Search Term: " Miochondrion "
4 matching the search criteria.
Scientists Say: Mitochondrion
May 27, 2017 07:14 PM
Author: Darrell Miller
Subject: Scientists Say: Mitochondrion
Mitochondria are crucial parts of cells, performing the integral function of glucose to ATP conversion, which provides energy for the function of the entire cell. They are found in the majority of cells, and they uniquely possess DNA, making them more complex than most other cellular structures. One theory behind mitochondrial DNA is that mitochondria originated from a living bacteria that lived with cells, and eventually joined together as a single unit. Mitochondria are an important identifying aspect of a cell, and are commonly regarded as a cell's most significant cellular structure.
Read more: Scientists Say: Mitochondrion
Benefits of L-Carnitine
February 12, 2006 03:24 PM
Author: Darrell Miller
Subject: Benefits of L-Carnitine
| Benefits |
Helps the body burn fat for energy*
L-Carnitine promotes energy production in cells by transporting fatty acids into the mitochondrion. Its primary function is to transfer long-chain fatty acids across the inner mitochondrial membrane. Fatty acid molecules are activated to coenzyme A (CoA) esters in the cytoplasm of the cell, and then esterified to L-Carnitine. The combination of a fatty acid molecule and L-Carnitine is called “acyl-carnitine.” Much of the body's L-Carnitine content is stored in the form of acyl-carnitine.1
The mitochondrion is the cell’s energy-generating furnace. Called an “organelle,” the mitochondrion is a self-contained structure inside the cell. Like all cellular structures, the mitochondrion is surrounded by a membrane. This membrane is an impenetrable barrier to acyl-CoA esters; passage across the membrane requires L-Carnitine as a transporter. On the inside of the mitochondrial membrane, the acyl-CoA esters are made available to be metabolized through the process of beta oxidation. One of the key metabolic byproducts of this process is acetyl-CoA, also called “active acetate,” which enters the Krebs cycle (also known as the “citric acid cycle”) to supply fuel for production of ATP, the cell’s primary energy “currency.” L-Carnitine shuttles excess fatty acid residues out of the mitochondrion, and in this role is essential for preventing toxic buildup of fatty acids inside the mitochondrion.
Evidence suggests that L-Carnitine and short chain acyl-carnitine esters can protect the mitochondrion from adverse effects of drugs and toxic chemicals. L-Carnitine has been shown to protect animals form cardiotoxins and decrease mortality rate in animals with diphtheria, due to this cardioprotective effect.2
Helps maintain a healthy heart and cardiovascular system*
Muscle tissue contains a high concentration of L-Carnitine. With its constant energy needs, heart muscle tissue is especially rich in L-Carnitine. If the body’s ability to biosynthesize L-Carnitine is compromised, energy production in muscle tissue is impaired, and a toxic buildup of fatty acids can occur.3 Defective production of L-Carnitine by the body can result from a variety of factors, including kidney or liver malfunction, increased catabolism or the inability of tissues to extract and retain L-Carnitine from the blood.
Along with glucose and lactate, fatty acids are the primary oxidation fuel for the heart. A considerable amount of scientific data from animal experiments indicates that L-Carnitine protects the heart under conditions of hypoxia, or low oxygen. In addition to the oxidation of fat for energy in the cell, L-Carnitine is involved in the metabolism of glucose.4 Evidence of L-Carnitine’s role in glucose metabolism was uncovered in a small trial on 9 diabetic individuals. Given intravenously, L-Carnitine improved insulin-mediated glucose utilization and insulin sensitivity.5
Depletion of the body’s L-Carnitine supply is linked to various abnormal states, especially of the heart muscle. The effect of L-Carnitine on hypoxic (oxygen-starved) isolated heart muscle tissue has been studied.6 At high concentrations, L-Carnitine demonstrates a clear-cut ability to potentiate the contractility of isolated heart muscle tissue, indicating the L-Carnitine has a strengthening effect on the heart. L-Carnitine has been shown to improve the performance of rats subjected to fatigue test.
