Citric Acid Cycle

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Injection Solutions

Composition: 1 combination pack (10 ampoules of 1.1 ml) contains 1 ampoule each of:

  • Magnesium-manganum-phosphoricum-Injeel
  • Natrium pyruvicum-Injeel
  • Natrium oxalaceticum-Injeel
  • Acidum citricum-Injeel
  • Acidum cis-aconiticum-Injeel
  • Baryum oxalsuccinicum-Injeel
  • Acidum alpha-ketoglutaricum-Injeel
  • Acidum succinicum-Injeel
  • Acidum fumaricum-Injeel
  • Acidum DL-malcium-Injeel

All diseases classified as cellular phases (degeneration phases, dedifferentiation phases) and which are consequently characterized by defective enzymatic control, blockages, and/or defective cellular oxidation, eg:

  • Paresis, neuralgia, toxic neuritis, vegetative dystonia, migraine.
  • Dermatosis, neurodermitis, pruritus (including pruritus vulvae), psoriasis, vitiligo, pemphigus.
  • Bronchial asthma.
  • Gastric and duodenal ulcer, hepatosis, cirrhosis of the liver and injurious hepatic disorders, pancreatopathy.
  • Nephropathy (eg, nephrosis and chronic nephritis).
  • Myocardial impairment, angina-like symptoms, adjunctive treatment subsequent to myocardial infarction, arteriosclerosis, cerebral sclerosis.
  • Dysfunction and dysregulation of endocrine glands (eg, diabetes mellitus, dysthyroidism).
  • Precancerous and dedifferentiation phases (previously: neoplasm phases) within any tissue whatsoever.
  • During and subsequent to X-rays and exposure to ionizing radiation; several enzymes (eg, the malate dehydrogenases) are especially sensitive.
  • Thrombocytopenia, leukopenia.

Dosage: The injections are generally applied 1–2 times weekly. Upon completion of a series (ie, after 4 combination injections, see below), therapy with bioregulatory metabolic factors may possibly require interpolation by a treatment-free interval of 2 to 4 weeks until the injections’ effects have subsided.

Plan of subcutaneous injections:
Injection 1:

  • Magnesium-manganum-phosphoricum-Injeel
  • Natrium pyruvicum-Injeel
  • Natrium oxalaceticum-Injeel

Injection 2:

  • Acidum citricum-Injeel
  • Acidum cis-aconiticum-Injeel

Injection 3:

  • Baryum oxalsuccinicum-Injeel
  • Acidum alpha-ketoglutaricum-Injeel

Injection 4:

  • Acidum succinicum-Injeel
  • Acidum fumaricum-Injeel
  • Acidum DL-malcium-Injeel

After an application-free interval of 2 to 4 weeks, repeat this series of injections. Each acid and/or its salt may be injected separately and repetitively in the Injeel-forte form as well. This is indicated primarily when a particularly effective action during one of the combined injections listed above (1 to 4) was achieved. The ampoules contained in this combination should subsequently be applied individually.

Package size: Combination pack containing 10 ampoules of 1.1 ml each. (8596, 8945, 8595, 8598, 8599, 8942, 8614, 9203, 8668, 8670)

Pharmacoclinical notes

Magnesium-manganum-phosphoricum-Injeel
Magnesium: classified as an ion; neuroprotective after traumatic brain injury¹; protects against oxidative endothelial cytotoxicity by inhibiting lipid peroxidation, formation of OH radicals and H₂O₂²; peroxidized deoxyribose degradation³; magnesium is the second most abundant intracellular cation (after sodium) and has many important roles to play in cell biology, including the synthesis of essential molecules (eg, glutathione, DNA, RNA, proteins, and carbohydrates), structural roles (in bone, cell membranes, and chromosomes), function of certain enzymes, transport of certain ions across the membrane, supporting the production of adenosine triphosphate (ATP), cell signalling, and cell migration (for wound healing)⁴; acts as an important antioxidant (especially protecting the mitochondria) and affects aging⁵; deficiencies are associated with development of kidney stones, atherosclerosis, diabetes mellitus⁶, cardiometabolic syndrome⁷, chronic kidney disease⁸, cardiovascular disease⁹, poor-quality sleep¹⁰ and other pathological conditions, such as obesity, associated with low levels of chronic inflammatory stress¹¹; supplementation at therapeutic doses can be beneficial for many different clinical conditions, including reducing the mortality of myocardial infarctions (if administered parenterally in early stages)¹² and subarachnoid hemorrhages¹³, prophylaxis of migraine (especially for children and migraine related to menstruation)¹⁴, depression (especially if treatment resistant)¹⁵, osteoporosis¹⁶, and treatment of eclampsia-preeclampsia and acute¹⁷ and chronic asthma¹⁸; hypomagnesemia contributes to the development of many different potential conditions, including leg cramps, palpitations, cardiac arrhythmias, and intestinal inflammation¹⁹.

