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Student No./10001Experiment: Glycoside Beta DrumminAssignment (type)Date1000 wordsStudent’s NameInstitutional Affiliation
Student No./10002Experiment: Glycoside Beta Drummin1) According to the Embden-Meyerhof pathway, the pentose cycle involves the conversionof glucose molecules (and fructose molecules) to CO2. Glycolysis involves the conversion ofglucose to produce ATP. 3 pentose phosphates elements are converted to form fructose 6-phosphate and triose phosphate1. The14C are used directly while the fructose 6-P is notbroken down to Glucose. As such, the14C is used up to complete for the pentose phosphatecycle due to randomized of14C metabolism use in the pentose cycle or glycolysis pathway. Insome cases, when the fructose-6-phosphate is equal or in equilibrium with glucose-6-phosphate, fructose-6-phosphate can be reversed. However, even when the process isreversed in glycolysis the use of14C from the substrates. Hence, randomized use of14C inglucose-6-phosphate is predicted for metabolism in order to complete the pentose cycle.2) The significance in lack of accumulation of lactate in the experiment is that noabnormalities would be experienced during the pentose cycle. Accumulation in lactate wouldlead to metabolic dysregulation which would result in reduced or abnormal metabolism ofpentose-phosphate2. Metabolism would affect the pH balance in pentose-phosphatemetabolism if lactate would be produced in high or excess amounts. The other explanationwould be the incorporation of the lactate-acid cycle. Since the process is anaerobic the use ofCO2to convert the lactate reduced the amount of carbon (IV) oxide. Nonetheless, asglycolysis is happening probably the lactate acid cycle is taking place. Therefore,based onthe results of the experiment, the equilibrium in CO2 and O2 at 50% reduced the productionof lactate.1Katz, J., Wood, H.G. “The use of glucose-C14 for the evaluation of the pathways ofglucose metabolism.” J. Biol. Chem. 235, 2165–2177, 20102Hoff, J., Støren, Ø., Finstad, A., Wang, E., Helgerud, J. “Increased blood lactate leveldeteriorates running economy in world class endurance athletes.” J. Strength Cond.Res. 30, 1373–1378, 2016.
Student No./100033) The enzymes necessary for metabolic activity may have been depleted or were lesscompared to the number of available enzymes were lower than substrates3. Therefore, therate of oxygen input in addition carbon (IV) oxide output may have reached an equilibrium.The isomerization of 14C in substrates as a result of reduction of substrates and enzymesnecessary for glycolysis. Another reason is that substrates may have reduced in amount whichmay have resulted in reduced metabolic activity leading to an equilibrium in oxygen inputand carbon (IV) oxide output.4) The opinion is that glycoside beta drummin may be an inhibitor to the enzymatic activityin glycolytic metabolism4.Glycolysis heavily relies on enzymatic action which is crucial tothe catalysis of the cycle resulting into the creation of carbon (IV) oxide and intake ofoxygen. As such, inability of the enzymes to induce metabolism, there was a reduced oxygenintake and carbon (IV) oxide output. The possible explanation is that the binding of theinhibitor, in this case, glycoside beta drummin, to the substrates, at concentration between 10-100mM created an imbalance in the enzyme-substrate complex as a result reducingmetabolism.5) The addition of inhibition to RSW did not alter any results and thus indicates thatglycoside beta drummin, can cause inhibition reaction in the glycolysis process. The plausibleexplanation is that glycoside beta drummin contains inhibitor molecules that either bind tothe substrate-enzyme complex or on the enzymes limiting their biochemical functionality5.3Canto, C., Menzies, K.J., Auwerx, J. “NAD+ metabolism and the control of energyhomeostasis: a balancing act between mitochondria and the nucleus.” Cell Metab. 22,31–53, 2015.4Vander Heiden, M.G., DeBerardinis, R.J. “Understanding the intersections betweenmetabolism and cancer biology.” Cell 168, 657–669, 2017.5Vander Heiden, M.G., DeBerardinis, R.J. “Understanding the intersections betweenmetabolism and cancer biology.”Cell 168, 657–669, 2017.