GALACTOSE 661 



effect of iilkali (KOII) is to form a salt, C^IIj — OK (or l\-incthylatc), wliicli heing 

 highly dissociable breaks down to give CHj and i\()H. The proportion of free 



II 

 methylene is therel)y enormously increased. What then befalls the methylene 

 will depend on the amount of oxygen i)resent and on the various other factors 

 which enter into the conditions of the experiment. These general principles arc 

 applicable directly to the polyatomic alcohols— the hexo.ses and other sugars — as 

 shown on prcccdinp; page. 



In the presence of sufHcient oxygen the methylene particle takes on oxygen 

 to form first an osone. In the alisence of oxygen it undergoes intramolecular 

 rearrangements, the details of which need not here l)e entered into. It is these 

 which gives rise to the (j-carbon acids known as the saccharines or saccliarinic 

 acids. 



GALACTOSE 



A normal individual weighing 75 kilos may eat about 50 grams of 

 galactose and show but a trace of melituria. More than this is likely 

 to cause the presence of measurable amounts of galactose in the 

 urine, the alimentary tolerance lintit for this sugar being therefore 

 about 0.6 to 0.8 grams per kilogram of body weight. We have no 

 direct data concerning the time within which 50 grams of galactose 

 are absorbed by a man of average weight. When given intravenously 

 at uniform rates, unchanged galactose appears in the urine of dogs 

 receiving slightly more than 0.1 per kilo per hour. The tolerance 

 for galactose appears to be lessened in phosphorus poisoning and in 

 many other conditions which cause apparent parenchj^matous changes 

 in the liver, so that after administration of 50 grams of gakictose by 

 mouth, as much as 10 to 12 grams may be excreted in the urine 

 (Bauer). On the other hand, ligation of the common duct does not 

 lessen the tolerance for galactose in rabbits (Reiss and Jehn, Hierose) 

 so that the lowered tolerance following phosphorus administration ap- 

 pears to be independent of the disturbed biliary function. Infants- 

 suffering from gastro-enteritis may show alimentary lactosuria, and 

 along with the lactose some of its constituent galactose may appear in 

 the urine. The question thus naturally arises as to whether the low- 

 ered tolerance for galactose in phosphorus poisoning and other liver dis- 

 eases may not be due to an increased permeabilit}- of the intestinal wall,, 

 or to changes elsewhere in the body besides the liver, ^^'orner found 

 that galactose injected directly into the portal vein was handled by 

 healthy and phosphorized rabbits in the same relative jiroportions as 

 when given to these animals by mouth, thus apparently exchuhng the 

 bowel as a contributer to the decreased tolerance. It is unlikf^Iy also- 

 that the kidneys in phosphorized animals were rendered abnormally- 

 permeable for galactose, since when the kidneys alone are phosphorized 

 without affecting the liver, the excretion of galactose after adminis- 

 tration by mouth or into a vein has been retarded rather than hastened. 

 These principles have become incorporated in a clinical test for dis- 

 ease of the hepatic parenchyma. When galactose is administered to a 

 fully diabetic animal it is capable of being converted quantitatively 

 into glucose. Existing data indicate that galactose, like diose and 



