GLYCOPROTEIN DEGENERatION OF MUSCLE FIBER
Authors: Nasu Tsuyoshi 
Published: December 2008

VII Summary

. 1. Degeneration products of so‐called basophilic (mucoid) degeneration show the properties of glycogen or glycogen‐protein complex in the initial stage, followed by formation of neutral and acid mucopolysaccharides. Judging from the steps taken in the occurrence of degeneration and from the histochemical characteristics, it is designated as mucopolysaccharide (MPS) degeneration.

2. Having discovered a new type of degeneration that forms crystalloid bodies, what is considered to be in the absorption stage of MPS degeneration, it was named as crystalloid degeneration. Histochemically in this degeneration characteristics of neutral mucopolysaccharide are demonstrated more frequently, but in a later stage some also reveal properties of hyaline protein or lipoprotein.

3. MPS degeneration and crystalloid degeneration set in from abnormal metabolism of sugars, especially of glycogen, and as the products resulting from misguided synthesis caused by disturbed enzyme systems there are formed various complexes of substances that chemically represent residual radicals of sugars, and of proteins. Therefore, it may be appropriate to designate these degeneration types taken together as glycoprotein (GP) degeneration.

4. Products of GP degeneration of heart muscles are not direct deposits of substances that infiltrated into the muscle fiber from outside but they are endogenous autochthonous metabolites. Moreover, this degeneration is closely associated with aging phenomena, and it develops, as a rule, not from specific nature of any particular disease but rather it sets in proportionately to underlying wasting conditions of the body.

5. Mentions were made on 3 cases of myoclonic epilepsy and on one case each of myeloma and X‐ray irradiated cancer of esophagus, as examples that developed markedly multiple GP degeneration in heart muscle as to present a classical state of myodegeneratio cordis.

6. GP degeneration develops not only in heart muscle but also in skeletal muscle and smooth muscle. In skeletal muscle it occurs at the time when the muscle is injured and also in myogenous cells during subsequent degeneration phase in the “abortive regeneration”.

7. There could be recognized intermediary forms between crystalloid degeneration substance to which lipoid was adsorbed and coarse lipofuscin clusters, suggesting that the formation of lipofuscin has a close relationship with GP degeneration.

8. GP degeneration of heart muscle was experimentally induced in rabbits. Namely, by injection of desoxycorticosterone acetate (DOCA) GP degeneration was developed approximately parallel to the degree of dysprotei'nemia in 8 of 11 animals. However, since the degeneration occurs even by repeated heart punctures, dysproteinemia is not an indispensable factor in the development of this degeneration. GP degeneration was observed in 6 of the 8 rabbits in experimental starvation and in 14 of the 26 rabbits exposed to a large dose of X‐ray irradiation. However, GP degeneration did not develop in the animals with experimental hypo‐ and hyperthyroidism.

9. In the experimental GP degeneration induced acutely within a short period of time, MPS‐type degeneration is found more frequently but formation of acid mucopolysaccharide is less than that in the human heart muscle. In addition, experimental GP degeneration induced chronically over a long period of time tends to be mostly of crystalloid‐type degeneration.

10. From these results it can be said that glycoprotein degeneration of muscle fibers represents energetic‐chemical insufficiency of the muscle function.