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Mitochondrially targeted effects of berberine [Natural Yellow 18, 5,6-dihydro-9,10-dimethoxybenzo(g)-1,3-benzodioxolo(5,6-a) quinolizinium] on K1735-M2 mouse melanoma cells: comparison with direct effects on isolated mitochondrial fractions. Pereira GC, Branco AF, Matos JA, Pereira SL, Parke D, Perkins EL, Serafim TL, Sardão VA, Santos MS, Moreno AJ, Holy J, Oliveira PJ. J Pharmacol Exp Ther. 2007 Nov;323(2):636-49. Epub 2007 Aug 17. PMID: 17704354 doi: 10.1124/jpet.107.128017 The present work shows that berberine is accumulated by mitochondria of a mouse melanoma cell line, leading to mitochondrial fragmentation and dysfunction, accompanied by decreased cellular energy charge. When the effect was compared with the results obtained on isolated mitochondrial fractions, it is observed that regardless of the system used, berberine is toxic for mitochondria. One major limitation of the present study (as in many others) is the lack of knowledge of the real concentration of berberine that reaches mitochondria in intact cells. Although we do not possess data regarding this aspect, it is wise to speculate that mitochondrial berberine concentrations will be much higher than in the bulk cytosol due to electrophoretic accumulation. We believe that the range of berberine concentrations accumulated by mitochondria in intact cells is within the range of concentrations used on isolated mitochondrial fractions in the present study. The present work not only provides insights on the mechanism by which berberine interferes with tumor cell proliferation, demonstrating previously unknown effects on mitochondrial physiology, but also raises a note of caution on the use of berberine as a nontoxic "natural" over-the-counter medication.

"Summer vs Winter Mode: Explaining AMPK Last year I read an article which made a statement that has not left my mind. The statement went as follows: "You are only good as your mitochondria." In fact, the more a dwell into the details of human metabolism, the more I sense that this is true - especially with the metabolic syndrome. For those who are not familiar with the concept of mitochondria, they are the tiny energy factories within the cells that produce cellular energy through aerobic means (meaning oxygen). Mitochondria utilize oxygen to ultimately produce Adenosine Triphosphate or simply ATP. ATP relays energy by donating a phosphate bond resulting in Adenosine Diphosphate (ADP). Another phosphate release would entail Adenosine Monophosphate or AMP. ATP is one of the main sources of cellular energy in the body."

"Summer vs Winter Mode: Explaining AMPK Last year I read an article which made a statement that has not left my mind. The statement went as follows: "You are only good as your mitochondria." In fact, the more a dwell into the details of human metabolism, the more I sense that this is true - especially with the metabolic syndrome. For those who are not familiar with the concept of mitochondria, they are the tiny energy factories within the cells that produce cellular energy through aerobic means (meaning oxygen). Mitochondria utilize oxygen to ultimately produce Adenosine Triphosphate or simply ATP. ATP relays energy by donating a phosphate bond resulting in Adenosine Diphosphate (ADP). Another phosphate release would entail Adenosine Monophosphate or AMP. ATP is one of the main sources of cellular energy in the body

Ultrastructural changes in regressing equine sarcoid tumours--mysterious role of mitochondria. Hallamaa RE. In Vivo. 2008 Jul-Aug;22(4):519-23. PMID: 18712182

CANCER BIO-IMMUNOTHERAPY CONTINUED Its effect on inductional control, triggered by hormones and mediated by transformed mitochondria by Thomas Tallberg Synopsis of presentations at the 3rd. World Congress on Cancer Darwin 25-27th, April 1997

