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Lesson Plan: Respiration Challenge General Description In this activity, students examine cellular respiration on a molecular level. In small teams, they solve problems focused on various inhibitors of respiration. Using limited data and their past learning of respiration, students “formulate and revise scientific explanations and models using logic and evidence”. Objectives 1. Students will examine cellular respiration at the molecular level. 2. Students will solidify their knowledge of the general process of cellular respiration. 3. Students will practice creating scientific explanations using logic. Concepts cellular respiration, glycolysis, Krebs cycle (citric acid cycle), electron transport system, phosphorylation, pH, enzyme Time 40 minutes Prerequisite Skills Students should be familiar with the general process of cellular respiration. Materials Question cards Take Home Worksheets Individual Accountability handouts ICE Inquiry-based Curriculum Enhancement

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Lesson Plan: Respiration Challenge

General Description

In this activity, students examine cellular respiration on a molecular level. In small teams,

they solve problems focused on various inhibitors of respiration. Using limited data and

their past learning of respiration, students “formulate and revise scientific explanations and

models using logic and evidence”.

Objectives

1. Students will examine cellular respiration at the molecular level.

2. Students will solidify their knowledge of the general process of cellular respiration.

3. Students will practice creating scientific explanations using logic.

Concepts

cellular respiration, glycolysis, Krebs cycle (citric acid cycle), electron transport system,

phosphorylation, pH, enzyme

Time

40 minutes

Prerequisite Skills

Students should be familiar with the general process of cellular respiration.

Materials

Question cards

Take Home Worksheets

Individual Accountability handouts

ICEInquiry-based Curriculum Enhancement

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UTI Instructions: Respiration Challenge

Introduction:

In this activity, students examine cellular respiration on a molecular level. In small teams,

they solve problems focused on various inhibitors of respiration. Using limited data but

their past learning of respiration, students “formulate and revise scientific explanations and

models using logic and evidence”.

Procedure:

Have students create teams of no more than three students. Distribute the question cards,

one card to each team. As you are doing so, describe the activity as a series of challenges

to their growing knowledge of cellular respiration and as a review of the basic process.

Remind the teams that they will be responsible for reporting to the class. Allow the teams

10-12 minutes to prepare answers to their questions. Provide a one-minute warning for

them to wrap up. Then have teams trade cards and again work to create answers to their

questions. Allow 8-10 minutes for this second round of thinking. When most teams appear

to be completing the questions, have the teams that traded cards compare answers, and

elect two spokespersons to report clear, succinct answers to the class. Allow about 5-8

minutes for comparisons (or as the progress of the class indicates). Have spokespersons

read their questions then present their teams’ answers. After only a few questions, the

students should realize that there are themes in the questions and should consider the

similarities in these questions and answers (you might have to prompt them in this

respect). After all teams have reported, answer any remaining questions and administer

the Individual Accountability question.

Additional Suggestions:

If you feel your class needs an additional introduction to cellular respiration, consider having

them individually write as much as they can remember about respiration and then sharing

with one or two neighbors. The assumption with this strategy is that most students are

familiar with the process, but no one student will remember everything necessary. The

students will confirm their knowledge and extend it with a short exchange. This whole

process can occur in less than ten minutes and can increase the success of the main

activity.

ICEInquiry-based Curriculum Enhancement

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In the 1940s, some physicians prescribedthe drug DNP (dinitrophenol) to help

patients lose weight. This treatment was

abandoned after several patients died.DNP works by uncoupling the

chemiosmotic machinery by making thelipid bilayer of the inner mitrochondrial

membrane leaky to H+.

A) Explain how DNP causes weight loss.

B) Suggest at least one other cellulareffect of DNP (i.e., what other aspects of

the cell might be affected by DNP), andprepare an explanation of this effect.

Cyanide is a chemical that irreversiblybinds to (i.e., prevents the functioning of)

the enzyme cytochrome oxidase, animportant enzyme in the electron

transport system.

A)Explain, at the cellular level, whycyanide is a lethal chemical.

B) Suggest at least one other cellular

consequence of cyanide (i.e., what elsehappens to the electron transport system

when cyanide is present), and prepare and

explanation of this effect.

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Rotenone is a naturally occurring chemical

derived from the roots of several tropical andsubtropical plants. Ingestion of rotenone can

be fatal. It inhibits chemiosmosis by

interfering with NADH dehydrogenasepreventing utilization of NADH as a proton andelectron donor in the electron transport chain.

A)Explain why rotenone exposure can be fatal.

B) Suggest at least one other cellular effect ofrotenone (i.e., what other parts of respiration

might be affected by rotenone), and preparean explanation of this effect.

DCCD (dicyclohexylcarbodiimide) inhibits

oxidative phosphorylation when thesubstrate is mitochondrial NADH. DCCD is

a drug that binds to ATP synthase and

blocks proton transport through the ionchannel.

