Heart damage caused by cancer with a link to free radicals
Cancer is a debilitating disease on its own and is a global medical disease that has tormented medical professionals for decades. To add fuel to the fire, Cancer becomes a systemic disease when new studies reveal heart damage caused by Cancer and Cancer treatments. Studies done on fruit flies and mice reveal the role of free radicals in cardiac dysfunction. These molecules called free radicals interact with specific cells in hearts which cause a decrease in the heart’s blood pumping capabilities.
Firstly, What are Free Radicals?
In chemistry, a free radical is an atom, molecule or ion that has at least one unpaired valence electron. This makes them highly chemically reactive.
In medicine, free radicals are unstable atoms that can damage cells, causing illness and ageing. They are highly reactive unstable molecular fragments that alter DNA creating mutant cells that proliferate out of control causing tumours throughout the body and bulges inside artery walls. In a way it is a double-edged sword as free radicals can be both toxic and beneficial compounds and can help or harm the body. The latter will be outlined in this article.
The study involved adding different types of antioxidants to food consumed by fruit flies with tumours which reversed the heart damage caused. This finding suggested that harm caused by free radicals was the likely link between cancer and cardiac dysfunction. Furthermore , the thread connecting cancer is heart damage also relates to the toxic effects of chemotherapy (a common treatment for cancer).
Mechanism: How do they attack?
Tumour suppressor genes are proteins that regulate a cell during cell division and replication. When a tumour suppressor gene is mutated by free radicals, the cell it used to regulate proliferates out of control, leading (a) to the growth and development of cancers; and (b) to abnormal growth and swelling between the endothelium lining and smooth muscle wall of arteries, which growths structurally resemble benign tumours. Free radical exposure precedes both cancer and atherosclerosis.
The study further revealed that an estimated 50 to 80% of cancer patients develop the muscle wasting condition called cachexia, which can lead to heart failure, and radiation and chemotherapy treatments are associated with toxicity-related damage to the heart muscle.
The research: A peek inside their brain
In fruit flies, the team overexpressed cancer-causing genes to trigger development of tumours in the flies' eyes. The scientists observed significantly lower ejection fraction and fractional shortening -- similar to what was seen in mice with tumours -- as well as an increase in heart rate in flies with tumours.
The researchers found a total-body increase in the rate of production as well as a higher total number of free radicals -- also known as reactive oxygen species -- in fruit flies with tumours compared to controls. The rate of reactive oxygen species production was also significantly higher in mice with tumours compared to controls.
To test whether supplements could reverse the tumour-related heart damage, four antioxidants were added to the fruit flies' food for seven days: Glutathione (GSH), vitamin E, CoQ10 or vitamin C.
Results showed that all but vitamin C restored the flies' cardiac function to normal levels.
Though this research zeroed in on one cancer-causing gene to study the mechanism of heart damage in fruit flies, the researchers initially tested the effects of several cancer-causing genes in the flies. The heart function affected and the intensity of the effects on the heart varied, depending on the gene.
Well, How do we protect ourselves?
Free radicals attack the smooth muscles in arteries. These attacks create mini-tumors within arterial walls. As each tumour grows, a tiny tear develops in the endothelium. The blood’s coagulation mechanism responds by depositing fibrin, a clotting protein that retracts to stop the loss of blood. This rough scab-like structure becomes a matrix that traps calcium, heavy metals, macrophages, and cellular debris. To prevent obstruction from additional debris becoming trapped in the burgeoning atherosclerotic matrix, the body covers it over with a smooth layer of cholesterol. Note that cholesterol is the last substance laid down in the arterial plaque and not the first. This outer layer of cholesterol tends to become oxidised from further free radical attack. Cholesterol thus appears to serve a dual protective role: (1) to improve blood flow by adding a smooth surface to the damaged arterial wall; and (2) to prevent free radicals from causing further damage to the artery itself.
Role of Antioxidants
Antioxidants like Vitamin E, Selenium, Manganese and Zinc have their role against these free radicals. They often act as free radical scavengers. These are enzymes produced by the body that act to neutralise as many free radicals as possible before they cause any harm. For example, Catalase breaks down hydrogen peroxide, glutathione peroxidase neutralises other peroxides, and superoxide dismutase (SOD) neutralises superoxide.
In conclusion, due to our modern lifestyle, these free radicals are running rampant in our body and are due to harm them in many ways. Fortunately, new genetic studies are being conducted and animal models created to control these highly reactive molecular fragments. This further leads to an insight of finding new and effective ways to treat cancer as this article subtly highlights the harm of chemotherapy.
Written by: Svasti Tewari
Bibliography:
D, R. (no date) Antioxidant therapy to protect against free radical damage implicated in coronary heart disease and cancer, OSP Journal of Health Care and Medicine. Open Scientific Publishers. Available at: https://www.ospublishers.com/Antioxidant-Therapy-to-Protect-Against-Free-Radical-Damage-Implicated-in-Coronary-Heart-Disease-and-Cancer.html (Accessed: December 26, 2022).
Maxwell, S.R. and Lip, G.Y. (1997) Free radicals and antioxidants in cardiovascular disease, British journal of clinical pharmacology. U.S. National Library of Medicine. Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2042858/ (Accessed: December 26, 2022).
Comments