Question

1) Sarin is a poison that prevents the breakdown of acetylcholine. Explain what sarin application will do to each of the following:

a) number of action potentials in the muscle cell

b) levels of Ca2+ in the sarcoplasmic reticulum

c) ability to control muscle contraction

2) Describe the role of the electron carriers (NADH and FADH2) in the production of ATP. Make sure to discuss the electron transport chain and the H+ gradient.

3) If a particular poison blocked the transfer of electrons from one electron carrier to another, would the amount of H+ in the intermembrane space increase or decrease? EXPLAIN.

Answer 1

1)

a) Number of action potential in the msucle cell increases

b) the level of calcium ion in the sarcoplassmic reticulum will decrease due the continuous contraction of the muscle, the level of the calcium ion in the sarcoplasm will increase.

c)Ability to control the muscle contraction is lossed, beacuse sarin is acetyl choline esterase inhibitor , this enzyme help the acetyl choline to hydrolyse . But when this enzyme is inhibited , their will be high amount of acetyl choline in the NMJ. it produce uncontrolled muscle contraction , later muscle become spastic.

sarin is a potent inhibitor of acetylcholinesterase, an enzyme that degrades the neurotransmitter acetylcholine after it is released into the synaptic cleft. In vertebrates, acetylcholine is the neurotransmitter used at the neuromuscular junction, where signals are transmitted between neurons from the central nervous system to muscle fibres. Normally, acetylcholine is released from the neuron to stimulate the muscle, after which it is degraded by acetylcholinesterase, allowing the muscle to relax. A build-up of acetylcholine in the synaptic cleft, due to the inhibition of acetylcholinesterase, means the neurotransmitter continues to act on the muscle fibre, so that any nerve impulses are effectively continually transmitted.

2)

• NADH is very good at donating electrons in redox reactions (that is, its electrons are at a high energy level), so it can transfer its electrons directly to complex I, turning back into NAD+. As electrons move through complex I in a series of redox reactions, energy is released, and the complex uses this energy to pump protons from the matrix into the intermembrane space.

• FADH2, is not as good at donating electrons as NADH (that is, its electrons are at a lower energy level), so it cannot transfer its electrons to complex I. Instead, it feeds them into the transport chain through complex II, which does not pump protons across the membrane.

Because of this "bypass," each FADH2 molecule causes fewer protons to be pumped (and contributes less to the proton gradient) than an NADH.

Electron transfer and proton pumping. As electrons are passed down the chain, they move from a higher to a lower energy level, releasing energy. Some of the energy is used to pump H+ions, moving them out of the matrix and into the intermembrane space. This pumping establishes an electrochemical gradient.

Splitting of oxygen to form water. At the end of the electron transport chain, electrons are transferred to molecular oxygen, which splits in half and takes up H+ to form water.

Gradient-driven synthesis of ATP. As H+ ions flow down their gradient and back into the matrix, they pass through an enzyme called ATP synthase, which harnesses the flow of protons to synthesize ATP

3) DECREASES

Electron transfer and proton pumping. As electrons are passed down the chain, they move from a higher to a lower energy level, releasing energy. Some of the energy is used to pump H+ions, moving them out of the matrix and into the intermembrane space. This pumping establishes an electrochemical gradient.