Effect of Vitamin E on Phosphofructokinase Activity in Acute Metabolically Stressed Rats

Reactive oxygen species and free radicals generated in oxidative stress, during conditions of metabolic stress as seen in illness, are occupied in tissue injury and dysfunction of the mitochondria with depletion of ATR A pro-oxidant/antioxidant imbalance is commonly found in disease states, and the excess of pro-oxidant may cause muscle cell injury. An increase in antioxidant status could be attained by diet supplementation, which will regain the favorable level of antioxidant status and slow the progress of disease by limiting the decline of phosphofructokinase (PFK) activity, a major enzyme in glycolysis. Intramuscular injections of an antioxidant, such as vitamin E, may help patients recover more rapidly without feeding. A rat model of metabolic stress was created using zymosan, (Z) a nonbacterial, nonendotoxic agent. Sixty male Wistar rats (BW 250-300 g) were obtained from Harlan and divided randomly into groups: Control, Pair-Fed, Zymosan-injected (ZI) day two, ZI day seven, vitamin E and ZI day two, and vitamin E and ZI day seven. Stressed rats received either Z (50 mg per / Kg BW) or Z and vitamin E injections. Surgeries were preformed two and seven days after injections; four muscles from both hind legs, the soleus, the extensor digitorum longus, and the red and white gastrochemius, were isolated and extracted by freeze clamping. Analysis of PFK activity is currently being performed by fluorescence using a Fluorscan Microplate Reader. We hypothesize the antioxidant vitamin, vitamin E, will inhibit the decline in activity of PFK observed in acute metaboiicaliy stressed rat models