Page 2

Effect of propionyl-L-carnitine on oscillatory potentials in electroretinogram in streptozotocin-diabetic rats
Hotta N.; Koh N.; Sakakibara F.; Nakamura J.; Hamada Y.; Hara T.; Fukasawa H.; Kakuta H.; Sakamoto N.
III Department of Internal Medicine, Nagoya University School of Medicine, 65 Tsuruma-cho, Showa-ku, Nagoya 466 Japan
European Journal of Pharmacology (Netherlands), 1996, 311/2-3 (199-206)

The effect of propionyl-L-carnitine, an analogue of L-carnitine, and insulin on the oscillatory potentials of the electroretinogram was determined in rats with streptozotocin-induced diabetes. Propionyl-L-carnitine was administered at a daily dose of 0.5 g/kg by gavage for 4 weeks, while other rats were treated with subcutaneous injections of insulin (8-10 U/day). Both treatments shortened the peak latencies of the oscillatory potentials in the electroretinogram, which were significantly prolonged in untreated diabetic rats (O1, O2 and O3, and Sigma(O1 + O2 + O3)) (P < 0.0001 vs. untreated normal rats). A significant decrease in the erythrocyte free carnitine level in diabetic rats was prevented by both treatments. Insulin produced a significant reduction of retinal glucose, sorbitol and fructose levels in diabetic rats, while propionyl-L-carnitine failed to do so. However, both treatments markedly reduced serum lipids levels in the diabetic rats. These findings provide information on the pathogenesis of diabetic retinopathy as well as suggesting the potential therapeutic value of propionyl-L-carnitine for retinopathy.

Abnormalities of retinal metabolism in diabetes or experimental galactosemia. III. Effects of antioxidants
Kowluru R.A.; Kern T.S.; Engerman R.L.; Armstrong D.
Dept. of Ophthalmology/Visual Sci., University of Wisconsin, 1300 University Ave., Madison, WI 53706-1532 USA
Diabetes (USA), 1996, 45/9 (1233-1237)

Effects of antioxidants on hyperglycemia-induced alterations of retinal metabolism were evaluated in rats diabetic or experimentally galactosemic for 2 months. Oxidative stress was estimated by measuring lipid peroxides (measured as thiobarbituric acid reactive substances (TBARS)) in retina and plasma. Erythrocyte osmotic fragility, another measure of oxidative stress, also was determined in the same groups of rats. In diabetic rats, TBARS were elevated by 74% in retina and 87% in plasma. In galactose-fed rats, TBARS were significantly elevated in retina (P < 0.05), but were normal in plasma. The administration of supplemental dietary ascorbic acid and alpha-tocopherol acetate for 2 months prevented the elevation of retinal TBARS and the decrease of Na+-K+-ATPase and calcium ATPase activities in retinas of diabetic animals without having any beneficial effect on plasma TBARS. In galactosemic rats, these antioxidants had a partial beneficial effect on the activity of retinal Na+-K+-ATPase, but failed to have any effect on calcium ATPase. The beneficial effects of antioxidants in diabetes and experimental galactosemia were not caused by the amelioration of hyperglycemia or retinal polyol accumulation. Erythrocyte osmotic fragility was increased by more than twofold in diabetes, but was normal in experimental galactesemia, and antioxidants prevented diabetes-induced increases in erythrocyte osmotic fragility. Diabetes-induced increased oxidative stress and subnormal ATPase activities in the retina can be inhibited by dietary supplementation with antioxidants.

Advanced glycation and the development of diabetic complications: Unifying the involvement of glucose, methylglyoxal and oxidative stress
Thornally P.J.
Department Biological Sciences, Central Campus, University of Essex, Wivenhoe Park, Colchester United Kingdom
Endocrinology and Metabolism (United Kingdom), 1996, 3/3 (149-166)