Research has revealed that in animals and humans with defective heart muscle, the amount of free L-Carnitine (not bound to fatty acids) is reduced. Administration of L-Carnitine to hamsters prevents damage to the heart muscle. Given to humans with angina, L-Carnitine was found to improve exercise tolerance. In a small study, patients with congestive heart failure showed gains in heart function with oral consumption of L-Carnitine, reportedly by restoring normal oxidation of fatty acids.7 In heart valve replacement patients, L-Carnitine has been shown to increase the valve tissue levels of ATP, pyruvate and creatine phosphate, which are key cellular energy substrates. In a controlled study, L-Carnitine was administered to 38 patients prior to open heart surgery. Prior to surgery, heart circulatory function, as assessed by measurements of hemodynamics, was “good” in all 38. While there was evidence of a “preserving” effect of L-Carnitine on heart cells, no differences in cardiac performance were observed. These results suggest that noticeable improvements in heart muscle performance with L-Carnitine are most likely to occur in people with compromised hearts.8
It has been suggested that L-Carnitine favorably influences blood lipids. Preliminary evidence of this was seen in a small open trial on 26 patients who took 3 grams of L-Carnitine daily for 40 days. Blood levels of cholesterol and triglycerides dropped substantially, while the ratio of total to HDL cholesterol–– a known marker of cardiovascular health––markedly improved.9
While L-Carnitine is not a treatment for heart disease, (nor should it be used as a substitute for medical treatment) the results of these and other studies suggest that oral consumption of L-Carnitine has a beneficial influence on maintaining a healthy heart and cardiovascular system.
Suggested Adult Use: Take 1 to 4 capsules daily without food.
L-Carnitine is considered to be very safe for oral consumption. L-Carnitine is generally well tolerated, even at doses as high as 15 grams daily. Toxicity or overdosage has not been reported.10
1. Wagenmakers, A. L-Carnitine supplementation and performance in man. Brouns, F. ed. Advances in Nutrition and Top Sport. Med Sport Sci. Basel, Karger, 1991;32:110-27.
2. Arrigoni-Martelli, E., Caso, V. Carnitine protects mitochondria and removes toxic acyls from xenobiotics. Drugs Exptl. Clin. Res. 2001;27(1):27-49)
3. Pepine, C.J. The therapeutic potential of carnitine in cardiovascular disorders. Clinical Therapeutics 1991;13(1):2-21.
4. Calvani, M., Reda, E., Arrigoni-Martelli, E. Regulation by carnitine of myocardial fatty acid and carbohydrate metabolism under normal and pathological conditions. Basic Research in Cardiology 2000;95(2):75-83.
5. Capaldo, B. et al. Carnitine improves peripheral glucose disposal in non-insulin-dependent diabetic patients. Diabetes Research and Clinical Practice 1991;14:191-96.
6. Fanelli, O. Carnitine and acetyl-carnitine, natural substances endowed with interesting pharmacological properties. Life Sciences 1978;23:2563-2570.
7. Kobayashi, A., Masumura, Y., Yamazaki, N. L-Carnitine treatment for congestive heart failure-experimental and clinical study. Japanese Circulation Journal 1992;56:86-94.
8. Pastoris, O. et al. Effect of L-Carnitine on myocardial metabolism: results of a balanced, placebo-controlled, double-blind study in patients undergoing heart surgery. Pharmacological Research 1998;37(2):115-22.
