What We Have In Common With Bananas, And How This Commonality Can Precipitate Parkinson’s Disease.
- Dr Joel Yong
- Jun 23, 2020
- 5 min read
Updated: Jul 26, 2020
Hint: It has something to do with the tyrosinase enzyme.
The banana is a carbolicious fruit that many of us do like snacking on. It’s a source of quick, “natural” energy. Professional athletes chomp down on them in between games to get their second wind. We love using it in other carby dishes, such as with ice cream (the banana split), pancakes, waffles or with bread. In fact, people who grew up in the UK in the 1980s and the 1990s would also have been exposed to little Eric Wimp, a wimpy looking kid who gains superhuman strength after eating a banana — and becoming Bananaman in the process.
But of course, given my background, I’m not here to wax lyrical on Bananaman.
Rather, I’d be looking at what our human body has in common with the banana. See the brown spots in the image? That’s what I’ll be discussing here.
What are those brown spots?
According to this article,
The dark spots on fruits such as bananas can be attributed to the presence of melanin.
Now, hang on a second. We do have melanin in our bodies too. In fact, the melanocyte cells in our bodies are responsible for producing this melanin, and the melanin that we have in our hair determines whether our hair has colour or not. A lack of melanin in the hair would be a good indicator that our hair would be greying or silvery, as I have discussed in Vanity and Aging As Linked By The Same Chemical, Really.
The mechanism behind the formation of those melanin spots The major controller behind the rate of melanin synthesis is the tyrosinase enzyme. Tyrosinase is an enzyme that oxidises the amino acid tyrosine (which we can find in the proteins that we consume). As it is written in this article, tyrosine is oxidised by tyrosinase to 3,4-dihydroxyphenylalanine (DOPA) to dopamine, which is then eventually converted into eumelanin, which is the most common type of melanin pigment occurring in humans. This sequence of biochemical reactions is known as the Raper-Mason pathway.
In the banana, any aging or damage sustained to the fruit triggers the activity of tyrosinase to convert tyrosine into melanin too. Hence, whole bananas “are prone to rapid browning during handling, peeling and slicing operations and even storage, if ripening is not adequately controlled”, because of the damage that they are sustaining during all the handling operations that are involved.
That’s what we have in common with bananas!
But what are the deeper implications of tyrosinase and melanin in our body? An improper regulation of tyrosinase enzyme activity can result in the development of melanomas, or skin cancer. The abnormal browning of the skin from the overproduction in melanomas can be attributed to an abnormal tyrosinase activity.
We also did briefly touch on the conversion process of tyrosine to DOPA to dopamine. Dopamine is an important neurotransmitter that is released in the brain after a feelgood meal has been consumed. Much like serotonin production, which I have covered in The Biochemistry Behind Anxiety And Depression — Mental Health Issues That We Wouldn’t Wish Anyone Would Go Through, a lack of dopamine production in the brain can also contribute to a lack of motivation and symptoms of depression.
And dopamine production comes from… tyrosinase activity.
Of course, tyrosinase can also directly oxidise dopamine into toxic aminochromes. The aminochrome “forms adducts with proteins such as alpha-synuclein-inducing and alpha-synuclein-stabilizing neurotoxic protofibrils”. The aggregation and misfolding of these alpha-synuclein protein adducts into Lewy bodies is thought to accelerate the death of the neuronal cells in the brain, which then precipitates into Parkinson’s disease. Some of these aminochromes can also end up tautomerising and polymerising into neuromelanin.
Of course, in some situations, dopamine can become oxidised by the oxidative stress that is caused by the reactive oxygen species that spill out of our cellular mitochondria during the energy generation process, which I have covered in Where Does The Body Get Its Energy And Stamina From?
But at the end of the day, an abnormal tyrosinase activity can be implicated in the pathogenesis of Parkinson’s disease, or just the misfolding and accumulation of alpha-synuclein into Lewy bodies can play a big role in the pathogenesis of Parkinson’s.
Modern medical treatments for Parkinson’s These include the use of drugs such as monoamine oxidase (MAO) inhibitors (MAOIs). MAOs are enzymes that degrade neurotransmitters in the brain and reduce the available concentration of these neurotransmitters for receptor stimulation. (I previously covered how Selective Serotonin Reuptake Inhibitors, or SSRIs, helped to prevent the reuptake of serotonin, so as to increase the concentration of available serotonin for treating depression in The Biochemistry Behind Anxiety And Depression — Mental Health Issues That We Wouldn’t Wish Anyone Would Go Through).
MAOIs inhibit MAO activity and hence prevent the degradation of dopamine, which is important considering that a lack of dopamine results in motor and movement issues that patients with Parkinson’s disease face. MAOs degrade dopamine into DOPAL. DOPAL is then sequentially converted by aldehyde dehydrogenase (ALDH) into DOPAC, before ultimately being converted into homovanillic acid for excretion. Unfortunately, DOPAL is a reactive aldehyde that can also contribute to Parkinson’s.
Another consideration is the use of L-DOPA, or levodopa, which is the product of tyrosine oxidation by tyrosinase. It can directly cross the blood-brain barrier (which dopamine cannot do), and get converted into dopamine. This increases the dopamine concentrations in the brain, and that can also help with motor functions.
Win win situation, ain’t it?
Unfortunately, what isn’t really explained to the Parkinson’s patients is that the oxidation of dopamine after it has outlived its usefulness is problematic. As it is mentioned in this article, Administration of L-dopa to PD (Parkinson’s disease) patients, especially long-time therapy, may cause side effects in the form of increased toxicity and inflammatory response.
And that’s precisely because the oxidation of dopamine into aminochromes, whether by tyrosinase, MAOs or oxidative stress, can precipitate the alpha-synucleins that will worsen the symptoms of Parkinson’s disease over time!
It’s interesting, though, how the dysregulation of one enzyme can deal that much damage to a person’s health. Excessive tyrosinase activity can precipitate Parkinson’s disease and/or carcinogenic melanomas. Would it be surprising to see Parkinson’s patients with odd skin discolourations? Not necessarily, if the tyrosinase activity were as dysregulated in the brain as it were dysregulated on the skin.
This is eerily similar to how the carbonic anhydrase enzyme can deal damage to one’s digestive system and their urine/blood pH control, as I have covered in The Effects Of Carbonic Anhydrase on Our Bodily Functions.
But again, it really boils down to the transfer of electrons. It Only Takes That Tiny Electron To Cause Those Health Problems, and again, the electron transfer in the oxidation of dopamine is a major player in Parkinson’s.
How do we support our own brain and mental health? Here are 12 brain boosting nutrients that we can consider.
Here's also more information about how our brains can degenerate - Brain Degeneration Ain't All That It's Cracked Up To Be.
For vanity and skincare purposes, do check out this skin brightening series that is targeted at inhibiting tyrosinase activity!
This article was originally published in Medium.
Comments