The formation of advanced glycation endproducts (AGE) and oxidative stress have been implicated in the development of diabetic complications. The evidence for advanced glycation mediated by glucose and methylglyoxal, and oxidative stress, in clinical diabetes mellitus and their association with diabetic complications is reviewed. Indeed, they are linked and mutually reinforcing. Glucose reacts non-enzymatically with N-terminal and lysyl side chain amino groups in proteins to form fructosamines which are early stage glycation products. Fructosamines degrade oxidatively and non-oxidatively to form AGE: N(epsilon)-carboxymethyl-lysine, N(epsilon)-lactatolysine, pentosidine and alpha-oxoaldehydes, 3-deoxyglucosone and 2-glucosulose; 3-deoxyglucosone reacts nonenzymatically with proteins to form pyrraline, imidazolone derivatives and bis(lysyl) crosslinks. The alpha-oxoaldehyde methylglyoxal is formed from triosephosphates, ketone body metabolism and the catabolism of threonine, and is detoxified by the glyoxalase system. It reacts non-enzymatically with proteins to form imidazolone derivatives and bis(lysyll) crosslinks, and with guanyl nucleotides in DNA and RNA to form imidazopurinone derivatives. Modification of proteins and nucleotides by AGE has functional consequences. Proteins minimally-modified by imidazolone derivatives are bound by cell surface receptors on monocytic cells, internalized and degraded; they are chemotactic and induce the synthesis and secretion of cytokines (interleukin-1beta, tumour necrosis factor-alpha and macrophage colony-stimulating factor). Crosslinking of proteins by pentosidine and bis(lysyl) crosslinks formed by methylglyoxal and 3-deoxyglucosone may stabilize collagen and contribute to basement membrane thickening. Modification of guanyl nucleotides by methyglyoxal induces mutagenesis and apoptosis. Oxidative stress has been implicated in the development of diabetic complications. The concentration of reduced glutathione (GSH) is decreased and lipid peroxidation is increased in blood cells, vascular cells and lens in diabetes. The oxidative stimulus may arise from the oxidative degradation of monosaccharides (monosaccharide autoxidation), the oxidative degradation of glycated proteins (glycoxidation) and the activation of the respiratory burst of phagocytes by the AGE-induced synthesis and secretion of cytokines. This leads to the oxidative modification of proteins and nucleotides, and the initiation of atherosclerosis. The formation of AGE and the metabolism of methylglyoxal have been logistically linked to the development of diabetic complications (retinopathy, neuropathy and nephropathy). Recently, a negative logistic link of GSH to diabetic complications was also found but only in a statistical model where variables related to the detoxification of alpha-oxoaldehydes by the glyoxalase system were included. GSH is a cofactor of the glyoxalase system. Decreased GSH and other cysteinyl thiols in diabetes both pre-disposes tissues to oxidative stress and alpha-oxoaldehyde-mediated protein glycation. Glycation and oxidative stress are mutually reinforcing. Strategies for the prevention of diabetic complications should therefore aim to prevent both the effects of glycation and oxidative stress.

Toxic amblyopia may be associated with Purtscher's retinopathy in alcohol-induced pancreatitis
Rover J.
Augenklinik, Stadtische Kliniken, Teutoburger Strasse 50, D-33604 Bielefeld Germany
Spektrum der Augenheilkunde (Austria), 1996, 10/3 (129-132)

2% of all patients with alcohol-induced pancreatitis develop visual disturbances presenting a retinal image similar to Purtscher's retinopathy. In a 38-year male Caucasian, suffering from chronic pancreatitis, acute retinal ischemia without vascular occlusion caused severe visual disturbances. Inspite of rapid improvement of the pancreatitis and the electroretinogram, the visual function did not recover due to severe loss of photoreceptor function and retinal nerve fibres. A lack of Vitamin B12 may have pronounced the ischemic damage of the optic nerve.

Clinical study of vitamin influence in diabetes mellitus
Hashizume N.
Dept. of Laboratory Medicine, Ohashi Hosp., Toho Univ. Sch. of Med., 2-17-6 Ohashi, Meguro, Tokyo Japan
Journal of the Medical Society of Toho University (Japan), 1996, 42/6 (577-581)

Vitamin deficiency is a result of an inadequale diet. Education on the importance of trace nutrients in diabetic patients with poor blood sugar control is examined. Those who prepare meals must consider the loss of vitamins in the process of cooking. Our study also suggested that marginal vitamin deficiency plays an indirect but important role in the development of diabetic complications. Vitamin-C as altering total cholesterol (T-ch) and vitamin E as altering triglyceride (TG) could modify diabetic angiopathy. Pharmacologically, niacin might be responsible for the decrease in Lipoprotein (a) and Vitamin-C would inhibit the influence of rapid blood glucose control on diabetic retinopathy.