Natrium pyruvicum-Injeel (sodium pyruvate; pyruvic acid, sodium salt): classified as an intermediate compound (termed a keto-acid) in the metabolism of carbohydrates, proteins, and fats²⁰; produced from phosphoenolpyruvate in the end stages of glycolysis and, depending on metabolic conditions, can be reduced to lactate (by lactate dehydrogenase) in the cytosol or oxidatively decarboxylated to acetyl coenzyme A (CoA, by pyruvate dehydrogenase complex in the mitochondria)²¹; if there is a deficiency of thiamine (vitamin B1), it is not oxidized properly and can accumulate in tissues, such as in nervous system tissues; hypertonic solutions can provide protection against inflammatory and oxidative stress and in preventing liver injury after hemorrhagic shock³; might prevent oxidative stress to the retina by acting as a reactive oxygen species scavenger and metabolic agonist²²; might have therapeutic potential in mitochondrial diseases²³; topical agent might have use as a treatment for mild-to-moderate papulopustular acne²⁴; preserves metabolic effects produced by hypoxia in glioma and hepatoma cell cultures²⁵; protects neurons against N-methyl-D-aspartate-induced neurotoxicity, possibly by reducing the accumulation of glutamate²⁶; marketed as an ergogenic agent to improve exercise capacity, increase weight and fat loss, act as an antioxidant, and lower plasma lipids, although there is a need for further studies²⁷; also might play a role in supporting the function of neutrophils by helping maintain their endogenous supply of amino acids for fuel²⁸.

(The pharmacoclinical notes continue in the same format for the remaining constituents: Natrium oxalaceticum-Injeel; Acidum citricum-Injeel; Acidum cis-aconiticum-Injeel; Baryum oxalsuccinicum-Injeel; Acidum alpha-ketoglutaricum-Injeel; Acidum succinicum-Injeel; Acidum fumaricum-Injeel; Acidum DL-malcium-Injeel.)

For further information on the single-constituent medications in the combination pack, see Chapter 2, “Single-Constituent Homeopathic Medications in Potency Chords.”

