Kyle J. Norton
Liver toxicity is a condition in which the liver is damaged due to an overdose of medicine or harmful substances.
In the US, the most common causes of liver toxicity are the results of the most common drug-induced liver injury including overdoses of acetaminophen.
Believe it or not, antibiotics are the class of drugs most commonly causing liver toxicity.
The liver is the largest internal organ that processes the function to filter out blood from the digestive tract before passing it to other parts of the body. Furthermore, the liver also produces cholesterol in a moderate amount which aids the digestive system in absorbing nutrients builds a strong cell wall, and produces vitamin D and steroid hormones.
However, overexpression in most cases caused by injection of fat from the dietary source can lead to plaque accumulating on the wall of the artery, leading to an increased risk of heart disease and stroke.
Liver damage can be hepatocellular caused by direct hepatotoxicity, or innate and adaptive immune responses, and cholestatic caused most commonly by the drug or the drug metabolite, or mixed.
Liver damage can lead to reduced function of liver hepatobiliary transporter systems that affect the bile formation and secretion of cholephilic substances and xenobiotics.
Acute liver toxicity can be cured if the cause is found. However, damage to the liver in some cases can be permanent, inducing the formation of irreversible scarring of liver tissue.
The most common symptoms of liver toxicity are jaundice, persistent itching, and abdominal pain.
Some patients may also experience symptoms of pain in the upper right portion of the abdomen fatigue, loss of appetite accompanied by gastrointestinal discomforts.
If you have some of the above symptoms, please check with your doctor to rule out the possibility.
Betanin is phytochemicals in the class of red and yellow indole-derived pigments of Betacyanins, belonging to the group of Betalains, found abundantly in beets, chard, etc.
With an aim to find a potential ingredient for the prevention of liver injury, researchers examined the protective effect of betanin (from natural pigments) against paraquat-induced liver injury in Sprague-Dawley rats.
Selected rats induced liver toxicity intraperitoneally, were randomly divided into four groups: a control group, a paraquat group, and two groups that received betanin at doses of 25 and 100mg/kg/day three days before and two days after they were administered paraquat.
Rats injected with paraquat showed a significant liver injury observed by the elevated levels of liver oxidative stress markers including serum aspartate aminotransferase and alanine aminotransferase levels.
Furthermore tested rats also led to oxidative stress, liver toxicity observed by the increased levels of increase of cytochrome P450 3A2 mRNA expression and histological changes of mitochondria, including mitochondrial damage, indicated by mitochondrial membrane swelling.
Moreover, the levels of protein-associated liver cell death also increased compared to the reduced mitochondrial cytochrome C due to cytochrome c release.
Administration of betanin inhibited the pathological damage and all of the above-mentioned markers.
In other words, paraquat rats treated with betanin showed lesser pathological damage compared to those of the untreated groups.
Based on the findings, researchers wrote, " Betanin had a protective effect against paraquat-induced liver damage in rats".
In order to reveal additional information about betanin anti-liver toxicity, scientists assessed whether betanin (a natural pigment) is able to mitigate some OPs-induced hepatotoxicity in primary rat hepatocytes.
According to the tested assays from observation of mitochondrial depolarization as toxicity markers., administration of betanin (25μM) in tested rats significantly increased cell viability, inhibited the ROS formation and LPO, restored the levels of the cellular antioxidant glutathione (GSH) produced by the host.
Furthermore, followed by the treatment of chlorpyrifos (CPF) (300μM), diazinon (DZN) (600μM) and dichlrovos (DDVP) (400μM) treatment, betanin exerted strongly mitochondrial protection against liver toxicity.
Collectively, Dr. Ahmadian E, the lead scientist said, "potential protective role of betanin in OPs-induced hepatotoxicity in which the mechanism appears to be inhibition of ROS formation and mitochondrial protection".
Taken altogether, betanin may be considered a supplement for the prevention and treatment of liver toxicity, pending the confirmation of a larger sample size and multicenter human study.
Intake of betanin in the form of supplements should be taken with extreme care to prevent overdose acute liver toxicity.
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Author Biography
Kyle J. Norton (Scholar, Master of Nutrition, All rights 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.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for Shorty Award over last 4 years
Some articles have been used as references in medical research, such as the international journal Pharma and Bioscience, ISSN 0975-6299.
Sources
(1) Betanin attenuates paraquat-induced liver toxicity through a mitochondrial pathway by Han J1, Zhang Z2, Yang S2, Wang J2, Yang X2, Tan D. (PubMhttps://www.ncbi.nlm.nih.gov/pubmed/24799198ed)
(2) Betanin reduces organophosphate induced cytotoxicity in primary hepatocyte via an anti-oxidative and mitochondrial dependent pathway by Ahmadian E1, Khosroushahi AY2, Eghbal MA, Eftekhari A. (PubMed)
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