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• W1982354125 abstract "Ever since cystinuria was first attributed to a renal and intestinal absorption defect, investigators have focused their research on determining the nature of membrane transport interactions between the amino acids involved. To that end, data were collected from experiments with humans, animal models, and the so-called cycloleucine model of cystinuria. In vivo and in vivo studies of the human disease helped define its genetic characteristics. Animal models found in nature show species particularities. For example, contrary to the human ailment, canine cystinuria is found only in the male population and cystinuric genets excrete excessive amounts of cystine without stone formation. Observation of the cycloleucine model, reproduced experimentally by intraperitoneal injections of this drug to rats, has led to the following conclusions: the transport defect results from a combination of influx inhibitions and efflux stimulations of one dibasic amino acid by another in renal and intestinal cells; the importance of cystine stems from the fact that both its influx and efflux across renal peritubular membranes are impaired by dibasic amino acids and cycloleucine; this double inhibition of cystine transport may be responsible for creating, in the experimental disease, a retrograde flow of intracellular cysteine toward the tubular lumen. Cystine leakage into tubular fluid is thought to occur in human cystinuria as a result of intracellular build-up of this amino acid secondary to its abnormal reentry from peritubular blood. Therefore, although the transport defects lead to similar manifestations in human and experimental diseases, the mechanisms may differ. Such fundamental differences together with others pertaining to genetics and side effects of cycloleucine make the experimental model a less than adequate representative of human cystinuria. Studies of the disease in its natural state remain the only means of describing its generic aspects. Nevertheless, the use of this experimental model coupled with new techniques in the field of membrane biology, and biophysical studies of amino acids and their synthetic analogs may become necessary to unveil the nature of transport defects in cystinuria and other aminoacidurias." @default.
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• W1982354125 date "1966-04-01" @default.
• W1982354125 modified "2023-10-15" @default.
• W1982354125 title "A common renal transport system for lysine, ornithine, arginine and cysteine" @default.
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• W1982354125 doi "https://doi.org/10.1016/0006-291x(66)90531-6" @default.
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