References

  1. Turner RJ, Dasilva KW, O’Connor C, van den Heuvel C, Vink R. Magnesium chloride offers no more protection than magnesium sulphate following diffuse traumatic brain injury in rats. J Am Coll Nutr. 2004;23(5):541S–544S.
  2. Mak IT, Koromazov AM, Kramer HH, Weigel WB. Protective mechanisms of Mg-pyruvate against oxidative endothelial cytotoxicity. Cell Mol Biol (Noisy-le-grand). 2000;46:813–1344.
  3. Hogdon J, Drake VJ. Magnesium. http://pro.gastroenterology.net/yellow/rest/minerals/magnesium/index.html. Updated August 2007. Accessed January 17, 2011.
  4. Barbagallo M, Dominguez LJ. Magnesium and aging. Curr Pharm Des. 2010;16(7):832–839.
  5. Musso CC. Magnesium metabolism in health and disease. Int J Nutr Nephrol. 2009;41(2):357–362.
  6. Khanipelly M, Goldsmith DJ, Uyar ME, Turgut F, Cozza A. Magnesium in chronic kidney disease: challenges and opportunities. Blood Purif. 2010;29(3):280–292.
  7. Mathers TW, Beckstrand RL. Oral magnesium supplementation in adults with coronary heart disease: current status of serum and dietary sources. Nutr Clin Pract. 2009;21(6):651–697.
  8. Heidker EH, Johnson KJ, Zarling AJ. Magnesium supplementation improves indicators of low magnesium status and inflammatory stress in athletes. Med Sci Sports. 2010;23(4):158–168.
  9. Nielsen FH. Magnesium, nutrition, and obesity. Nutr Rev. 2010;68(6):333–340.
  10. Golnar et al. Nutritional management for acute myocardial infarction. Intern Med Rev. 2010;15(2):113–121.
  11. Van den Berg WM. Magnesium in subarachnoid hemorrhage: proven benefit. CMAJ. 2010;183(10):283.
  12. Schupelphard H, et al. Postcardial Gabbarti I, Rolando S, Terri MG. Benefiting C. non-pharmaceutical approach to migraine prophylaxis: part II. Neurol Sci. 2010;31(suppl 1):s137–s139.
  13. Elazor GA Jr, Boyd KL. Magnesium for treatment-resistant depression: a review and hypothesis. Med Hypotheses. 2010;74(4):649–660.
  14. Meheller AC, Singer RR, Gruber RH, DeLosa ML. The effect of Mg in migraine. Headache. 2010;39(2):131–141.
  15. Eeusdar, Yoe. Lithium treatment. J Electrocardiol. 2010;29(2):131–141.
  16. Muhl A, Tsiang H, Nicodemius KA, et al. Effects of alpha-ketoglutarate on retinoceptor network and ROS production. Ann Nutr Metab. 2011;59:124–130.
  17. Bunik VI, Fernie AR. Metabolic control exerted by the 2-oxoglutarate dehydrogenase reaction: a cross-linkage between energy production and nitrogen assimilation. Biochem J. 2009;422(3):405–421.
  18. Harirson AP. Piezowski SG. Biological effects of 2-oxoglutarate with particular emphasis on the regulation of protein, mineral and lipid absorption. J Physiol Pharmacol. 2008;59(suppl 1):91–106.
  19. Syrobor LA. The use of alpha-ketoglutarate salts in clinical nutrition and metabolic care. Curr Opin Clin Nutr Metab Care. 1999;2(1):33–37.
  20. Succinate acid: compound summary. http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=110 Accessed February 8, 2011.
  21. Kharzov VA, Kiselal AA, Vasiliev KY. Chernysheva GA. Cardioprotective effects of trimetazidine in a combination of succinic and malic acids during acute myocardial ischemia. Bull Exp Biol Med. 2008;146(2):218–222.
  22. Mazey EE, Paskov AB, Uchitel MI, et al. A succinate-based composition based on succinic–malic acid mixture for correction of mitochondrial dysfunction. Biochemistry (Mosc). 2007;72(10):947–950.
  23. Acyl et al. Role of gamma-aminobutyric acid in succinate-induced attenuation of metabolic acidosis. Clin Chem. 2009;55(10):1910–1916.
  24. Gurvitch AM, Mustukina EA, Zarutskaya VV, et al. Prophylaxis of encephalopathies and risk factors of atherogenesis development in the postresuscitation period. Vestn Ross Akad Med Nauk. 2008;6:65–71.
  25. Fumaric acid: compound summary. http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=449472&loc=ec_rcs. Accessed February 8, 2011.
  26. Brewer LR, Rogers SJ. Fumaric acid esters in the management of severe psoriasis. Clin Exp Dermatol. 2007;32(3):246–249.