A)Explain what the consequences are of

DCCD on cellular energy production.

B) Suggest at least one other cellulareffect of DCCD, and prepare an

explanation of this effect.

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Sometimes the supply of oxygen in active

muscle tissue is not adequate for thedemands of oxidative phosphorylation.When this situation occurs, the electron

transport system slows.

A)Explain on a cellular level theconsequences of low oxygen supply.

B) Suggest a respiration-basedexplanation for why deep breathing

continues even after strenuous exercise

has stopped.

How much energy would be generated inthe cells of a person who consumed a diet

of pyruvate instead of glucose?

Contrast the energy production of a highcarbohydrate diet and a high protein diet.

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Do mitochondria raise or lower the pH ofthe region of the cell in which they are

found? Why?

Describe the relative pHs of thecytoplasm, the mitrochondrialintermembrane space, and the

mitochondrial matrix, with an explanationof the origin of this pattern.

Glucosamine is a common compoundthat inhibits hexokinase action (the

transfer of a phosphate group to

glucose during glycolysis).

A) Describe the consequences ofglucosamine exposure on cellular

respiration.

B) Is glucosamine exposure fatal?Why or why not?

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Vitamin B3 (niacin) is a component ofNAD+ (or NADH). Niacin isacquired through the diet.

A) Describe the consequences ofniacin deficiency on energy

production.

B) Invent two strategies a cell mightuse to maintain energy production

under niacin deficiency.

Anemia is characterized by lowhemoglobin levels or a reduced number

of red blood cells (both of whichtransport oxygen to cells). A common

symptom of anemia is tiredness.

A) Explain what the consequences are ofanemia on cellular energy production.

B) Suggest at least one other cellular

effect of anemia, and prepare anexplanation of this effect.

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Bongkrekic acid is a toxic compoundproduced by the bacterial speciesBurkholderia gladioli. If ingested,

bongkrekic acid most often results indeath. Bongkrekic acid inhibits theadenine nucleotide transporter that

shuttles ADP across the innermitochondrial membrane.

A) Describe the consequences of bongkrekic

acid poisoning on cellular respiration.

B) Suggest two chemical cues that mightindicate bonkrekic acid poisoning.

Antimycin A is a pesticide in useworldwide. It is recognized as a

respiration inhibitor, since it blocks the

electron transport chain betweencytochrome b and cytochrome c1.

A)Describe why antimycin A is a

successful pesticide.

B) Describe the effects of antimycin Aexposure on cellular respiration in terms

of the byproducts of the process.

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Oligomycin is an antibiotic compoundproduced by actinomycete bacteria

(these bacteria can cause the condition

known as lumpy jaw). Oligomycinbinds to a protein in the ATP synthase

complex.

A) Describe the consequences ofoligomycin on cellular respiration.

B) Describe the energy production

capacity of a cell affected byoligomycin.

The antibiotic valinomycin is one exampleof an ionophore, a chemical that makes

the inner mitochondrial membrane

permeable to protons.

A) Describe why valinomycin is aneffective antibiotic agent.

B) Suggest three biochemicalconsequences of valinomycin on

cellular respiration.

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Pre-Activity Worksheet: Respiration Challenge

General Description

In the activity you will do this week during your learning/discussion group, you will be

examining how respiration in an individual’s cells change under different conditions. In

order to be prepared for this activity, complete this worksheet.

Reading

Browse the “Cellular Respiration” chapter in your text. Pay particular attention to figures

9.5, 9.6, 9.8, 9.12, 9.15, 9.16, 9.18, and 9.19. Read the section The Process of Cellular

Respiration beginning on pg. 160.

Definitions

Write a definition of the following words. Use your text, textbook glossary, and your

previous knowledge to create the best definition possible. Remember to connect your

definitions to respiration.

1) enzyme

2) glycolysis

3) electron transport

4) phosphorylation

Questions

Answer the following questions. You will explore your answers to these questions in-depth

during learning/discussion group.

1) Which enzyme in the process of cellular respiration is the most important? Why is this

enzyme more important than the others?

2) Describe substrate-level phosphorylation. What characteristics distinguish substrate-

level and oxidative phosphorylation.

3) Suggest at least two different reasons why the electron transport chain is comprised of

so many different versions of the same proteins.

ICEInquiry-based Curriculum Enhancement

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Individual Accountability: Respiration Challenge

Demonstrate your new understanding of cellular respiration by answering the following

question:

Which process within the overall process of cellular respiration is the most critical to energy

production? Defend your answer in four or five sentences.

ICEInquiry-based Curriculum Enhancement

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Take Home Worksheet: Respiration Challenge

All of the following questions are the same or similar to ones discussed in class today. One

good strategy for working with these questions is to answer them on your own to the best

of your ability, then compare your answers with a fellow student. Together you will be able

to create good answers to the questions. In all cases, be prepared to explain your

reasoning clearly and succinctly.