Cardio Defend™ Only $49/bottle - Limited Time Offer Flat Sale ONLY For Today - Special Offer Save Upto $120 + Special 71% Discount + 180 Day Money Back Guarantee CardioDefend Cardio Defend Rated FDA Approved CardioDefend Rated 5 Star Order TODAY And Save Up To $120! Save Over 71%! Cardio Defend is a dietary supplement that supports a healthy heart naturally. The lifestyle of individuals has evolved drastically, and with this evolution, mankind has seen a rise in individuals suffering from heart-related diseases. It supports healthy blood circulation and reduces blood pressure & the risk of heart disease naturally. Try CardioDefend For Over 71% OFF Today! Regular Price: $147.99/per bottle Only for: $49/per bottle Buy Cardio Defend Proven By Thousands Shannon Curry Mark Angelman Robert S Why Choose Cardio Defend? Made In The USA Made In The USA CardioDefend is manufactured on US soil. Cardio Defend 100% All Natural 100% All Natural All ingredients are pure, natural, and carefully sourced. FDA Approved Facility FDA Approved Facility CardioDefend is manufactured according to the latest standards. CardioDefend Supplement Cardio Defend Facts What is Cardio Defend? Heart disease is one of the top causes of death in the United States, but consumers continue to forgo the nourishment that they need. Even with all of the opportunities to eat better and exercise more, some people still struggle to improve their blood circulation and improve their heart health. Luckily, formulas like Cardio Defend can help a lot. CardioDefend is a dietary supplement that supports a healthy heart naturally. The lifestyle of individuals has evolved drastically, and with this evolution, mankind has seen a rise in individuals suffering from heart-related diseases. Even though exercise and healthy diets may help to reduce the risk of these conditions, they may not be 100% effective. The heart is an extremely important organ and must be taken good care of. CardioDefend naturally supports healt

Scientists have discovered the key to the ability of spicy foods to kill cancer cells. They found capsaicin, an ingredient of jalapeno peppers, triggers cancer cell death by attacking mitochondria - the cells' energy-generating boiler rooms.

Simultaneously Blocking Glycolysis and Fat Metabolism Can the use of DCA and a fatty acid metabolism blocker together force more cancer cells into using aerobic metabolism? Tim McGough used green tea extract, which contains EGCG, in his fantastic response. DCA works by reactivating mitochondria and shifts metabolism from glycolysis to glucose oxidation. Hopefully the cancer cell will then undergo apoptosis. However, cancer cells have an alternate energy source: fat metabolism. This page explores to possibility of blocking fat metabolism to help force the cell into apoptosis. Oral squamous cell carcinoma is a cancer that does not respond well to DCA. This study, Head and Neck Cancer Cell Lines Are Resistant to Mitochondrial-Depolarization-Induced Apoptosis states: "Results: ΔΨm in head and neck cell lines started to show slight loss of ΔΨm, while HL-60 showed significant loss of ΔΨm after 30 min of treatment. All cell lines demonstrated complete mitochondrial depolarization within 24 h, however, only the control cell line HL-60 underwent apoptosis. In addition, HNSCC cell lines did not demonstrate cytoplasmic cytochrome c release despite significant mitochondrial membrane depolarization, while HL-60 cell initiated apoptosis and cytochcrome c release after 24 h of treatment. Conclusions: Head and neck cancer cell lines exhibit defects in mitochondrial-membrane-depolarization-induced apoptosis as well as impaired release of cytochrome c despite significant mitochondrial membrane depolarization. Proximal defects in the mitochondrial apoptosis pathway are a feature of HNSCC.(head and neck squamous cell carcinoma)" Note that although the cell lines were depolarized, apoptosis did not occur. So I checked to see if fatty acid metabolism is used by squamous cell carcinoma.

"Susceptible strains of rodents fed high-fat diets overeat, gain fat and become profoundly insulin resistant. Dr. Jianping Ye's group recently published a paper showing that the harmful metabolic effects of a high-fat diet (lard and soybean oil) on mice can be prevented, and even reversed, using a short-chain saturated fatty acid called butyric acid (hereafter, butyrate). The butyrate-fed mice remained lean and avoided metabolic problems. Butyrate increased their energy expenditure by increasing body heat production and modestly increasing physical activity. It also massively increased the function of their mitochondria, the tiny power plants of the cell."

"Coenzyme Q10 (also known as ubiquinone, ubidecarenone, coenzyme Q, and abbreviated at times to CoQ10 - pronounced like "ko-cue-ten" -, CoQ, Q10, or simply Q) is a 1,4-benzoquinone, where Q refers to the quinone chemical group, and 10 refers to the isoprenyl chemical subunits. This oil-soluble vitamin-like substance is present in most eukaryotic cells, primarily in the mitochondria. It is a component of the electron transport chain and participates in aerobic cellular respiration, generating energy in the form of ATP. Ninety-five percent of the human body's energy is generated this way.[1][2] Therefore, those o

"Coenzyme Q10 (CoQ10) is a compound found naturally in the energy-producing center of the cell known as the mitochondria. CoQ10 is involved in the making of an important molecule known as adenosine triphosphate (ATP). ATP serves as the cell's major energy source and drives a number of biological processes including muscle contraction and the production of protein. CoQ10 also works as an antioxidant."

