Wednesday 11 December 2019

Cranberry Inhibited Oxidation Induced Liver Mitochondrial Damage

By Kyle J. Norton

The liver is the largest internal organ located in the upper right portion of the abdomen, beneath your diaphragm and above your stomach.

The liver not only plays a critical role to filter the blood coming from the intestine before passing them to other parts of the body but also protects our body against toxin by detoxifying chemicals and metabolizes drugs.

Additionally, the liver also inhibits oxidative stress by producing the antioxidant enzyme that counters the expression of free radicals in the body.

Mitochondria are power generators of the cell found abundantly in the liver and play a critical role in converting oxygen and nutrients to power the cell's metabolisms.

In other words, mitochondria convert nutrients from the cell into energy for cell functioning.

Mitochondrial permeability transition (MPT) and the mitochondrial generation of oxidative stress have been found to initiate hepatic mitochondrial dysfunction caused by hepatocellular necrosis and apoptosis.

 Liver mitochondrial damage has been found to orchestrate the symptoms, jaundice, vomiting, weakness, low blood sugar levels and sleepiness and an increased amount of lactic acid in the blood.

Cranberry is an evergreen dwarf shrub, genus Vaccinium, belongings to the family Ericaceae, native to Northern America and Southern Asia. Because of its health benefits, cranberry has been cultivated in some parts of the world for commercial profit and used in traditional and herbal medicine to treat wounds, urinary disorders, diarrhea, diabetes, stomach ailments, and liver problems.

On finding a potential compound for the treatment of diseases associated with oxidative stress, researchers investigated the cranberry flavonoids prevent toxic rat liver mitochondrial damage.

The study included rat induced mitochondrial damage by chronic carbon tetrachloride-induced intoxication.

According to the tested analysis, the treatment of cranberry flavonoids (7 mg/kg) protected the liver mitochondrial damage by inhibiting the fragmentation, rupture and local loss of the outer mitochondrial membrane.

Moreover, cranberry flavonoids also acted as free radical scavengers that inhibit oxidative stress in inducing liver mitochondrial damage by effectively scavenged nitric oxide (IC50  = 4.4 ± 0.4 µg/ml), superoxide anion radicals (IC50  = 2.8 ± 0.3 µg/ml) and hydroxyl radicals (IC50  = 53 ± 4 µg/ml).

In liposomal membranes and glutathione oxidation in liver erythrocytes, flavonoids isolated from cranberry exerted some protective activity against lipid peroxidation induced by UV irradiation or organic hydroperoxides.

Based on the findings, researchers wrote, "The hepatoprotective potential of cranberry flavonoids could be due to specific prevention of rat liver mitochondrial damage. The mitochondria-addressed effects of flavonoids might be related both to radical-scavenging properties and modulation of various mitochondrial events".

Taken altogether, cranberry combined with other herbal medicine for the protection of liver mitochondrial damage, pending to the confirmation of the larger sample size and multicenter human study.

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Author Biography
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.,.
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 international journal Pharma and Bioscience, ISSN 0975-6299.

Sources
(1) Cranberry flavonoids prevent toxic rat liver mitochondrial damage in vivo and scavenge free radicals in vitro by Lapshina EA1, Zamaraeva M2, Cheshchevik VT1, Olchowik-Grabarek E2, Sekowski S2, Zukowska I2, Golovach NG1, Burd VN1, Zavodnik IB. (PubMed)

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