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Diabetic retinopathy is a complex disease for which new therapeutic possibilities are always sought.
Recent literature shows that diabetes results in an excess of superoxide anion from the mitochondrial chain of transport. This seems to result in the damage caused by the diabetic syndrome.
The damage manifested by the retina tissue is two-fold:
• neurosensorial damage: this is present at an early stage and can also be seen in the absence of diabetic retinopathy
• vascular damage: this occurs later on, with possible neoangiogenesis.
It is necessary to intervene during the early stages of the illness with suitable remedies to prevent the clinical picture deteriorating or, at least, to stabilize its course. Therapeutic intervention involves careful control of diabetes and the administration of preparations with a positive effect on the vascular and metabolic component of the eye tissues, in particular, the retina.
 
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Info in Vista 2006 N.1 RETINOPARIA DIABETICA

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4. Chung SS, Ho EC, Lam KS, Chung SK. Contribution of polyol pathway to diabetes-induced oxidative stress. J Am Soc Nephrol. 2003 Aug;14(8 Suppl 3):S233-6. Review

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6. Nishikawa T, Edelstein D, Du XL, Yamagishi S, Matsumura T, Kaneda Y, Yorek MA, Beebe D, Oates PJ, Hammes HP, Giardino I, Brownlee M. Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage. Nature. 2000 Apr 13;404(6779):787-90.

7. Brownlee M. Biochemistry and molecular cell biology of diabetic complications. Nature. 2001 Dec 13;414(6865):813-20.

8. Du X, Matsumura T, Edelstein D, Rossetti L, Zsengeller Z, Szabo C, Brownlee M. Inhibition of GAPDH activity by poly(ADP-ribose) polymerase activates three major pathways of hyperglycemic damage in endothelial cells. J Clin Invest. 2003 Oct;112(7):1049-57.

9. Obrosova IG, Li F, Abatan OI, Forsell MA, Komjati K, Pacher P, Szabo C, Stevens MJ. Role of poly(ADP-ribose) polymerase activation in diabetic neuropathy. Diabetes. 2004 Mar;53(3):711-20.

10. Spitaler MM, Graier WF. Vascular targets of redox signalling in diabetes mellitus. Diabetologia. 2002 Apr;45(4):476-94. Review.

11. Ceriello A. New insights on oxidative stress and diabetic complications may lead to a "causal" antioxidant therapy. Diabetes Care. 2003 May;26(5):1589-96. Review.

12. Han Y, Bearse MA Jr, Schneck ME, Barez S, Jacobsen CH, Adams AJ. Related Articles, Links Multifocal electroretinogram delays predict sites of subsequent diabetic retinopathy. Invest Ophthalmol Vis Sci. 2004 Mar;45(3):948-54.

13. Bearse MA Jr, Han Y, Schneck ME, Adams AJ. Related Articles, Links Retinal function in normal and diabetic eyes mapped with the slow flash multifocal electroretinogram. Invest Ophthalmol Vis Sci. 2004 Jan;45(1):296-304.

14. Lund-Andersen C, Frost-Larsen K, Starup K. Acta Ophthalmol (Copenh). 1987 Aug;65(4):481-6 Natural history of diabetic retinopathy in insulin-dependent juvenile diabetics. A longitudinal study.

15. Chidlow G, Schmidt KG, Wood JP, Melena J, Osborne NN. Alpha-lipoic acid protects the retina against ischemia-reperfusion. Neuropharmacology. 2002 Nov;43(6):1015-25.

16. Low PA, Nickander KK, Tritschler HJ. The roles of oxidative stress and antioxidant treatment in experimental diabetic neuropathy. Diabetes. 1997 Sep;46 Suppl 2:S38-42.

17. van Dam PS. Oxidative stress and diabetic neuropathy: pathophysiological mechanisms and treatment perspectives. Diabetes Metab Res Rev. 2002 May-Jun;18(3):176-84. Review.

18. Baydas G, Donder E, Kiliboz M, Sonkaya E, Tuzcu M, Yasar A, Nedzvetskii VS. Neuroprotection by alpha-lipoic acid in streptozotocin-induced diabetes. Biochemistry (Mosc). 2004 Sep;69(9):1001-5.

19. Stevens MJ, Obrosova I, Cao X, Van Huysen C, Greene DA. Effects of DL-alpha-lipoic acid on peripheral nerve conduction, blood flow, energy metabolism, and oxidative stress in experimental diabetic neuropathy. Diabetes. 2000 Jun;49(6):1006-15.

