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Karl Gaede (1913–1980)
TIBS - September 1980
Neuropathy Monekosso and Wilson TM studied tropical ataxic syndrome in Nigerian patients from an area where cassava is eaten and they found that plasma thiocyanate concentrations were elevated. Osuntokun u reported tropical ataxie neuropathy in Western Nigeria and from an epidemiological study discovered that this condition is found in people who consume large amounts of cassava. The suggestion has been made that this neuropathy is caused by chronic ingestion of cyanide from cassava. In effect this suggestion is in agreement with, the first theory advanced by Moore TM and Clark x3 that amblyopia (dimness of vision caused by the action of noxious agents on the optic nerve) in West Africa may be a manifestation of chronic cassava poisoning. Studies of the myelin of the brains of rats exposed to small doses of cyanide ~4 demonstrated that the principal effect of these neuropathological changes is demyelination. Although the chemical composition of the brain is relatively constant, it is affected by dietary deficiencies during the early periods of growth and development. We have studied the effect of cassava feeding on rat brain cerebrosides and sphingomyelin xS. Two groups of rats were fed for four weeks on a standard diet with and without cassava and the analysis of brain cerebrosides and sphingomyelin showed lower concentrations in the cassava-fed rats than in the control rats ~5. Histological examination of the brains of the rats demonstrated degenerative changes in the brain cells. This was indicated by large numbers of mitochondrialike bodies in the nerve cells of the brain. Odutuga has also reported a lower proportion of cerebrosides and sphingomyelin in rats deficient in essential fatty acids TM. It appears that a decrease in the proportion of the two myelin lipids is one of the early steps in demyelination caused by cassava toxicity. In discussing cassava toxicity it is necessary to realize that the toxic effects of cyanide are probably not due to the cyanide ion but to its detoxification product, thiocyanate. The rhodanasemediated conversion of cyanide into thiocyanate is the main detoxification process of cyanide, and people who have cyanide in the diet produce increasing amounts of the enzyme rhodanase. The sulphur required for the conversion of cyanide into thiocyanate comes from the sulphur-containing amino acids. It has been suggested that the thiocyanate may be carried by cobalamin in the blood in a sul-
XI
phur transfer cyclexT. It is also pertinent to realize that in the estimation of cyanide in the tissues, thiocyanate may be included. The colorimetrie method depends on the bromination of either cyanide or thiocyanate and does not distinguish between the two. Furthermore estimation of thiocyanate either in the blood or urine does not give a simple index o f the amount of cyanide ingested. This is because there are other metabolic pathways for thiocyanate. There is a large thiocyanate metabolic pool in the body which varies with the dietary intake of preformed thiocyanate. It is also known that thiocyanate is present in considerable, but variable, amounts in green vegetables and milk. References 1 Seigler,D. S. (1975)Phytochemistry 14, 9 2 Ekpechi, O. L., Dimitriadou, A. and Fraser, R. (1966) Nature (London) 210, 1137 3 Osuntokun, B. O. (1971) Trans. R. Soc. Trop. Med. Hyg. 65,454
4 Adams, C. W. M., Fernand, V. S. V. and Schnieden, H. (1958) Br. L Exp. Path. 39, 393 5 Ononogbu, I. C. and Emole, I. (1978) Atherosclerosis 31,101 6 Uwaeziozi, A. B. (1978) B.Sc. Thesis, University of Nigeria, Nsukka 7 Coursey, D. G. and Haynes, P. H. (1970) World Crops July/Aug, 261-265 8 Rees, K. R. (1964) in Metabolism and Physiological Significance of Lipids (Dawson, R. M. C. and Rhodes, D. N. eds), p. 447, John Wiley, London 9 Nwosu, A. I. (1979) B.Sc. Thesis, University of Nigeria, Nsukka l0 Monekosso, G. L. and Wilson,J. (1966) Lancet i, 1062 11 Osuntokun, B. O.(1968)Brain 91,215 12 Moore, D. G. F. (1934)Ann. Trop. Med. ParasitoL 28, 295 13 Clark, A. (1936) L Trop. bled. Hyg. 39, 269 14 Smith, A. D. M., Duckett, S. and Waters, A. H. (1963)Nature (London) 200, 179 15 Ilouno, L. C. (1979) B.Sc. Thesis, University of Nigeria, Nsukka 16 Odutuga, A. A. (1979) Biochim. Biophys. Acta 487, 1 17 Wokes, F. and Picard, C. W. (1955)Am. J. Clin. Nutr. 3,383
