Chapter 10: Vitamins (Continued)

Question 1

Describe the rhodopsin receptor.

Answer 1

is a 7-pass receptor coupled to the trimeric G protein transducin (Gt)

Question 2

How does light affect cGMP in rod cells?

Answer 2

The pathway activates cGMP phosphodiesterase, which lowers cGMP levels shutting the Na+/Ca2+ channels

Question 3

Rhodopsin and transducin are found where on the rod cell?

Answer 3

rhodopsin and transducin are embedded in the disk membranes in the outer rod segment

Question 4

Why is the rod cell unusual compared to other excitable cells?

Answer 4

the membrane is partially depolarized (~ -30 mV) at rest (in darkness) and hyperpolarizes on stimulation

Question 5

In the dark the rod cell membrane is partially depolarized what neurotransmitter is continuously released? What is the effect of this neurotransmitter being released?

Answer 5

glutamate inhibits the optic nerve bipolar cells with which the rod cells synapse.

Question 6

Explain the biochemical mechanism by which it is easier to see with light than in the dark?

Answer 6

Light ends up hyperpolarizing the rod cell membrane, light stops the release of glutamate, relieving inhibition of the optic nerve bipolar cell and thus initiating a signal into the brain

Question 7

What is the most common cause of blindness in developing countries?

Answer 7

Vit A deficiency

Question 8

What molecule is B-carotene cleaved into?

Answer 8

cleaved into 2 molecules of retinal by an intestinal enzyme, each retinal molecule is then converted to all-trans-retinol then absorbed by interstitial cells

Question 9

What are characteristics of Vit A toxicity?

Answer 9

if ingested at levels greater than 15x RDA:

excessive sweating
diarrhea
brittle nails
hypercalcemia,
hepatotoxicity
vertigo,
nausea/vomiting

Question 10

Is beta-carotene toxic at high levels?

Answer 10

beta carotene not toxic at high levels

Question 11

Describe y-carboxylation of glutamic acid.

Answer 11

Where Vit K is required to introduce Ca2+ binding sites on several calcium dependent proteins. (especially those in coag pathway) This modification introduces the Ca2+ binding site through y-carboxylation of glutamyl residue (s) in these proteins.

Question 12

What type of gene modification is Vit. K dependent carboxylation? (post or co translational)

Answer 12

co-translational modification

Question 13

What are conditions that expose one to vit K deficiency?

Answer 13

• fat malabsorption (bile duct occlusion)
• prolonged treatment with broad-spectrum antibiotics (eliminate intestinal bacteria that supply vitamin K
• Breast-fed newborns (little intestinal flora, breast milk very low in vitamin K), esp. in home birth where a postnatal injection of vit K may not be given
• Infants whose mothers have been treated with certain anticonvulsants during pregnancy such as phenytoin (dilantin)

Question 14

Compare and contrast Vit K deficiency to Vit C deficiency PT times.

Answer 14

increased PT in vit K def
Normal PT in vit C def

Question 15

Compare and contrast BT in Vit K def. vs Vit C deficiency.

Answer 15

increased BT in Vit. C deficiency
Normal BT in Vit K deficiency

Question 16

Why is warfarin and dicumarol good competitive inhibitors of Vit. K?

Answer 16

They have similar shapes

Question 17

Why can warfarin and dicumarol only prevent coagulation only in vivo?

Answer 17

because clotting factors have already been made and are already in test tube. These drugs prevent y-carboxylation preventing new factors from being made and take time to work

Question 18

High blood levels of Vit E can cause hemorrhage in patients given what drug?

Answer 18

warfarin