, F. A.; Far&h, A.; Hadi, S. M. Photoinduction of strand scission in DNA by uric acid and Cu(I1). Free Radic. Biol. Med. 19(2):189-196; 1995. 2. Proctor, P. H. Electron-transfer factors in psychosis and dyskinesia. Physiol. Chem. Phys. 4:349-360; 1972. 3. Proctor, P. H. Similar functions of uric acid and ascorbate in man. Nature 228~868; 1970. 4. Lowrey, .I. C. An unusual diet-derived dernnatosis in dalmatian dogs responds to orgotein. Vet. Med. Small Anim. Clin. 71:289295; 1976.
5. Proctor, P. H.; McGinness, J. E.; Kirkpatrick, D. S. Superoxide dismutase therapy in hyperuricemic syndromes. Lancer ii:9596; 1978.
6. Proctor, P. H.; Reynolds, E. S. Free radicals and disease in man. Physiol. Chem. Phys. Med. NMR 1:175-195; 1984. 7. Proctor, P. H. Free radicals and human disease. In: Miguel, J.; et al., eds. CRC handbook of free radicals and antioxidants, vol. 1. Boca Raton, FL; CRC Press; 1989:209-221.
OF DR. PETER
To the Editor: We regret not having referred to Peter H. Proctor’s earlier work on uric acid. However, this was an over-
H. PROCTOR
sight possibly caused by the fact that our paper on uric acid-Cu (II) -mediated DNA damage evolves from our interest in DNA damage activities of natu-
761
0891-5849(95)02155-8
ELSEVIER
+
& Medicine, Vol. 20, No. 5, pp. 761-762, 1996 Copyright 0 1996 Elsevier Science Inc. Printed in the USA. All rights reserved 0891-5849/96 $15.00 + .OO
Letters to the Editors FREE
RADICALS,
URIC
ACID,
Shamsi and Hadi ’ report that uric acid in the presence of copper oxidatively cleaves DNA. This reaction apparently involves superoxide and is augmented by light. There is an older literature supporting this work. For example, decades ago2 we reported that urate similarly promotes the free radical-mediated autooxidation of epinephrine. The possible role of transition-series metals in this reaction was suggested, but not examined. Nor was the radical species identified. This followed a still earlier suggestion that the reducing properties of uric acid might explain its physiological and evolutionary role-e.g., as a substitute for ascorbate,3 another “antioxidant,” which also has occasional prooxidant properties.
Peter H. Proctor 4126 SW Freeway, suite 1616 Houston, TX 77027, USA
We also noted2 that free radical mechanisms might figure in the etiology of such hyperuricemic syndromes as Gouty arthritis and the Lesch-Nyhan Syndrome. Similarly, because of common symptomology with other putative free radical diseases such as manganism, I furthur suggested a potential role for radical processes in other diseases such as, e.g., homocystinuria and alcaptonuria. Like the Lesch-Nyhan syndrome, such diseases are associated with the chronic presence of autooxidation-catalyzing charge-transfer agents. Thus, for example, the role of homocysteine-derived active oxygen species in homocystinuria and atherosclerotic disease was also recently independently rediscovered. Further, electronically activated mechanisms likely also explain certain aspects of the Hyperuricemic Syndrome in Dalmatian dogs.4,5 These include skin hyperpigmentation and “bronzing” as well as a clinical re-
TO THE LETTER
DISEASE
sponse to ectopic superoxide dismutase in its veterinary form 0rgotein4 These skin pigmentary changes were predicted’ on the basis that putative free radical diseases are often associated with skin pigmentation abnormalities, presumably secondary to some pigment-cell response to electronically activated species. They are particularly relevant to Shamsi and Hadi’s demonstration of the photoproduction of oxygen radicals in the presence of uric acid.’ Likewise, a response to SODase treatment implies a role for superoxide in this animal disease. This early work was followed up in several review articles.6’7 It is good to see that this question has now been revived.
To the Editors:
REPLY
AND HUMAN
REFERENCES
1. Shamsi, F. A.; Far&h, A.; Hadi, S. M. Photoinduction of strand scission in DNA by uric acid and Cu(I1). Free Radic. Biol. Med. 19(2):189-196; 1995. 2. Proctor, P. H. Electron-transfer factors in psychosis and dyskinesia. Physiol. Chem. Phys. 4:349-360; 1972. 3. Proctor, P. H. Similar functions of uric acid and ascorbate in man. Nature 228~868; 1970. 4. Lowrey, .I. C. An unusual diet-derived dernnatosis in dalmatian dogs responds to orgotein. Vet. Med. Small Anim. Clin. 71:289295; 1976.
5. Proctor, P. H.; McGinness, J. E.; Kirkpatrick, D. S. Superoxide dismutase therapy in hyperuricemic syndromes. Lancer ii:9596; 1978.
6. Proctor, P. H.; Reynolds, E. S. Free radicals and disease in man. Physiol. Chem. Phys. Med. NMR 1:175-195; 1984. 7. Proctor, P. H. Free radicals and human disease. In: Miguel, J.; et al., eds. CRC handbook of free radicals and antioxidants, vol. 1. Boca Raton, FL; CRC Press; 1989:209-221.
OF DR. PETER
To the Editor: We regret not having referred to Peter H. Proctor’s earlier work on uric acid. However, this was an over-
H. PROCTOR
sight possibly caused by the fact that our paper on uric acid-Cu (II) -mediated DNA damage evolves from our interest in DNA damage activities of natu-
761