20. Packer L, Kraemer K, Rimbach G. Molecular aspects of lipoic acid in the prevention of diabetes complications. Nutrition. 2001 Oct;17(10):888-95. Review.

21. Nickander KK, McPhee BR, Low PA, Tritschler H. Alpha-lipoic acid: antioxidant potency against lipid peroxidation of neural tissues in vitro and implications for diabetic neuropathy. Free Radic Biol Med. 1996;21(5):631-9.

22. Baydas G, Donder E, Kiliboz M, Sonkaya E, Tuzcu M, Yasar A, Nedzvetskii VS Neuroprotection by alpha-lipoic acid in streptozotocin-induced diabetes. Biochemistry (Mosc). 2004 Sep;69(9):1001-5. 26)

23. Morris TW, Reed KE, Cronan JE Jr. Lipoic acid metabolism in Escherichia coli: the lplA and lipB genes define redundant pathways for ligation of lipoyl groups to apoprotein. J Bacteriol. 1995 Jan;177(1):1-10.

24. Kolobova E, Tuganova A, Boulatnikov I, Popov KM. Regulation of pyruvate dehydrogenase activity through phosphorylation at multiple sites. Biochem J. 2001 Aug 15;358(Pt 1):69-77.

25. Packer L, Witt EH, Tritschler HJ. alpha-Lipoic acid as a biological antioxidant. Free Radic Biol Med. 1995 Aug;19(2):227-50. Review.

26. Biewenga GP, Haenen GR, Bast A. The pharmacology of the antioxidant lipoic acid. Gen Pharmacol. 1997 Sep;29(3):315-31. Review.

27. Kowluru RA, Odenbach S. Effect of long-term administration of alpha-lipoic acid on retinal capillary cell death and the development of retinopathy in diabetic rats. Diabetes. 2004 Dec;53(12):3233-8.

28. Campbell N A Biologia Zanichelli

29. Davidson GE et all The metabolic conseguences of vitamin B12 / methionine deficienty in rats. Biochim biophiys acta 1975 jun 12;392(2): 207 - 215

30. Murata M, Kador PF, Sato S. Vascular endothelial growth factor (EGF) enhances the expression of receptors and activates mitogen-activated protein (MAP) kinase of dog retinal capillary endothelial cells. J Ocul Pharmacol Ther. 2000 Aug;16(4):383-91.

31. Akiyama T, Ishida J, Nakagawa S, Ogawara H, Watanabe S, Itoh N, Shibuya M, Fukami Y. Genistein, a specific inhibitor of tyrosine-specific protein kinases. J Biol Chem. 1987 Apr 25;262(12):5592-5.

32. Hayashi A, Weinberger AW, Kim HC, de Juan E Jr. Genistein, a protein tyrosine kinase inhibitor, ameliorates retinal degeneration after ischemia- reperfusion injury in rat. Invest Ophthalmol Vis Sci. 1997 May;38(6):1193-202.

33. Chung MJ, Kang AY, Lee KM, Oh E, Jun HJ, Kim SY, Auh JH, Moon TW, Lee SJ, Park KH. Water-soluble genistin glycoside isoflavones up-regulate antioxidant metallothionein expression and scavenge free radicals. J Agric Food Chem. 2006 May 31;54(11):3819-26.

34. Nakajima M, Cooney MJ, Tu AH, Chang KY, Cao J, Ando A, An GJ, Melia M, de Juan E Jr. Normalization of retinal vascular permeability in experimental diabetes with genistein. Invest Ophthalmol Vis Sci. 2001 Aug;42(9):2110-4.

35. Buchler P, Reber HA, Buchler MW, Friess H, Lavey RS, Hines OJ Antiangiogenic activity of genistein in pancreatic carcinoma cells is mediated by the inhibition of hypoxia-inducible factor-1 and the down-regulation of VEGF gene expression. Cancer. 2004 Jan 1;100(1):201-10.

36. Wang B, Li H, Yan H, Xiao JG. Genistein inhibited hypoxia-inducible factor-1alpha expression induced by hypoxia and cobalt chloride in human retinal pigment epithelium cells. Methods Find Exp Clin Pharmacol. 2005 Apr;27(3):179-84.

37. Wang B, Zou Y, Li H, Yan H, Pan JS, Yuan ZL. Genistein inhibited retinal neovascularization and expression of vascular endothelial growth factor and hypoxia inducible factor 1alpha in a mouse model of oxygen-induced retinopathy. J Ocul Pharmacol Ther. 2005 Apr;21(2):107-13.