9. Pola, P. et al. Carnitine in the therapy of dyslipidemic patients. Current Therapeutic Research 1980;27(2):208-16.
10. L-Carnitine. PDR for Nutritional Supplements. First Ed. 2001.Montvale, NJ:Medical Economics.
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Benefits of Acetyl-L-Carnitine
February 12, 2006 01:55 PM
Author: Darrell Miller
Subject: Benefits of Acetyl-L-Carnitine
| Benefits |
Supports cognitive function*
ALC has been studied for its effect on cognitive performance and emotional health in the elderly. In a single-blind, placebo-controlled trial, 481 elderly subjects exhibiting mild memory impairment improved their scores on a memory test after taking 1500 mg of ALC a day for 90 days.2 Hospitalized elderly people taking ALC have shown improvements in mental outlook.3 While ALC is not a treatment or cure for Alzheimer's disease, double-blind studies suggest it may help slow the rate at which early-stage Alzheimer's patients deteriorate.4 In particular, ALC seems to benefit short-term memory in these patients.5
Supports biosynthesis of acetylcholine, a key neurotransmitter for brain and nerve function* Brain function requires coordinated communication between brain cells. Brain and nerve cells ("neurons") communicate across tiny cell-to-cell gaps called "synapses." The passage of an electrical impulse from one neuron to the next requires a "neurotransmitter." When an electrical signal arrives at the synaptic junction, the neuron releases a neurotransmitter into the synapse. The neuron on the other side of the synapse contains receptors for the neurotransmitter; these receptors bind the neurotransmitter, triggering a series of chemical events that sends a new electrical signal down the membrane of the receiving neuron. Neurotransmitters work together like an orchestra to transmit information throughout the brain and nervous system. Acetylcholine is the most abundant neurotransmitter in the body, regulating activities of vital organs, blood vessels and communication between nerves and muscles. In the brain, acetylcholine helps facilitate memory and learning as well as influence emotions. ALC is structurally similar to acetylcholine, and brain neurons stimulated by acetylcholine are receptive to stimulation by ALC.6 It has been shown experimentally that ALC supplies acetyl groups for the biosynthesis of acetylcholine.7 ALC's hypothesized cholinomimetic (acts like acetylcholine) activity has led researchers to investigate its effects on mental function and emotional health.8
Helps supply the brain with energy by improving energetics in the mitochondrion*
The acetyl groups donated by ALC can be used to synthesize acetyl-CoA, the key substrate for energy metabolism in the mitochondrion. 9 Acetyl-CoA enters the Krebs cycle, the mitochondrial mechanism that generates cellular energy in the form of ATP. ALC easily crosses the blood-brain barrier, allowing it to play various roles in maintaining brain neuron (nerve cell) function. When given by oral administration, the concentration of ALC is increased in the blood and cerebrospinal fluid.10
Stabilizes intracellular membranes*
ALC was found to improve membrane phospholipid metabolism in early-stage Alzheimer's patients.11 Phospholipids are structural components of brain cell membranes that regulate neuron function. ALC donates acetyl groups that can be used to modify the functional activity of proteins in neuronal membranes.12 ALC thus plays a role in maintaining membrane function. ALC also increases membrane stability and structural integrity.13
Increases nerve growth factor production*
The body produces various specialized proteins called "growth factors" which are essential to growth and repair of tissue. Nerve Growth Factor (NGF) protects neurons from death, prolonging survival of neurons in both the central and peripheral nervous systems. It is theorized that aging of the central nervous system is associated with a loss of NGF. ALC has shown the ability to reverse age-related decrease in the binding of NGF to its receptors in neuron membranes.14 Given to aged rats, ALC increases the level and utilization of NGF in the rats. ALC protects cholinergic neurons (nerve cells stimulated by acetylcholine) in rats from degeneration due to lack of NGF.15 These results, together with other data from animal studies, suggest that ALC positively influences NGF activity.16
Has a protective influence on brain neurons*
Several animal studies have revealed that ALC exerts a protective effect on neurons. In one experiment, brain cells from rats exposed to NMDA, a known neurotoxin, were protected by being simultaneously exposed to ALC.17 Rats injected with ALC were protected from mortality caused by the neurotoxin MPP+.18 ALC has been shown to raise levels of glutathione, a highly valuable antioxidant, in isolated mouse brain tissue.19 ALC prevents buildup of malondyhaldeyde, a marker of lipid peroxidation.20 ALC is also a chelator of iron, which can generate free radicals. It also reinforces antioxidant mechanisms in the brain.21 As a whole, data from test tube and animal studies, showing that ALC has a protective, restorative effect on brain neurons and neuronal energetic processes, suggest that ALC is an anti-aging nutrient for the brain. This hypothesis is supported by human studies demonstrating measurable benefits for brain function in elderly persons taking ALC by oral consumption.
Suggested Adult Use: 1 to 4 capsules daily.
ALC is considered safe and well-tolerated when consumed orally. ALC has been administered in doses as high as 3 grams per day for periods of two to six months, with no reports of serious side effects. Some patients have experienced occasional mild abdominal discomfort, nausea, skin rash, restlessness, vertigo and headache. The severity and incidence of these side effects are reported as minor.22
1. Pettegrew, JW, Levine, J, McClure, RJ. Acetyl-L-carnitine physical-chemical, metabolic, and therapeutic properties: relevance for its mode of action in Alzheimer's disease and geriatric depression. Molecular Psychiatry 2000;5:616-32.
