Oxidative Stress and alcohol

Question 1

What are the two types of free radicals?

Answer 1

rOS (reactive oxygen species) and RNS (reactive nitrogen species)

Question 2

How can oxygen behave as a radical?

Answer 2

An oxygen molecule is a biradical, and has two unpaired electrons, and when an electron is added a superoxide molecule can be produced, which can then go on to produce hydrogen peroxide, which can go on to produce an OH which is the most dangerously reactive free radical.

Question 3

What is nitric oxide an important radical?

Answer 3

Can with superoxide to produce peroxydide deoxynitrate, which is not a free radical but a powerful oxidative species that can cause a lot of damage.

Question 4

How does ROS damage DNA.

Answer 4

It can either react with the base which can lead to misparing and mutation, or reaction with the sugar causing the strand to break and mutation to occur upon repair. This dna mutation and damage can lead to cancer.m

Question 5

How can ROS damage proteins?

Answer 5

It can either damage the amino acid backbone leading to fragmentation and protein degradation, or can damage the side chain and this can cause a change in protein primary, secondary or tertiary structure, which can cause a gain or loss of function and potentially degradation.

Question 6

How can ROS damage lipids?

Answer 6

The free radical can extract oxygen from a polyunsaturated amino acid and this can form a lipid peroxyidil radical which can start a chain reaction that can disrupt structures such as phospholipid bilayer ps.m

Question 7

What are the endogenous sources of biological oxidants?

Answer 7

The electron transport chain, perioxidases, nitric oxide synthase, lipooxygenesis, NADPH oxidases, xathine oxidases, monoamine oxidases.

Question 8

What are the exogenous sources of biological oxidants?

Answer 8

Exogenous, radiation, UV light, pollutants. Drugs, promaquine, toxins.

Question 9

How does the electron transport chain produce biological oxidants?

Answer 9

Electrons can escape the chain and react with o2 to form superoxides.

Question 10

How can nitric oxide syntheses produce biological oxidants?

Answer 10

Inducable nitric oxide synthase produce NO which is used for toxic affects in phagocytosis, as was as eNOS and nNOS which produce NO for signalling purposes.

Question 11

How does a respiratory burst produce free radicals?

Answer 11

This is a rapid increase in production of superoxide and hydrogen peroxide (NADPH oxidase is used to produce superoxide )

Question 12

How does Glutathione protect against oxidative damage?

Answer 12

The thiol group of the cysteine residue donates electron to ROS, and GSH reacts with another GSH to produce a disulphide bond using the glutathione peroxidase enzyme. It is reduced back to GSH by gluthaione reductase, which requires a transfer of electrons from NADPH to the disulphide bond.

Question 13

How does the superoxide dimutase enzyme protect against oxidative stress?

Answer 13

This is an enzyme that coverts superoxide to hydrogen peroxide and oxygen.

Question 14

How do free radical scavengers protect against oxidative stress?

Answer 14

They reduce oxidative damage by donating hydrogen atoms to free radicals in a non-enzymatic reaction.

Question 15

How do vitamin E and vitamin C act as free radical scavengers?

Answer 15

Vitamin c is a vitamin soluble antioxidant that is important for protection against lipid per-oxidants, vitamin c is water soluble and is important in regenerating the reduced form of vitamin e.

Question 16

How is galactosemia a sign of oxidative stress?

Answer 16

There is a deficiency in the galactokinase or uridyl transferase enxpzyme, which leads to a increased activity of the aldose reductase enzyme and this uses up NADPH, which compromises protection against ROS damage, such as denaturation of proteins in the eye.

Question 17

How is G6PDH deficiency an example of oxidative stress?

Answer 17

This limits the amount of NADPH, which lowers the amount of GSH as it is not being transformed back to its reduced form, which can lead to formation of lipid per oxidation and cell membrane damage, heiz bodies and potentially haemolysis.

Question 18

How doe ischemia reperfusion in injury lead to oxidative stress?

Answer 18

Reperfusion of blood after ischameia can cause more damage as incompletly metabolised products can cause ROS to be formed, antioxidants have been lost during injury and influx of calcium and influx of leukocytes.

Question 19

What is a free radical?

Answer 19

An atom or molecule that contains one or more unpaired electrons.m

Question 20

How os alcohol metabolised?

Answer 20

The enzyme alcohol dehydrogenase converts alcohol to acetaldehyde, and the enzyme aldehyde dehydrogenase converts acetaldehyde to acetate (both reactions convert NAD+ to NADH), which combines to coA to form acetyl CoA.

Question 21

Where is alcohol metabolised?

Answer 21

90% is metabolised in the liver, and the remainder is passively excreted in urine and breath.

Question 22

What is the impact of decrease NAD +/NADH ratio?

Answer 22

Inadequate NAD+ for conversion of lactate to pyruvate, lactate accumulates in the blood, inadequate NAD+ for glycerol metabolism, so the kidneys ability to secrete uric acid will be reduced, and there will be a deficit in gluconeogenesis which can result in hypoglycaemia.

Question 23

What is the impact of increase acetyl CoA after alcohol metabolism?

Answer 23

Increased synthesis of fatty acids and ketone bodies, increased formation of triglycerol which can lead to a fatty liver.

Question 24

What are the different causes of liver damage from alcohol metabolism?

Answer 24

Prolonged, excessive alcohol consumption leads to a sufficient acetaldehyde concentration to cause liver damage, and excessive NADH and acetyl CoA can lead to alcohol cirrhosis, alcohol hepatitis, and a fatty liver.

Question 25

How is disulfram used to treat chronic alcohol dependance?

Answer 25

It is an inhibitor of aldehyde dehydrogenase, and so acetaldehyde will acculmate causing the symptoms of a hangover.