  27. Saccharin Q, Koch HJ. Long-term treatment of psoriasis using fumaric acid esters. Br J Dermatol. 1999;141:110–115.
  28. Garcia-Caballero M, Mari-Belfa M, Medina MA, Quesada AR. Dimethylfumarate inhibits angiogenesis in vitro and in vivo: a possible role for its antioxidant properties. Pharmacol Res. 2008;58(3):395–401.
  29. DITCH et al. Fumaric acid esters: clinical and experimental background. Dermatology. 1998;196(suppl 2):7–12.
  30. Huse R, Callea M. Metabolism of mass spectrometry of succinate in patients with multiple sclerosis. Trace Elem Res. 2005;112(1):18–22.
  31. Wolany H, Kolnikowski T. Therapeutic relevance of succinic–malic acid in metabolic syndrome. J Clin Endocrinol Metab. 2003;88(2):545–552.
  32. Nagy D, Marosi M, Kis Z, et al. Oxaloacetate decreases the infarct size and attenuates the reduction in evoked responses after photothrombotic focal ischemia in the rat cortex. Cell Mol Neurobiol. 2009;29(6-7):827–835.
  33. Citric acid: compound summary. http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=311&loc=ec_rcs. Accessed February 8, 2011.
  34. The citric acid cycle. In: Nelson DL, Cox MM, eds. Lehninger Principles of Biochemistry. 5th ed. New York, NY: WH Freeman; 2008:615–641.
  35. Nagar R, Ragai M, Shimaski N, Baynes WJ, Fujiwara I. Citric acid inhibits development of cataracts, proteinuria and ketosis in streptozotocin (type I) diabetic rats. Biochem Biophys Res Commun. 2010;393(1):118–122.
  36. Baynes JW, Murray B. The metal chelators, triennate and citrate, inhibit the development of diabetic pathology in the Zucker diabetic rat. Exp Diabetes Res. 2009;2009:696378.
  37. Kosa N, Atyapcui BN, Yilmaz N, et al. Citric acid as a decalcifying agent for the excised calcified human heart valves. Anatol J Cardiol Derg. 2008;8(2):94–98.
  38. Cis-aconitate: compound summary. http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=5459816&loc=ec_rcs. Accessed February 8, 2011.
  39. Ricciardolo FL. Mechanisms of citric and induced bronchoconstriction. Am J Med. 2001;111(suppl A8):18S–24S.
  40. Kar S, Kar B, Bhattacharya PK, Ghosh DK. Experimental visceral leishmaniasis: role of trans-aconitic acid in combined chemotherapy. Antimicrob Agents Chemother. 1993;37(11):2459–2465.
  41. Oxalosuccinic acid: compound summary. http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=912&loc=ec_rcs. Accessed February 8, 2011.
  42. Alpha-ketoglutarate acid: compound summary. http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=164533&loc=ec_rcs. Accessed February 8, 2011.
  43. Leimer J, Mindlau Y, Auger C, et al. Acquisicio AA, Appanna VP, Appanna VD. Histidine is a source of the antioxidant, alpha-ketoglutarate, in Pseudomonas fluorescens challenged by oxidative stress. FEMS Microbiol Lett. 2010;309(2):170–177.
  44. Mallouki R, Berkary L, Leriner J, et al. The tricarboxylic acid cycle, an ancient metabolic network with a new dimension. PLoS One. 2007;2(8):e890.
  45. Muhling J, Tusing F, Nicodemius KA, et al. Effects of alpha-ketoglutarate on glutathione and amino acid biosynthesis and ROS production. Amino Acids. 2010;38(1):167–177.
  46. Bunik VI, Fernie AR. Metabolic control exerted by the 2-oxoglutarate dehydrogenase reaction: a cross-talk between energy production and nitrogen assimilation. Biochem J. 2009;422(3):405–421.
  47. Harrison AP. Piezowski SG. Biological effects of 2-oxoglutarate with particular emphasis on the regulation of protein, mineral and lipid absorption. J Physiol Pharmacol. 2008;59(suppl 1):91–106.
  48. Gurvitch AM, Mustukina EA, Zarutskaya VV. et al. Prophylaxis of encephalopathies and risk factors of atherogenesis development in the postresuscitation period. Vestn Ross Akad Med Nauk. 2008;6:65–71.
  49. Fumaric acid: compound summary. http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=449472&loc=ec_rcs. Accessed February 8, 2011.
  50. Brewer LR, Rogers SJ. Fumaric acid esters in the management of severe psoriasis. Clin Exp Dermatol. 2007;32(3):246–249.