2. Salvioli, G. Neri , M. L-acetylcarnitine treatment of mental decline in the elderly. Drugs Exptl. Clin. Res. 1994; 20(4):169-76.
3. Tempesta, E, et al. L-acetylcarnitine in depressed elderly subjects. A cross-over study vs. placebo. Drugs Exptl. Clin. Res. 1987;8(7):417-23.
4. Spagnoli, A et al. Long-term acetyl-L-carnitine treatment in Alzheimer's disease. Neurology 1991;41:1726-32.
5. Rai, G et al. Double-blind, placebo-controlled study of acetyl-L-carnitine in patients with Alzheimer's dementia. Curr. Med Res. Opin. 1990;11:638-47.
6. Falchetto, S, Kato, G, Provini, L. The action of carnitines on cortical neurons. Can J Physiol Pharmacol 1971; 49(1):1:7.
7. Dolezal, V., Tucek, S. Utilization of citrate, acetylcarnitine, acetate, pyruvate and glucose for the synthesis of acetylcholine in rat brain slices. J Neurochem 1981;36(4):1323.30.
8. Passeri, M, et al. Mental impairment in aging: selection of patients, methods of evaluation and therapeutic possibilities of acetyl-L-carnitine. Int. J. Clin. Pharm. Res. 1988;8(5):367-76.
9. Pettegrew, JW, Levine, J, McClure, RJ. Acetyl-L-carnitine physical-chemical, metabolic, and therapeutic properties: relevance for its mode of action in Alzheimer's disease and geriatric depression. Molecular Psychiatry 2000;5:616-32.
10. Parnetti, L, et al. Pharmacokinetics of IV and oral acetyl-L-carnitine in multiple dose regimen in patients with senile dementia of Alzheimer type. Eur. J. Clin Pharmacol 1992;42:89-93.
11. Pettegrew, JW, et al. Clinical and neurochemical effects of acetyl-L-carnitine in Alzheimer's disease. Neurobiology of Aging 1995;16(1):1-4.
12. Pettegrew, JW, Levine, J, McClure, RJ. Acetyl-L-carnitine physical-chemical, metabolic, and therapeutic properties: relevance for its mode of action in Alzheimer's disease and geriatric depression. Molecular Psychiatry 2000;5:616-32.
13. Arduni, A, et al. Effect of L-carnitine and acetyl-L-carnitine on the human erythrocyte membrane stability and deformability. Life Sci 1990;47(26):2395-2400.
14. Taglialatela, G, et al. Stimulation of nerve growth factor receptors in PC12 by acetyl-L-carnitine. Biochem Pharmacol 1992;44(3):577-85.
15. Taglialatela, G, et al. Acetyl-L-carnitine treatment increases nerve growth factor levels and choline acetyltransferase activity in the central nervous system of aged rats. Exp Gerontol 1994;29(1):55-56.
16. Pettegrew, JW, Levine, J, McClure, RJ. Acetyl-L-carnitine physical-chemical, metabolic, and therapeutic properties: relevance for its mode of action in Alzheimer's disease and geriatric depression. Molecular Psychiatry 2000;5:616-32.
17. Forloni, G, Angeretti, N, Smiroldo, S. Neuroprotective activity of acetyl-L-carnitine: studies in vitro. J Neurosci Res 1994;37(1):92-6.
18. Steffen, V, et al. Effect of intraventricular injection of 1-methyl-4-phenylpyridinium: protection by acetyl-L-carnitine. Hum Exp Toxicol 1995;14(11):865-71.
19. Fariello, RG, et al. Systemic acetyl-L-carnitine elevates nigral levels of glutathione and GABA. Life Sci 1988;43(3):289-92.
20. Calvani, M, et al. Action of acetyl-L-carnitine in neurodegeneration and Alzheimer's disease. Ann Ny Acad Sci 1992;663:483-86.
21. Calvani, M, Carta, A. Clues to the mechanism of action of acetyl-L-carnitine in the central nervous system. Dementia 1991;2:1-6.
22. Zdanowicz, M. Acetyl-L-carnitine's healing potential. Continuing Education Module. New Hope Institute of Retailing. October, 2001.