Oxidative stress and diabetic vascular complications
Giugliano D.; Ceriello A.; Paolisso G.
Via Emilia I, 80021 Afragola (NA) Italy
Diabetes Care (USA), 1996, 19/3 (257-267)

Long-term vascular complications still represent the main cause of morbidity and mortality in diabetic patients. Although prospective randomized long-term clinical studies comparing the effects of conventional and intensive therapy have demonstrated a clear link between diabetic hyperglycemia and the development of secondary complications of diabetes, they have not defined the mechanism through which excess glucose results in tissue damage. Evidence has accumulated indicating that the generation of reactive oxygen species (oxidative stress) may play an important role in the etiology of diabetic complications. This hypothesis is supported by evidence that many biochemical pathways strictly associated with hyperglycemia (glucose autoxidation, polyol pathway, prostanoid synthesis, protein glycation) can increase the production of free radicals. Furthermore, exposure of endothelial cells to high glucose leads to augmented production of superoxide anion, which may quench nitric oxide, a potent endothelium- derived vasodilator that participates in the general homeostasis of the vasculature. In further support of the consequential injurious role of oxidative stress, many of the adverse effects of high glucose on endothelial functions, such as reduced endothelial-dependent relaxation and delayed cell replication, are reversed by antioxidants. A rational extension of this proposed role for oxidative stress is the suggestion that the different susceptibility of diabetic patients to microvascular and macrovascular complications may be a function of the endogenous antioxidant status.

[Erythrocyte and plasma antioxidant activity in diabetes mellitus type I].
Ndahimana J, Dorchy H, Vertongen F
Service de Chimie medicale, Universite Libre de Bruxelles, Belgique.
Presse Med 1996 Feb 10;25(5):188-92

Objectives: Some biologic parameters involved in cell defence against oxygen radicals (plasmatic vitamins C and E, erythrocyte glutathione peroxidase, glutathione reductase and superoxide dismutase) were measured in single blood samples from 119 diabetic infants, adolescents and young adults.

Methods: Data were studied in relation to residual insulin secretion determined by C peptide, level of metabolic control appreciated by glycosylated haemoglobin, lipid abnormalities and subclinical complications (retinopathy, neuropathy and nephropathy).

Results: There was no change in antioxidant parameters with insulin secretion. Patients with poor glycaemic control and high plasma lipids had higher levels of plasma vitamin E. Patients with nephropathy had lower plasma Vitamin-C levels and those with neuropathy showed lower erythrocyte glutathione peroxidase activity. Plasma Vitamin-C concentrations and erythrocyte glutathione reductase activities were negatively correlated with the age of the patients and the duration of the disease. Conclusion: Higher transport capacity of vitamin E probably explains the elevated levels of vitamin E observed in patients with high lipid levels and long lasting illness. The lower levels of Vitamin-C in the presence of nephropathy may be due to an increased renal excretion of this vitamin. The reduction of glutathione peroxidase, glutathione reductase activities and Vitamin-C levels confirms the existence of an oxidative stress in type 1 diabetes.

A deficiency of vitamin B6 is a plausible molecular basis of the retinopathy of patients with diabetes mellitus.
Ellis JM; Folkers K; Minadeo M; VanBuskirk R; Xia LJ
Department of Medicine, Titus County Hospital, Mt. Pleasant, Texas.
Biochem Biophys Res Commun. 1991 Aug 30. 179(1). P 615-9

Eighteen patients with diabetes mellitus, some of whom had variously retinopathy, pregnancy, and the carpal tunnel syndrome, and were variously treated with steroids and vitamin B6, have been overviewed for periods of 8 months to 28 years. We have established an association of a deficiency of vitamin B6 with diabetes by monitoring the specific activity of the erythrocyte glutamic oxaloacetic transaminase and again by the association with the carpal tunnel syndrome (C.T.S.). It has been known for a decade that C.T.S. is caused by a B6 deficiency. The absence of retinopathy in vitamin B6-treated diabetic patients over periods of 8 months - 28 years appears monumental. These observations are like discovery and constitute a basis for a new protocol to establish the apparent relationship of a deficiency of vitamin B6 as a molecular cause of diabetic neuropathy. Blindness and vision are so important that the strength or weakness of the observations are not important; the conduct of a new protocol is important.