Obituary Karl Gaede (1913-1980) Karl August Ernst Gaede Jaekel, Professor and Head of the Department of Biochemistry at the Instituto Venezolano de Investigaciones Cientificas (IVIC), died on 8 April, 1980. Karl Gaede was well known to biochemists in the Americas for his enthusiastic support of the proposal to found the Pan-American Association of Biochemical Societies (PAABS). He acted as its unofficial chairman during 1969 until PAABS came into official existence in 1970 and gave PAABS its first major visibility by organizing the first Congress, held in Caracas in 1971. At the same time he was the founder and first President of the Asociacion Venezolana de Bioquimica, a charter member of PAABS, and now also the Adhering Body to the IUB from Venezuela. Karl Gaede was born in Gltickstadt, Germany on 11 January, 1913 and obtained his Dr Med. qualification from the University of Hamburg in 1948. He published pioneering papers on glucagon and its role in regulating carbohydrate metabolism as an insulin antagonist (e.g. Klin. Wochenschr. (1950) 28, 388). He emigrated to Venezuela in 1955, became a Venezuelan citizen and from 1958 to his death held his post at IVIC.
Karl Gaede
Biochemical teaching and research in Venezuela was almost non-existent until Karl Gaede's arrival. Now it is flourishing, thanks to his efforts, and Venezuelan biochemists are solidly integrated into international activities. Karl Gaede's pioneering activities within and without Venezuela laid the cornerstone of these achievements. RAFAEL APITZ-CASTRO (IVIC) WILLIAM J. WHELAN (IUB)
Neuropathy Monekosso and Wilson TM studied tropical ataxic syndrome in Nigerian patients from an area where cassava is eaten and they found that plasma thiocyanate concentrations were elevated. Osuntokun u reported tropical ataxie neuropathy in Western Nigeria and from an epidemiological study discovered that this condition is found in people who consume large amounts of cassava. The suggestion has been made that this neuropathy is caused by chronic ingestion of cyanide from cassava. In effect this suggestion is in agreement with, the first theory advanced by Moore TM and Clark x3 that amblyopia (dimness of vision caused by the action of noxious agents on the optic nerve) in West Africa may be a manifestation of chronic cassava poisoning. Studies of the myelin of the brains of rats exposed to small doses of cyanide ~4 demonstrated that the principal effect of these neuropathological changes is demyelination. Although the chemical composition of the brain is relatively constant, it is affected by dietary deficiencies during the early periods of growth and development. We have studied the effect of cassava feeding on rat brain cerebrosides and sphingomyelin xS. Two groups of rats were fed for four weeks on a standard diet with and without cassava and the analysis of brain cerebrosides and sphingomyelin showed lower concentrations in the cassava-fed rats than in the control rats ~5. Histological examination of the brains of the rats demonstrated degenerative changes in the brain cells. This was indicated by large numbers of mitochondrialike bodies in the nerve cells of the brain. Odutuga has also reported a lower proportion of cerebrosides and sphingomyelin in rats deficient in essential fatty acids TM. It appears that a decrease in the proportion of the two myelin lipids is one of the early steps in demyelination caused by cassava toxicity. In discussing cassava toxicity it is necessary to realize that the toxic effects of cyanide are probably not due to the cyanide ion but to its detoxification product, thiocyanate. The rhodanasemediated conversion of cyanide into thiocyanate is the main detoxification process of cyanide, and people who have cyanide in the diet produce increasing amounts of the enzyme rhodanase. The sulphur required for the conversion of cyanide into thiocyanate comes from the sulphur-containing amino acids. It has been suggested that the thiocyanate may be carried by cobalamin in the blood in a sul-