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Benfotiamine raises the blood level of thiamine pyrophosphate (TPP)
August 02, 2005 03:52 PM
Author: Darrell Miller
Subject: Benfotiamine raises the blood level of thiamine pyrophosphate (TPP)
Benfotiamine raises the blood level of thiamine pyrophosphate (TPP), the biologically active co-enzyme of thiamine.4
Thiamine and its Co-enzyme, TPP
Thiamine (vitamin B1) plays an essential part in the metabolism of glucose, through actions of it co-enzyme TPP (thiamine pyrophosphate). TPP is formed by the enzymatically-catalyzed addition of two phosphate groups donated by ATP to thiamine. TPP also goes by the name "thiamine diphosphate." In the cytoplasm of the cell, glucose, a 6-carbon sugar, is metabolized to pyruvic acid, which is converted into acetyl-CoA, otherwise known as "active acetate." Acetyl CoA enters the mitochondrion, where it serves as the starting substrate in the Kreb’s cycle (citric acid cycle). The Krebs cycle is the primary source of cellular metabolic energy. TPP, along with other co-enzymes, is essential for the removal of CO2 from pyruvic acid, which in turn is a key step in the conversion of pyruvic acid to acetyl CoA. CO2 removal from pyruvic acid is called "oxidative decarboxylation," and for this reason, TPP was originally referred to as "cocarboxylase." TPP is thus vital to the cell’s energy supply. Benfotiamine helps maintain healthy cells in the presence of blood glucose. Acting as a biochemical "super-thiamin," it does this through several different cellular mechanisms, as discussed below.
Benfotiamine and Glucose Metabolism Benfotiamine normalizes cellular processes fueled by glucose metabolites.
As long as glucose remains at normal levels, excess glucose metabolites do not accumulate within the cell. The bulk of the cell’s glucose supply is converted to pyruvic acid, which serves as substrate for production of acetyl CoA, the primary fuel for the Krebs cycle. Of the total amount of metabolic energy (in the form of ATP) released from food, the Krebs cycle generates about 90 percent.5 In the presence of elevated glucose levels, the electron transport chain, the final ATP-generating system in the mitochondrion, produces larger than normal amounts of the oxygen free radical "superoxide." This excess superoxide inhibits glyceraldehyde phosphate dehydrogenase (GAPDH), as key enzyme in the conversion of glucose to pyruvic acid, resulting in an excess of intermediate metabolites known as "triosephosphates." Increase triosephophate levels trigger several cellular mechanisms that result in potential damage to vascular tissue. Cells particularly vulnerable to this biochemical dysfunction are found in the retina, kidneys and nerves.
Benfotiamine has been shown to block three of these mechanisms: the hexosamine pathway, the diaglycerol-protein kinease C pathway and the formation of Advanced Glycation End-poducts. As discussed below, benfotiamine does this by activating transketolase, a key thiamin-dependent enzyme.6 Benfotiamine stimulates tranketolase, a cellular enzyme essential for maintenance of normal glucose metabolic pathways.* Transketolase diverts the excess fructose-6-phosphate and glyceraldehydes-3-phosphate, (formed by the inhibition of GAPDH, as mentioned above), into production of pentose-5-phosphates and erythrose-4-phosphate and away from the damaging pathways. Benfotiamine activates transketolase activity in bovine aortic endothelial cells incubated in glucose.6 To test benfotiamine’s ability to counteract these metabolic abnormalities caused by elevated blood glucose, studies have been done in diabetic rats. Benfotiamine increases transketolase activity in the retinas of diabetic rats, while concomitantly decreasing hexosamine pathway activity, protein kinase C activity and AGE formation.6
Benfotiamine and Protein glycation Benfotiamine controls formation of Advanced Glycation End-products (AGEs).