Pharmacological prevention of diabetic microangiopathy
Guillausseau P.J.
Diabete Metabol. (France), 1994, 20/2 BIS (219-228)

The development of drugs in order to block metabolic pathways of glucose responsible for diabetic vascular dysfunction is in progress. Aldose reductase inhibitors prevent or reduce the different components of vascular dysfunction, cataract, neuropathy and nephropathy in animal models of diabetes. Promising results have been observed in diabetic patients concerning the prevention of neuropathy and of retinopathy. Larger scale studies with the second generation compounds are in progress. Glycation inhibitors, mainly aminoguanidine, have been shown to prevent or reduce vascular dysfunction and microvascular complications in animal models. Trials in diabetic patients with aminoguanidine are just beginning. Anti-oxidant therapy is also at its early stage of development (vitamine E, vitamine C, alpha lipoic acid). Antiplatelet agents (aspirin, ticlopidine) have been demonstrated to reduce the progression of non proliferative diabetic retinopathy. Angiotensin converting enzyme inhibitors are of particular interest in preventing diabetic glomerulopathy.

Erythrocyte and plasma antioxidant activity in type I diabetes mellitus
Ndahimana J.; Dorchy H.; Vertongen F.
Presse Medicale (France), 1996, 25/5 (188-192)

Objectives: Some biologic parameters involved in cell defence against oxygen radicals (plasmatic vitamins C and E, erythrocyte glutathione peroxidase, glutathione reductase and superoxide dismutase) were measured in single blood samples from 119 diabetic infants, adolescents and young adults.

Methods: Data were studied in relation to residual insulin secretion determined by C peptide, level of metabolic control appreciated by glycosylated haemoglobin, lipid abnormalities and subclinical complications (retinopathy, neuropathy and nephropathy).

Results: There was no change in antioxidant parameters with insulin secretion. Patients with poor glycaemic control and high plasma lipids had higher levels of plasma vitamin E. Patients with nephropathy had lower plasma Vitamin-C levels and those with neuropathy showed lower erythrocyte glutathione peroxidase activity. Plasma Vitamin-C concentrations and erythrocyte glutathione reductase activities were negatively correlated with the age of the patients and the duration of the disease.

Conclusion: Higher transport capacity of vitamin E probably explains the elevated levels of vitamin E observed in patients with high lipid levels and long lasting illness. The lower levels of Vitamin-C in the presence of nephropathy may be due to an increased renal excretion of this vitamin. The reduction of glutathione peroxidase, glutathione reductase activities and Vitamin-C levels confirms the existence of an oxidative stress in type 1 diabetes.

Lipid peroxidation in insulin-dependent diabetic patients with early retina degenerative lesions: Effects of an oral zinc supplementation
Faure P.; Benhamou P.Y.; Perard A.; Halimi S.; Roussel A.M.
European Journal of Clinical Nutrition (United Kingdom), 1995, 49/4 (282-288)

Design: Placebo for 3 months, followed by 30 mg/day zinc gluconate in identical capsules.

Setting: Diabetic out patients clinic at the University Hospital, Grenoble.

Subjects: Diabetic patients cared for type I diabetes mellitus. 22 patients began the study, 4 dropped out. 10 patients suffered of an early retinopathy, 8 patients had no retinopathy. Interventions: In this order: T0 biological measurements, 3 months placebo treatment, T1 biological measurements, 3 months zinc gluconate treatment, T2 biological measurements. Plasma Zn, Cu, Se, thiobarbituric acid reactants and antioxidant enzymes were measured (plasma and red glutathione peroxidase (Se-GPx), red cell superoxide dismutase (Cu-Zn-SOD)). Results: Lower plasma zinc level in the two groups. An increase in zinc level was observed and was more important in diabetic patients with no retinopathy (P = 0.05). The thiobarbituric acid reactants were above the reference values in all the patients, and were decreased at T2 (P < 0.05). Increase of GPx activity after zinc supplementation in patients with retinopathy.

