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Part I

SIDNEY LERMAN, M.D.

AMA Arch Ophthalmol. 1960;63(1):128-131.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Kalckar et al.^1,2 have recently succeeded in demonstrating the locus of the metabolic block which occurs in the red cell and liver of individuals suffering from congenital galactosemia. A similar block has been demonstrated in the lenses obtained from a child who died of this disease.³ In all these tissues there is a relative or absolute lack of the enzyme galactose-1-phosphate uridyl transferase with the subsequent accumulation of galactose-1-phosphate (Gal-l-P) in the red cell, liver,^1,2 and in the lens.⁴ This ester apparently accumulates to about ten times the level normally present in these tissues.^1,2,4 Since the metabolism of glucose provides the lens with its main source of energy, it seems likely that an accumulation of Gal-1-P within the lens may be the precipitating factor in the development of both the human and the experimental galactose cataract.

There are several possible loci where this ester could . . . [Full Text PDF of this Article]

Author Affiliations
Rochester, N.Y.

From the Department of Surgery, Division of Ophthalmology, The University of Rochester School of Medicine and Dentistry.

Footnotes
Submitted for publication July 8, 1959.

This investigation was supported by research funds granted by the Rochester Eye Bank and Research Society.

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