[Suppression of phosphofructokinase (PFK) by sera from cancer patients, and mechanism of the antagonistic effect of PSK].
Body fluids from cancer patients (sera, pleural effusions and ascites) tended to inhibit phosphofructokinase (ATP: D-fructose-6-phosphate 1-phosphotransferase, EC 2.7.1.11) (PFK), the rate-limiting key enzyme in the glycolysis pathway, when analysed using aqueous ATP solution separately from the main reaction mixture. A protein-bound polysaccharide from Coliolus versicolor QUEL (Krestine, PSK) antagonistically elevated the activity of the enzyme. It was found that PSK stabilized PFK in a similar way to certain enzyme stabilizers such as proteins and polysaccharides. Furthermore, it was clarified that PSK worked as an ion radical scavenger that could capture 1O2, O-2, and OH X radicals released from lipoperoxides. In other words PSK protects PFK from hyperoxidation by lipoperoxides.
D002021:Buffers; D004305:Dose-Response Relationship, Drug; D004355:Drug Stability; D006801:Humans; D066298:In Vitro Techniques; D010655:Phenylenediamines / Q000037:antagonists & inhibitors; D010732:Phosphofructokinase-1 / Q000037:antagonists & inhibitors* / Q000097:blood; D011509:Proteoglycans / Q000494:pharmacology*; D013274:Stomach Neoplasms / Q000097:blood*
D002021:Buffers; D010655:Phenylenediamines; D011509:Proteoglycans; C010770:polysaccharide-K; C034193:1,2-diaminobenzene; D010732:Phosphofructokinase-1