Conclusions: Zinc deficiency in insulin-dependent diabetic patients is corrected by a zinc supplementation. Moreover this supplementation decreases lipid peroxidation. The effects of zinc are different in diabetic patients with or without retinopathy. The increase in Se-GPx activity observed in patients with retinopathy could be linked to the protective effect of zinc on the protein itself.

Angioid streaks associated with abetalipoproteinemia
Gorin M.B.; Paul T.O.; Rader D.J.
Ophthalmic Genet. (Netherlands), 1994, 15/3-4 (151-159)

Angioid streaks were observed in two patients with abetalipoproteinemia. The progression of the angioid streaks was minimal over the years that these patients received vitamin A and E supplementation, though in one patient the development of subretinal neovascular membranes within the angioid streaks was the cause of rapid central visual loss. The simultaneous appearance of two rare entities in unrelated individuals strengthens the relationship between these two disorders that has been suggested by previous case studies. The authors propose a common metabolic pathway involving trace element deficiencies that may account for this relationship as well as the association of angioid with other rare disorders such as Paget's disease, hypoparathyroidism, lead poisoning, hyperphosphatemia, and a number of hemoglobinopathies. Their study of these two patients underscores the need for further investigations as to the role of copper, zinc and omega-3 fatty acids in the pathogenesis of retinopathy in abetalipoproteinemia. Abnormalities of retinal metabolism in diabetes or galactosemia II.

Comparison of gamma-glutamyl transpeptidase in retina and cerebral cortex, and effects of antioxidant therapy
Kowluru R.; Kern T.S.; Engerman R.L.
Curr. Eye Res. (United Kingdom), 1994, 13/12 (891-896)

Levels of the intracellular antioxidant, glutathione, become subnormal in retina in diabetes or experimental galactosemia. In order to investigate the cause and significance of this abnormality, activity of gamma-glutamyl transpeptidase (an enzyme important in the synthesis and degradation of glutathione) and levels of reduced glutathione have been measured in retinas of diabetic rats and dogs and of experimentally galactosemic rats and dogs. Retinal gamma-glutamyl transpeptidase activity and glutathione level were significantly less than normal after 2 months of diabetes or galactosemia. In contrast, cerebral cortex from the same diabetic rats and galactosemic rats showed no significant reduction in either gamma-glutamyl transpeptidase activity or glutathione level. These different responses of the two tissues to hyperglycemia might help account for the difference in microvascular disease in these two tissues in diabetes. Consumption of the antioxidants, ascorbic acid (1.0%) plus alpha-tocopherol (0.1%), by diabetic rats and galactosemic rats inhibited the decrease of gamma- glutamyl transpeptidase activity and glutathione levels in retina, suggesting that defects in glutathione regulation in the retina are secondary to hyperglycemia-induced 'oxidative stress'.

Status of antioxidants in patients with diabetes mellitus with and without late complications
Oels C.; Elmadfa J.
Aktuel. Ernahr.Med. Klin. Prax. (Germany), 1994, 19/3 (155-159)

The role of antioxidative vitamins in the therapy of diabetes mellitus is of growing importance. The development of diabetic late complications (cataract, retinopathy, nephropathy and neuropathy and others) is associated with an increased presence of free radicals, and therefore, elevated oxidative stress of the human body. The aim of the present study was the evaluation of the vitamin and selenium status of diabetics. Thirty-eight patients of the age of 35-58 years had been diabetics for 8-27 years and their plasma concentration of haemoglobin was 6.7-7.5%. The diabetics of type I were treated with a functional insulin therapy with dietary restrictions, whereas the type II diabetics received oral antidiabetica (sulfonyl urea, biguanids) and had to comply with a fixed diet. Any supplementation of vitamins was omitted. The nutritional intake was monitored by a weighed record over 7 days. The plasma concentrations of vitamin A, beta-carotone, K and E were determined by reversed-phase-PLC. For the assessment of Vitamin-C concentrations, a photometric method was used, and selenium concentrations was determined by electrothermal atomic absorption spectrometry. Mean values of plasma concentrations were: vitamin A 36-50 microg/dl, beta-carotene 35-42 microg/dl, vitamin K: 0.5-0.6 ng/ml, vitamin E: 1.1-1.6 mg/dl, selenium: 72-75 microg/l. The values of Vitamin-C concentration of the diabetics type I without late complications and of type II diabetics were at 0.8 mg/dl and, therefore, at the borderline. Diabetics of type I with late complications showed marginal values of 0.6 plus or minus 0.3 mg/dl. The critical value for the prevention of scorbut has been fixed at 0.4 mg/dl. The results of this confirm the importance and efficiency of vitamins, especially of ascorbic acid. Positive effects of this antioxidative vitamin in respect of the prevention of diabetic side effects and subsequent disease should therefore be expected.