AGEs have an affinity for proteins such as collagen, the major structural protein in connective tissue. AGEs are formed through abnormal linkages between proteins and glucose. This occurs via a non-enzymatic glycosylation reaction similar to the "browning reaction" that takes place in stored food.7 At high glucose concentrations, glucose attaches to lysine, forming a Schiff base, which in turn forms "early glycosylation products." Once blood glucose levels return to normal levels, the amount of these early glycosylation products decreases, and they are not particularly harmful to most tissue proteins. On long-lived proteins such as collagen, however, early glycosylation products are chemically rearranged into the damaging Advanced Glycation End-products. AGE formation on the collagen in coronary arteries causes increased vascular permeability. This vessel "leakiness" allows for abnormal cross-linking between plasma proteins and other proteins in the vessel wall, comprising vascular function and potentially occluding the vessel lumen. A number of other potentially harmful events may also occur, including production of cytokines that further increase vascular permeability. Endothelin-1, a strong vasoconstrictor, is over produced, increasing the possibility of thrombosis and generation of oxygen free radicals is stimulated.8 It is vitally important to support normal glucose metabolic pathways so that formation of AGEs is minimized. Benfotiamine, in the test tube (in vitro) prevents AGE formation in endothelial cells cultured in high glucose by decreasing the glucose metabolites that produce AGEs.9 Endothelial cells make up the membranes that line the inner walls of organs and blood vessels. In a rat study comparing the effects of Benfotiamine with water-soluble thiamin, Benfotiamine inhibited AGE formation in diabetic rats while completely preventing formation of "glycooxidation products," which are toxic by products of chronic elevated blood glucose. AGE levels were not significantly altered by thiamin.10 Benfotiamine also normalized nerve function in the animals. After three months of administration, "nerve conduction velocity (NCV)," a measure of nerve function, was increased by both benfotiamine and thiamin; at six months, NCV was normalized by benfotiamine, whereas thiamin produced no further increases in this parameter.
Dysfunctional glucose metabolic pathways leading to AGE formation occurs in endothelial cells of the kidneys. In a recent animal study, benfotiamine was administered to rats with elevated glucose levels. Benfotiamine increased transketolase activity in the kidney filtration system of these rats, while at the same time shifting triosephophates into the pentose pathway and preventing protein leakage.11
Benfotiamine has an excellent tolerability profile and can be taken for long periods without adverse effects.3,12 The statements in this fact sheet have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.
1. Bitsch R, Wolf M, Möller J. Bioavailability assessment of the lipophilic benfotiamine as compared to a water-soluble thiamin derivative. Ann Nutr Metab 1991;35(2):292-6.
2. Schreeb KH, Freudenthaler S, Vormfelde SV, et al. Comparative bioavailability of two vitamin B1 preparations: benfotiamine and thiamine mononitrate. Eur J Clin Pharmacol 1997; 52(4):319-20.
3. Loew D. Pharmacokinetics of thiamine derivatives especially of benfotiamine. Int J Clin Pharmacol Ther 1996;34(2):47-50.
4. Frank T, Bitsch R, Maiwald J, Stein G. High thiamine diphosphate concentrations in erythrocytes can be achieved in dialysis patients by oral administration of benfontiamine. Eur J Clin Pharmacol. 2000;56(3):251-7.
5. Pike RL, Brown ML. Nutrition, An Integrated Approach, 3rd Ed. New York:MacMillan; 1986:467.
6. Hammes H-P, Du X, Edlestein D, et al. Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic neuropathy. Nat Med 2003;9(3):294-99.
7. Monnier VM, Kohn RR, Cerami A. Accelerated age-related browning of human collagen in diabetes mellitus. Proc Natl Acad Sci 1984;81(2):583-7.
8. Brownlee M. The pathological implications of protein glycation. Clin Invest Med 1995;18(4):275-81.
9. Pomero F, Molinar Min A, La Selva M, et al. Benfotiamine is similar to thiamine in correcting endothelial cell defects induced by high glucose. Acta Diabetol 2001;38(3):135-8.
10. Stracke H, Hammes HP, Werkman D, et al. Efficacy of benfotiamine versus thiamine on function and glycation products of peripheral nerves in diabetic rats. Exp Clin Endocrinol Diabetes 2001;109(6):300-6.
11. Babaei-Jadidi R, Karachalias N, Ahmed N, et al. Prevention of incipient diabetic nephropathy by high-dose thiamine and benfotiamine. Diabetes 2003;52(8):2110-20.
12. Bergfeld R, MatsumaraT, Du X, Brownlee M. Benfotiamin prevents the consequences of hyperglycemia induced mitochondrial overproduction of reactive oxygen specifies and experimental diabetic neuropathy (Abstract) Diabetologia 2001; 44(Suppl1):A39.
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