Vitamin C antagonizes the cytotoxic effects of antineoplastic drugs.\nHeaney ML, Gardner JR, Karasavvas N, Golde DW, Scheinberg DA, Smith EA, O'Connor OA.\nCancer Res. 2008 Oct 1;68(19):8031-8.\nPMID: 18829561

Lifestyle-induced metabolic inflexibility and accelerated ageing syndrome: insulin resistance, friend or foe? Nunn AV, Bell JD, Guy GW. Nutr Metab (Lond). 2009 Apr 16;6:16. PMID: 19371409 doi:10.1186/1743-7075-6-16

Traditional chinese medicine in treatment of metabolic syndrome. Yin J, Zhang H, Ye J. Endocr Metab Immune Disord Drug Targets. 2008 Jun;8(2):99-111. Review. PMID: 18537696 Berberine from rhizoma coptidis is an oral hypoglycemic agent. It also has anti-obesity and anti-dyslipidemia activities. The action mechanism is related to inhibition of mitochondrial function, stimulation of glycolysis, activation of AMPK pathway, suppression of adipogenesis and induction of low-density lipoprotein (LDL) receptor expression.

Neuroprotective effects of berberine on stroke models in vitro and in vivo. Zhou XQ, Zeng XN, Kong H, Sun XL. Neurosci Lett. 2008 Dec 5;447(1):31-6. Epub 2008 Sep 30. PMID: 18838103 doi:10.1016/j.neulet.2008.09.064 Findings of this study suggest that berberine protects against ischemic brain injury by decreasing the intracellular ROS level and subsequently inhibiting mitochondrial apoptotic pathway.

"5' AMP-activated protein kinase or AMPK or 5' adenosine monophosphate-activated protein kinase is an enzyme that plays a role in cellular energy homeostasis. It consists of three proteins (subunits) that together make a functional enzyme, conserved from yeast to humans. It is expressed in a number of tissues, including the liver, brain, and skeletal muscle. The net effect of AMPK activation is stimulation of hepatic fatty acid oxidation and ketogenesis, inhibition of cholesterol synthesis, lipogenesis, and triglyceride synthesis, inhibition of adipocyte lipolysis and lipogenesis, stimulation of skeletal muscle fatty acid oxidation and muscle glucose uptake, and modulation of insulin secretion by pancreatic beta-cells.[1] It should not be confused with cyclic AMP-activated protein kinase (protein kinase A), which, although being of similar nature, may have opposite effects.[2]"

Mechanisms of berberine (natural yellow 18)-induced mitochondrial dysfunction: interaction with the adenine nucleotide translocator. Pereira CV, Machado NG, Oliveira PJ. Toxicol Sci. 2008 Oct;105(2):408-17. Epub 2008 Jul 3. PMID: 18599498 doi: 10.1124/jpet.107.128017 The data from the present work appear to show that berberine also presents some degree of toxicity to "nontumor" systems, which should be carefully understood. ANT inhibition in nontumor cells by berberine would be responsible for a decrease in energy production and could also result in MPT induction. To the best of our knowledge, no full toxicity assessment exists for berberine in humans, although its use in several commercially available supplements suggests that the compound may present a relatively wide safety interval. In fact, a study with patients with congestive heart failure treated with 1.2 g/day of oral berberine revealed low toxicity and resulted into an average plasma concentration of 0.11 mg/l which would translate into 0.3µM (Zeng and Zeng, 1999Go). Repeated cumulative treatments, alternative forms of formulation (e.g., topical application vs. injection) or more importantly, active mitochondrial accumulation due to its positive charge would be expected to increase its concentration in cells into the range of concentrations used in this study. Empirical data from nontraditional medicines plus the use of extensive clinical assays would allow the use of berberine as a promising antimelanoma agent while maintaining its safety for humans. In radial/vertical forms of melanoma, a possible topical application of berberine would also be possible, thus minimizing side effects on other organs. In conclusion, the present work identifies the ANT as an important target for berberine, with clear relevance for its proposed antitumor effects.