Vitamins for seeing
[No authors listed]
Compr. Ther. (USA), 1990, 16/4 (62)

It has long been known that an inadequate diet lacking in certain essential vitamins can cause ocular disorders. On an Egyptian papyrus dated about 1500 BC, it is recorded that liver was used as a food to cure night blindness. Healthy eyes depend on a well-balanced diet. Vitamin A maintains the normal function of the epithelial cells of the eye and is essential for the synthesis of visual photosensitive pigments. Deficiencies of vitamin A lead to clinical manifestations including night blindness, conjunctival pigmentation, and dry eyes. The B vitamins are important for maintaining good vision. Vitamin B1 (thiamine) deficiency produces optic nerve dysfunction. Vitamin B12 deficiency can produce vascular changes in the retina. Deficiency of riboflavin (part of the B complex) has been implicated in the formation of cataracts and may also be a factor in producting xerophthalmia (dry eyes). Vitamin-C is necessary to prevent scurvy. The scorbutic manifestations in the eyes are bleeding from the lids, conjunctiva, anterior chamber, and retina. Vitamin-C deficiency may also be a factor in cataract formation. Finally, vitamin K deficiency causes retinal hemorrhages in neonates. Deficiencies of vitamin D and E have not been shown to have a negative effect on the visual process, but vitamin E therapy improves retrolental fibroplasia (retinopathy of prematurity).

The regional distribution of vitamins E and C in mature and premature human retinas
Nielsen J.C.; Naash M.I.; Anderson R.E.
Invest. Ophthalmol. Visual Sci. (USA), 1988, 29/1 (22-26)

Vitamin E is used to ameliorate retinopathy of prematurity, but little is known about baseline vitamin E levels in retinas of premature infants or the effect of vitamin E supplementation on these levels. Vitamin E and C levels were measured in mature retinas (1 month to 73 years) and in retinas of premature infants (22 to 33 weeks of gestation). The infants fell into two groups: (1) those who survived <12 hr and received no vitamin E, and (2) those who survived >4 days and received vitamin E supplementation. Premature infants are born with 5 to 12 percent the vitamin E levels found in mature retinas. Vitamin E levels in vascular and avascular retina of premature infants increased with gestation. Infants born >27 weeks gestation and surviving at least 4 days with vitamin E supplementation demonstrated markedly elevated vitamin E levels in vascular and avascular retina when compared to supplemented infants <27 weeks gestation. Premature infants possessed 35-50% higher levels of retinal Vitamin-C than those found in mature retinas. These data demonstrate that premature infants are born with relatively low levels of retinal vitamin E, particularly in the avascular region, but contain an abundance of retinal Vitamin-C. These data further suggest that vitamin E supplementation results in a rapid increase in retinal vitamin E levels, particularly in infants >27 weeks gestational age.

Oral vitamin E supplements can prevent the retinopathy of abetalipoproteinaemia
Runge P, Muller DP, McAllister J, Calver D, Lloyd JK, Taylor D
Br J Ophthalmol 1986 Mar;70(3):166-73

Six patients with abetalipoproteinaemia are described who received large doses of oral vitamin E for between 12 and 18 years in addition to a low fat diet and supplements of the other fat soluble vitamins. The progressive retinopathy observed in untreated abetalipoproteinaemia was substantially modified and most probably prevented by this therapy. Angioid streaks were noted in one patient. Treatment with vitamin A alone did not prevent or arrest the progression of the retinal lesion.

