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Respiration Scientific Lab

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Cellular Respiration Scientific Lab: lose control
Adriana Resendiz
Brandon Morse
Halle Vogelpohl
Clackamas Community College

Cellular Respiration Scientific Lab: Lose Control
Introduction
My group wanted to find out the effects of an increase of mitochondrial suspension on the rate of aerobic cellular respiration. Specifically we're focusing on the second step of this process, The Kreb’s Cycle. Before the Kreb’s Cycle, the process of Glycolysis breaks glucose into 2 Pyruvate molecules, which is then oxidized into 2 Acetyl CoA. The two-carbon acetyl part of Acetyl CoA enters the Kreb’s Cycle with help from Coenzyme A, the latter of which is then recycled. The acetyl group combines with a four carbon molecule, marking a six carbon molecule …show more content…
Finally, two of the carbon atoms are removed as CO2, then the four carbon molecule regenerates. The Kreb’s Cycle yields 1 ATP, 1 FADH2, and 3 NADH per Acetyl CoA that enters the cycle. Since two Acetyl CoA enter the cycle, it yields a total 2 ATP, 2 FADH2, and 6 NADH by the end. (Lerner, 2008) The Kreb’s Cycle occurs in the mitochondria of the cell, and we ran an experiment during which we observed cellular respiration rates. We placed a mixture of mitochondrial suspension from ground up Lima beans, a buffer, DCPIP, and succinate of different proportions into labeled cuvettes. DCPIP is a blue chemical used to observe and measure the rates of cellular respiration, as it loses its color as cellular respiration occurs. For one set of three trials, we will keep the amount of mitochondrial suspension at .3 mL. For our experimental trial, we will increase the mitochondrial suspension for each cuvette. Our hypothesis is that if we increase the amount of mitochondrial suspension, then more cellular respiration would occur. If …show more content…
The percentages go up in tubes 2 and 3 but after 10 minutes the measured absorbance starts to decline, signaling the start of mitochondrial production. PTU is definitely limited in its effect of being a non-competitive inhibitor, once it is used up the remaining and unaffected mitochondria will continue cellular respiration. Through these results we can rationalize that if a human were to come in contact with the PTU toxin the effects can be limited to time.
Another experiment also tested PTU as an inhibitor to catechol oxidase, a type of enzyme found in fruits. This enzyme is found in several places of a plant cell, one of these places is also in the mitochondria (Shomer, I., 1979). The solution of PTU used was at 0.02 Molarity with 0.02 to 0.12 concentration of catechol oxidase. One of the graphs given help proves our hypothesis, that PTU does indeed halt mitochondrial production. Their graph shows that PTU stunts the browning of a banana, an effect caused by the oxidation of catechol by aerobic respiration

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