XI
phur transfer cyclexT. It is also pertinent to realize that in the estimation of cyanide in the tissues, thiocyanate may be included. The colorimetrie method depends on the bromination of either cyanide or thiocyanate and does not distinguish between the two. Furthermore estimation of thiocyanate either in the blood or urine does not give a simple index o f the amount of cyanide ingested. This is because there are other metabolic pathways for thiocyanate. There is a large thiocyanate metabolic pool in the body which varies with the dietary intake of preformed thiocyanate. It is also known that thiocyanate is present in considerable, but variable, amounts in green vegetables and milk. References 1 Seigler,D. S. (1975)Phytochemistry 14, 9 2 Ekpechi, O. L., Dimitriadou, A. and Fraser, R. (1966) Nature (London) 210, 1137 3 Osuntokun, B. O. (1971) Trans. R. Soc. Trop. Med. Hyg. 65,454
4 Adams, C. W. M., Fernand, V. S. V. and Schnieden, H. (1958) Br. L Exp. Path. 39, 393 5 Ononogbu, I. C. and Emole, I. (1978) Atherosclerosis 31,101 6 Uwaeziozi, A. B. (1978) B.Sc. Thesis, University of Nigeria, Nsukka 7 Coursey, D. G. and Haynes, P. H. (1970) World Crops July/Aug, 261-265 8 Rees, K. R. (1964) in Metabolism and Physiological Significance of Lipids (Dawson, R. M. C. and Rhodes, D. N. eds), p. 447, John Wiley, London 9 Nwosu, A. I. (1979) B.Sc. Thesis, University of Nigeria, Nsukka l0 Monekosso, G. L. and Wilson,J. (1966) Lancet i, 1062 11 Osuntokun, B. O.(1968)Brain 91,215 12 Moore, D. G. F. (1934)Ann. Trop. Med. ParasitoL 28, 295 13 Clark, A. (1936) L Trop. bled. Hyg. 39, 269 14 Smith, A. D. M., Duckett, S. and Waters, A. H. (1963)Nature (London) 200, 179 15 Ilouno, L. C. (1979) B.Sc. Thesis, University of Nigeria, Nsukka 16 Odutuga, A. A. (1979) Biochim. Biophys. Acta 487, 1 17 Wokes, F. and Picard, C. W. (1955)Am. J. Clin. Nutr. 3,383
Obituary Karl Gaede (1913-1980) Karl August Ernst Gaede Jaekel, Professor and Head of the Department of Biochemistry at the Instituto Venezolano de Investigaciones Cientificas (IVIC), died on 8 April, 1980. Karl Gaede was well known to biochemists in the Americas for his enthusiastic support of the proposal to found the Pan-American Association of Biochemical Societies (PAABS). He acted as its unofficial chairman during 1969 until PAABS came into official existence in 1970 and gave PAABS its first major visibility by organizing the first Congress, held in Caracas in 1971. At the same time he was the founder and first President of the Asociacion Venezolana de Bioquimica, a charter member of PAABS, and now also the Adhering Body to the IUB from Venezuela. Karl Gaede was born in Gltickstadt, Germany on 11 January, 1913 and obtained his Dr Med. qualification from the University of Hamburg in 1948. He published pioneering papers on glucagon and its role in regulating carbohydrate metabolism as an insulin antagonist (e.g. Klin. Wochenschr. (1950) 28, 388). He emigrated to Venezuela in 1955, became a Venezuelan citizen and from 1958 to his death held his post at IVIC.
Karl Gaede
Biochemical teaching and research in Venezuela was almost non-existent until Karl Gaede's arrival. Now it is flourishing, thanks to his efforts, and Venezuelan biochemists are solidly integrated into international activities. Karl Gaede's pioneering activities within and without Venezuela laid the cornerstone of these achievements. RAFAEL APITZ-CASTRO (IVIC) WILLIAM J. WHELAN (IUB)