1. In the 1940s, some physicians prescribed the drug DNP (dinitrophenol) to help patients

lose weight. This treatment was abandoned after several patients died. DNP works by

uncoupling the chemiosmotic machinery by making the lipid bilayer of the inner

mitrochondrial membrane leaky to H+. A) Explain how DNP causes weight loss. B) Suggest

at least one other cellular effect of DNP (i.e., what other aspects of the cell might be

affected by DNP), and prepare an explanation of this effect.

2. Cyanide is a chemical that irreversibly binds to (i.e., prevents the functioning of) the

enzyme cytochrome oxidase, an important enzyme in the electron transport system. A)

Explain, at the cellular level, why cyanide is a lethal chemical. B) Suggest at least one other

cellular consequence of cyanide (i.e., what else happens to the electron transport system

when cyanide is present), and prepare and explanation of this effect.

3. Rotenone is a naturally occurring chemical derived from the roots of several tropical and

subtropical plants. Contact, particularly ingestion, with rotenone can be fatal. It inhibits

chemiosmosis by interfering with NADH dehydrogenase preventing utilization of NADH as a

proton and electron donor in the electron transport chain. A) Explain why rotenone

exposure can be fatal. B) Suggest at least one other cellular effect of rotenone (i.e., what

other parts of respiration might be affected by rotenone), and prepare an explanation of this

effect.

4. DCCD (dicyclohexylcarbodiimide) inhibits oxidative phosphorylation when the substrate is

mitochondrial NADH. DCCD is a drug that binds to ATP synthase and blocks proton

transport through the ion channel. A) Explain what the consequences are of DCCD on

cellular energy production. B) Suggest at least one other cellular effect of DCCD, and

prepare an explanation of this effect.

5. Sometimes the supply of oxygen in active muscle tissue is not adequate for the demands

of oxidative phosphorylation. When this situation occurs, the electron transport system

slows. A) Explain on a cellular level the consequences of low oxygen supply. B) Suggest a

respiration-based explanation for why deep breathing continues even after strenuous

exercise has stopped.

6. How much energy would be generated in the cells of a person who consumed a diet of

pyruvate instead of glucose? Contrast the energy production of a high carbohydrate diet

and a high protein diet.

7. Do mitochondria raise or lower the pH of the region of the cell in which they are found?

Why? Describe the relative pHs of the cytoplasm, the mitrochondrial intermembrane space,

and the mitochondrial matrix, with an explanation of the origin of this pattern.

8. Glucosamine is a common compound that inhibits hexokinase action (the transfer of a

phosphate group to glucose during glycolysis). A) Describe the consequences of

ICEInquiry-based Curriculum Enhancement

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glucosamine exposure on cellular respiration. B) Is glucosamine exposure fatal? Why or

why not?

9. Vitamin B3 (niacin) is a component of NAD+ (or NADH). Niacin is acquired through the

diet. A) Describe the consequences of niacin deficiency on energy production. B) Invent

two strategies a cell might use to maintain energy production under niacin deficiency.

10. Anemia is characterized by low hemoglobin levels or a reduced number of red blood

cells (both of which transport oxygen to cells). A common symptom of anemia is tiredness.

A) Explain what the consequences are of anemia on cellular energy production. B) Suggest

at least one other cellular effect of anemia, and prepare an explanation of this effect.

11. Antimycin A is a pesticide in use worldwide. It is recognized as a respiration inhibitor,

since it blocks the electron transport chain between cytochrome b and cytochrome c1. A)

Describe why antimycin A is a successful pesticide. B) Describe the effects of antimycin A

exposure on cellular respiration in terms of the byproducts of the process.

12. Bongkrekic acid is a toxic compound produced by the bacteria species Burkholderia

gladioli. If ingested, bongkrekic acid most often results in death. Bongkrekic acid inhibits

the adenine nucleotide transporter that shuttles ADP across the inner mitochondrial

membrane. A) Describe the consequences of bongkrekic acid poisoning on cellular

respiration. B) Suggest two chemical cues that might indicate bonkrekic acid poisoning.

13. Oligomycin is an antibiotic compound produced by actinomycete bacteria (these bacteria

can cause the condition known as lumpy jaw). Oligomycin binds to a protein in the ATP

synthase complex. A) Describe the consequences of oligomycin on cellular respiration. B)

Describe the energy production capacity of a cell affected by oligomycin.

14. The antibiotic valinomycin is one example of an ionophore, a chemical that makes the

inner mitochondrial membrane permeable to protons. A) Describe why valinomycin is an

effective antibiotic agent. B) Suggest three biochemical consequences of valinomycin on

cellular respiration.