38. Constantinescu A, Han D, Packer L. Vitamin E recycling in human erythrocyte membranes. J Biol Chem. 1993 May 25;268(15):10906-13.

39. Kagan VE, Serbinova EA, Forte T, Scita G, Packer L. Related Articles, Links Recycling of vitamin E in human low density lipoproteins. J Lipid Res. 1992 Mar;33(3):385-97.

40. Stoyanovsky DA, Goldman R, Darrow RM, Organisciak DT, Kagan VE. Endogenous ascorbate regenerates vitamin E in the retina directly and in combination with exogenous dihydrolipoic acid. Curr Eye Res. 1995 Mar;14(3):181-9

41. Xu DP, Wells WW. alpha-Lipoic acid dependent regeneration of ascorbic acid from dehydroascorbic acid in rat liver mitochondria. J Bioenerg Biomembr. 1996 Feb;28(1):77-85.
 
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tioretin_compresse
Composition
Alpha-lipoic acid (thioctic acid) 400 mg
Genistein 80 mg
Vitamin C 30 mg
Vitamin PP 9 mg
Vitamin E 5 mg
Vitamin B6 2 mg
Vitamin B2 1,6 mg
Vitamin B1 1,4 mg
Vitamin B12 1 mg
Excipients  
 
Description

Dietary supplement of lipoic acid, genistein and vitamins

A new approach to the treatment of Diabetic Retinopathy

TIORETIN® tablets is a preparation based on lipoic acid, genistein and vitamins

Lipoic acid, also known as alpha-lipoic acid or thioctic acid, is a substance which is produced by almost all animals and has an important role in the energy metabolism of cells.
Lipoic acid has a highly antioxidant effect, but its most important characteristic is tied to the fact that, within cells, it is a cofactor in fundamental enzymatic processes which are needed for the metabolism of glucose, fatty acids and other substances useful to the human body.
As an antioxidant it is able to protect the body by combating damage caused by the formation of free radicals and contributing to the regeneration of other important antioxidants already present in various tissues, such as vitamin E, vitamin C and glutathione.
 
illustrazione

Once taken orally, lipoic acid is distributed throughout the body and easily passes into the cells where it is effective.
Diabetes is a high risk factor since it can result in the development of cardiovascular illnesses, damage to the kidneys, nerves and sight.
Lipoic acid is particularly important for those patients affected by diabetes since is has a beneficial effect on glycemia and on the complications which often follow on from this illness.
Lipoic acid may be very useful in diabetic retinopathy as it has a very beneficial effect on the retina and helps to protect the cells needed for vision.
Even though the human body is able to produce lipoic acid, a dietary supplement of this substance could be an important requirement, particularly in those patients who have greater need or have illnesses in which free radicals play a significant part.

Genisteinis a substance which, recent studies have shown, is able to reduce damage caused by the increased permeability of the blood vessels of the retina and prevent macular oedema which is considered the main reason for the loss of vision caused by diabetes.
Genisteinis also appears able to reduce the formation of new vessels in the retina. This therefore further contributes to better protecting vision during diabetic illness.

The presence of the vitamin B complex in TIORETIN® tablets increases the neuroprotective effect in synergy with that of lipoic acid. Vitamin C and vitamin E also optimize the antioxidant effect of lipoic acid which, in turn, facilitates the regeneration of these vitamin factors.

pill

The special technology used in the production of TIORETIN® tablets makes it possible to achieve the release of the active ingredients in a diversified manner. One part, the fast release delivery system, is rapidly made available, whilst the remaining content of the tablet is released slowly via controlled release over a period of time. This technology makes the effect of TIORETIN® tablets more long-lasting.

 
 
Product Use

TIORETIN® tablets are indicated in the case of an increased need for those nutrients which they contain or in the event of reduced dietary intake.
TIORETIN® tablets can be an effective specific nutritional aid for trophism of the eye, above all in those patients whose eyes function in a diminished capacity.
TIORETIN® tablets, as a result of their antioxidant effect, may also be useful to supplement the diet of those patients who need to improve cellular metabolism or prevent vascular damage to the eye tissue as a result of the excessive production of free radicals in the eye.

DOSAGE AND ADMINISTRATION
1 tablet per day.

PRECAUTIONS AND WARNINGS
Patients being treated with TIORETIN® tablets who take antidiabetic drugs must regularly check their level of glycemia.

PACKAGE
Box containing a blister pack of 30 double layer tablets to be swallowed.

 
 
 
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