Cardiotoxicity is a condition caused by toxin accumulated in the heart that leads to damage to the heart muscle.
Cardiotoxicity reduced the heart pumping blood capability, leading to a decrease in oxygen-rich blood to nourish the body tissues and organs.
Most common symptoms of cardiotoxicity, are tiredness fatigue, chronic cough, water retention and shortness of breath.
If you have experienced some of the aforementioned symptoms that can be healed within a week or 2, please check with your doctor to rule out the possibility.
Most common causes of cardiotoxicity are associated with patients receiving chemotherapy and intake of certain medications. However, infection, excessive alcohol consumption, medical condition such as diabetes and thyroid disease, high blood pressure and thiamine and Vitamin B deficiency have also been found to induce cardiotoxicity.
Some researchers suggested that the promotion of a high-fat diet over the past few decades that facilitate widespread obesity may increase the cardiotoxicity risk of obese who are treated by chemotherapy.
Dr. Mitra MS, the lead scientist said, "Often, chemotherapy by doxorubicin (Adriamycin) is limited due to life-threatening cardiotoxicity in patients during and posttherapy. Recently, we have shown that moderate diet restriction remarkably protects against doxorubicin-induced cardiotoxicity".
And, "HFD-induced obese rats are highly sensitized to doxorubicin-induced cardiotoxicity".
In other words, non-obese patients who follow the recommended diet before taking chemotherapy are for the treatment of cancer are less sensitive to doxorubicin-induced cardiotoxicity compared to a high-fat diet obese.
Alliin (S-allyl-L-cysteine-S-oxide) is a phytochemical compound sulfoxide,. a derivative of the amino acid cysteine, belonging to the class of sulfur compounds, found abundantly in fresh garlic and onion.
With an aim to find a potential compound with cardioprotective activity, researchers examined the effect of S-allyl cysteine sulphoxide (SACS) in isoproterenol (ISO)-induced cardiotoxicity in male Wistar rats.
The study included myocardial infarction was induced by subcutaneous injection of ISO (150 mg/kg) once a day for 2 days followed by SACS (40 and 80 mg/kg) as pretreatment orally daily for a period of 35 days using an intragastric tube.
SACS pretreatment showed significantly lowered levels of free radicals and increased antioxidant activities of mitochondrial superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione S-transferase (GST), and glutathione (GSH).
Furthermore, SACS pretreatment not only decreased the levels of mitochondrial cholesterol, free fatty acids (FFAs), triglycerides (TGs) and calcium, associated with plaque accumulation and the activity of xanthine oxidase (XOD) involved the production of the free radicals in the heart, but also increased significantly the levels of mitochondrial phospholipids of the inner membrane of the heart against damage.
Moreover, pretreatment of SACS also protected the heart mitochondrial fraction by increasing the activities of isocitrate dehydrogenase (ICDH), succinate dehydrogenase (SDH), alpha-ketoglutarate dehydrogenase (alpha-KGDH), NADH-dehydrogenase, and cytochrome C-oxidase.
Interestingly, oral administration of SACS for a period of 35 days showed no cardio effect in normal control rats.
In other words, SACS modulated heart function against mitochondrial cardiotoxicity without affecting the heart function in healthy control.
Based on the findings researchers said, "The effect at a dose of SACS 80 mg/kg was more effective than the dose 40 mg/kg. The results of the study conclude that SACS protect the mitochondria of the ISO-induced myocardial-infarcted rats".
In order to know more information about SACS cardioprotective activity, researchers examined the preventive role of SACS on glycoproteins and hematology in experimentally induced myocardial infarction in rats for 2 days.
Injection of SACS restored the abnormally significant increase in the levels of serum iron, uric acid and blood glucose, Na(+) and Ca(2+) characterized by heart damage and elevated blood glucose.
Furthermore, the significant decrease in the levels of plasma iron binding capacity, serum total protein, albumin/globulin ratio, heart K(+) and heart glycogen induced by isoproterenol (ISO) associated with heart tissues damage were also inhibited by the treatment of SACS in myocardial infarcted rats.
Moreover, SACS also modulated the immune response in the production of pro-inflammatory cytokines induced by isoproterenol (ISO) toxicity.
Additional differentiation of the results suggested that oral pretreatment with SACS (40 and 80 mg kg(-1)) daily for a period of 35 days prevents cardiotoxicity by improving all the biochemical parameters studied in ISO-induced rats.
Taken altogether, alliin may be considered supplements for the prevention and treatment of cardiotoxicity, depending on the confirmation of the larger sample size and multicenter human study.
Intake of alliin in the form of supplement should be taken with extreme care to prevent overdose acute liver toxicity.
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Kyle J. Norton (Scholar, Master of Nutrition, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published online, including worldwide health, ezine articles, article base, health blogs, self-growth, best before it's news, the karate GB daily, etc.,.
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Some articles have been used as references in medical research, such as international journal Pharma and Bioscience, ISSN 0975-6299.
(1) Preventive effect of S-allyl cysteine sulphoxide (Alliin) on mitochondrial dysfunction in normal and isoproterenol induced cardiotoxicity in male Wistar rats: a histopathological study by Sangeetha T1, Darlin Quine S. (PubMed)
(2) Protective effect of S-allyl cysteine sulphoxide (alliin) on glycoproteins and hematology in isoproterenol induced myocardial infarction in male Wistar rats by Sangeetha T1, Quine SD. (PubMed)
(3) High fat diet-fed obese rats are highly sensitive to doxorubicin-induced cardiotoxicity by Mitra MS1, Donthamsetty S, White B, Mehendale HM. (PubMed)
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