The Biochemistry Behind Oxidation And Reduction

The electron is a particle that is responsible for transporting electric currents.

Between two different chemicals, though, the transfer of electrons from Chemical A to Chemical B can result in a change in their chemical structures.

That's when the concepts of oxidation and reduction come in.

If Chemical A is able to extract electrons from Chemical B, we say that Chemical B is getting oxidised (loss of electrons), while Chemical A is a pro-oxidising agent that is getting reduced.

If Chemical B can maintain a stable chemical form upon oxidation, then it is a good antioxidant. However, if it cannot, then it turns into a highly unstable reactive oxygen species (ROS) that has to oxidise something else to extract electrons to maintain its stability. The propagation of these ROS oxidation reactions will generate even more unstable ROS species, which can also be termed as "free radicals".

The Redox Potential

A stable form of Chemical B reduces the probability of ROS propagation. Different A-B pairings will result in the development of different reduction-oxidation (redox) potentials, as highlighted in the table below:

What do these numbers mean? Let's take oxygen/water at +0.82 V and glutathione oxidised/reduced at -0.24 V, for example.

In the scheme of things, oxygen is the oxidising agent and water is its reducing counterpart, whereas oxidised glutathione is the oxidising agent and reduced glutathione is its reducing counterpart.

As the oxygen/water pair has a redox potential that is higher than the oxidised/reduced glutathione pair, with a net redox potential of 0.82 - (-0.24) = 1.06 V, if oxygen were to come into contact with reduced glutathione, oxygen would oxidise reduced glutathione into oxidised glutathione, and oxygen would get reduced to water in the process.

If water were to come into contact with oxidised glutathione, the net redox potential would be -0.24 - 0.82 = -1.06 V, and no electron transfer would occur.

In that same vein, can you work out that reduced Vitamin C is able to regenerate oxidised Vitamin E back to its reduced form (and in doing so, get oxidised into oxidised Vitamin C)?

Problems Associated With An Under-Regulated Electron Transfer

The redox activity in our bodies is generally well regulated. While our cell mitochondria are responsible for producing a lot of the ROS in our cells, ROS activity is kept in check by the glutathione antioxidants that are produced by the nuclear factor-erythroid 2 p45-related factor 2 (or nuclear respiratory factor 2, nrf2) transcriptional pathway in the body.

However, if our cells end up producing more ROS than the glutathione antioxidants can handle, the second line of defence that we do have comes from the antioxidants in our diets, such as Vitamin C and Vitamin E.

However, if all that cannot handle all the ROS that the body is producing, then there will be an "imbalance between reactive oxygen species and antioxidant reserve, referred to as oxidative stress", which can result in "the altered structure and function of proteins, lipids and DNA".

While oxidative stress appears to be a chemical problem on the surface, we do have to note that under the tip of the iceberg lies a massive change in how the biological components of our body function. Especially when the proteins, lipids and DNA of our cells can get damaged by oxidative stress.

If one were under a ton of psychological stress, could we expect them to make the right decision under pressure? Most people would crack. Now, if our cells were subjected to these biochemical stressors, how can we expect them to operate as if there was no problem at all?

Let's Look At The Regulation Of Our Blood Pressure

Our blood vessels are lined by a layer of cells known as the endothelial cells. These cells produce an enzyme known as endothelial nitric oxide synthase (eNOS), which are coupled together by a cofactor known as tetrahydrobioopterin (BH4) to produce nitric oxide (NO) to signal our blood vessels to dilate/enlarge (vasodilation).

When one is experiencing oxidative stress, there are a few things that can happen:

1. NO is oxidised into peroxynitrite radicals, which have zero capability in regulating vasodilation.

2. BH4 can be oxidised into dihydrobiopterin (BH2), which leads to eNOS decoupling and an inability to produce NO for vasodilation.

Therefore, the endothelial cells are unable to function properly with oxidative stress.

With insufficient vasodilation, the blood vessels are constricted more easily, which necessitates the heart to generate a higher pumping pressure to force blood through those constricted vessels.

Would that not lead into hypertension if our blood vessels were perpetually constricted from a lack of NO signalling?

Therefore, is hypertension not a problem with our cell functions, then?

Excessive Alcohol Consumption Can Be Bad For Our Health, Too.

A similar analysis can be conducted with the effects of excessive drinking. As I did mention in What Bearing Does A Cocktail Crisis Have On Our Health, alcohol metabolism in the liver is dependent on its conversion rates into acetaldehyde and acetate (vinegar):

The cells in our liver take 2 steps to metabolise ethanol (alcohol) into acetate (vinegar).

1. Initially, the alcohol dehydrogenase (ADH) enzyme converts ethanol into acetaldehyde.

2. The acetaldehyde dehydrogenase (ALDH) enzyme then converts acetaldehyde into acetate.

Both these reactions are oxidation reactions, where electrons are removed from the ethanol (Step 1) and acetaldehyde (Step 2). These electrons are transferred to nicotinamide adenine dinucleotide (NAD+), which then reduces NAD+ down to its reduced state of NADH.

Unfortunately, the rate of Step 2 activity tends to be slower than the rate of Step 1, hence when one drinks alcohol in excessive amounts, their faces tend to go red, they get nauseous, and they get dizzy. Those are symptoms of acetaldehyde toxicity right there.

This is essentially why alcoholics are at greater risk of developing liver cancer.

Their liver has to metabolise all the alcohol that they are consuming. If they drink themselves drunk on a regular basis, there will be constant periods of time when their blood acetaldehyde levels are higher than normal, which then has a higher propensity to cause greater amounts of damage to their liver cells. As more damage is sustained to the liver, the probability of developing liver cancer/health complications would then be much greater, no?

And that's really how the unseen transfer of electrons in reduction/oxidation reactions can be so damaging. Imagine one particle that cannot be seen by the naked eye. Lighter and smaller than a coronavirus particle, and yet so much more damaging to the human body over the long term!

Joel Yong, PhD, is a biochemical engineer/scientist, an educator and a writer. He has authored 1 ebook (which is available on Amazon.com in Kindle format) and co-authored 6 journal articles in internationally peer-reviewed scientific journals. His main focus is on finding out the fundamentals of biochemical mechanisms in the body that the doctors don’t educate the lay people about, and will then proceed to deconstruct them for your understanding — as an educator should. Do visit his website here or his Patreon site here to connect.