  51. Saccharin Q, Koch HJ. Long-term treatment of psoriasis using fumaric acid esters. Br J Dermatol. 1999;141:110–115.
  52. Garcia-Caballero M, Mari-Belfa M, Medina MA, Quesada AR. Dimethylfumarate inhibits angiogenesis in vitro and in vivo: a possible role for its antioxidant properties. Pharmacol Res. 2008;58(3):395–401.
  53. Lutz M, Lyall B, Moser DG, et al. Pharmacology of succinic acid derivatives. Ther Adv Neurol Disord. 2010;3(2):53–60.
  54. Nagy D, Marosi M, Kis Z, et al. Oxaloacetate decreases the infarct size and attenuates the reduction in evoked responses after photothrombotic focal ischemia in the rat cortex. Cell Mol Neurobiol. 2009;29(6-7):827–835.
  55. Citric acid: compound summary. http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=311&loc=ec_rcs. Accessed February 8, 2011.
  56. The citric acid cycle. In: Nelson DL, Cox MM, eds. Lehninger Principles of Biochemistry. 5th ed. New York, NY: WH Freeman; 2008:615–641.
  57. Nagar R, Ragai M, Shimaski N, Baynes WJ, Fujiwara I. Citric acid inhibits development of cataracts, proteinuria and ketosis in streptozotocin (type I) diabetic rats. Biochem Biophys Res Commun. 2010;393(1):118–122.
  58. Baynes JW, Murray B. The metal chelators, triennate and citrate, inhibit the development of diabetic pathology in the Zucker diabetic rat. Exp Diabetes Res. 2009;2009:696378.
  59. Kosa N, Atyapcui BN, Yilmaz N, et al. Citric acid as a decalcifying agent for the excised calcified human heart valves. Anatol J Cardiol Derg. 2008;8(2):94–98.
  60. Cis-aconitate: compound summary. http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=5459816&loc=ec_rcs. Accessed February 8, 2011.
  61. Ricciardolo FL. Mechanisms of citric and induced bronchoconstriction. Am J Med. 2001;111(suppl A8):18S–24S.
  62. Kar S, Kar B, Bhattacharya PK, Ghosh DK. Experimental visceral leishmaniasis: role of trans-aconitic acid in combined chemotherapy. Antimicrob Agents Chemother. 1993;37(11):2459–2465.
  63. Oxalosuccinic acid: compound summary. http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=912&loc=ec_rcs. Accessed February 8, 2011.
  64. Alpha-ketoglutarate acid: compound summary. http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=164533&loc=ec_rcs. Accessed February 8, 2011.
  65. Leimer J, Mindlau Y, Auger C, et al. Acquisicio AA, Appanna VP, Appanna VD. Histidine is a source of the antioxidant, alpha-ketoglutarate, in Pseudomonas fluorescens challenged by oxidative stress. FEMS Microbiol Lett. 2010;309(2):170–177.
  66. Mallouki R, Berkary L, Leriner J, et al. The tricarboxylic acid cycle, an ancient metabolic network with a new dimension. PLoS One. 2007;2(8):e890.
  67. Muhling J, Tusing F, Nicodemius KA, et al. Effects of alpha-ketoglutarate on glutathione and amino acid biosynthesis and ROS production. Amino Acids. 2010;38(1):167–177.
  68. Bunik VI, Fernie AR. Metabolic control exerted by the 2-oxoglutarate dehydrogenase reaction: a cross-talk between energy production and nitrogen assimilation. Biochem J. 2009;422(3):405–421.
  69. Harrison AP, Piezowski SG. Biological effects of 2-oxoglutarate with particular emphasis on the regulation of protein, mineral and lipid absorption. J Physiol Pharmacol. 2008;59(suppl 1):91–106.
  70. Gurvitch AM, Mustukina EA, Zarutskaya VV, et al. Prophylaxis of encephalopathies and risk factors of atherogenesis development in the postresuscitation period. Vestn Ross Akad Med Nauk. 2008;6:65–71.
  71. Fumaric acid: compound summary. http://pubchem.ncbi.nlm.nih.gov/summary/summary.cgi?cid=449472&loc=ec_rcs. Accessed February 8, 2011.
  72. Brewer LR, Rogers SJ. Fumaric acid esters in the management of severe psoriasis. Clin Exp Dermatol. 2007;32(3):246–249.
  73. Saccharin Q, Koch HJ. Long-term treatment of psoriasis using fumaric acid esters. Br J Dermatol. 1999;141:110–115.
  74. Garcia-Caballero M, Mari-Belfa M, Medina MA, Quesada AR. Dimethylfumarate inhibits angiogenesis in vitro and in vivo: a possible role for its antioxidant properties. Pharmacol Res. 2008;58(3):395–401.