The role of taurine in developing rat retina
Lepore D.; Antico L.; Balzano L.; Molle F.
Ophtalmologie (France), 1995, 9/3 (283-286)

Taurine is the most abundant free aminoacid in the retina. A recent study hypothesises the existence of two different functional pools of taurine in the retina: one Ca2-dependent, the other related to high K+ concentration, and to the subsequent cell volume adjustment. Many pathologic conditions, such as hypoxia or ischemia, can induce cell swelling: photoreceptors could prevent volume alteration by a taurine release. The mechanism allowing membrane protection by taurine is still unclear (modification of calcium ion fluxes and inhibition of protein phosphorylation), but many evidence of a key-role played by taurine have been found: we already know that the mother diet-free taurine produce a reduction of neonate optique nerve fibers. We studied the uptake system of taurine with 0.1 mM and 4 mM solution in 7(PN) and 15(PN15) days old rats retina, grown in environmental standard conditions, compared with adult rats. We also studied the effect of neonatal oxygen supplementation (80% O2 in the air followed by 9 days recovery in room air). The data demonstrate that PN 15 rats have a taurine uptake similar to the adult. The PN 7 rats have an hyperactive uptake of this aminoacid. The AA hypothesise that the developing rat retina has a good protection against damages induced by cell swelling during absolute or relative hypoxia. At PN 7 taurine could also play a key role for retinal growth. The oxygen, damaging the taurine uptake system, could stop the normal development of the optic pathway.

Taurine: Review and therapeutic applications (Part I)
Barbero Hernandez M.J.; Martin Sances M.S.; Damas Fernandez-Figares M.
J. Farm. Clin. (Spain), 1990, 7/7 (580-600)

No abstract.

Supplemental taurine in diabetic rats: Effects on plasma glucose and triglycerides
Goodman H.O.; Shihabi Z.K.
Biochem. Med. Metab. Biol. (USA), 1990, 43/1 (1-9+8)

The present study has indicated that significant shifts in plasma, urinary, and tissue taurine and in non-taurine dialyzable amines occur in the STZ-induced diabetic rat, especially in the kidney. Taurine administration at relatively low dosage ameliorated only kidney taurine concentration. Anticipated alterations in plasma glucose and creatinine were observed but neiher of these changes was affected by taurine administration. Similarly, urinary output of creatinine, gluycose, and NAG increased significantly among diabetic rats, but none of these were detectably influenced by taurine. Increases in plasma triglycerides observed in STZ-induced diabetes appear to be attenuated by taurine administration, and although cholesterol concentrations were lower in taurine-treated rats, the differences were not statistically significant. These findings should encourage further studies of these effects in rats as a useful model for several complications of human diabetes including atherosclerosis, retinopathy, and nephropathy

Taurine deficiency retinopathy in the cat
Barnett K.C.; Burger I.H.
J. Small Anim. Pract. (England), 1980, 21/10 (521-534)

The literature on feline central retinal degeneration is reviewed and an experiment reported which investigates whether taurine is essential in cats fed a purified diet. The development of taurine deficiency retinopathy is described and illustrated. The histopathological, ultrastructural and ERG changes are also described. Other retinal degenerations in the cat are discussed.

[Clinical experimentation with pyridoxylate in treatment of various chorioretinal degenerative disorders (50 cases)]
Boudet C; Philippot M; Arnaud B
Bull Soc Ophtalmol Fr. 1969 Dec. 69(12). P 1145-50

No abstract.

Rationales for micronutrient supplementation in diabetes
McCarty MF; Rubin EJ
Med Hypotheses. 1984 Feb. 13(2). P 139-51

Available evidence--some well-documented, some only preliminary--suggests that properly-designed nutritional insurance supplementation may have particular value in diabetes. Comprehensive micronutrient supplementation providing ample doses of antioxidants, yeast-chromium, magnesium, zinc, pyridoxine, gamma-linolenic acid, and carnitine, may aid glucose tolerance, stimulate immune defenses, and promote wound healing, while reducing the risk and severity of some of the secondary complications of diabetes. Refs: 125.

Magnesium and potassium in diabetes and carbohydrate metabolism. Review of the present status and recent results.
Durlach J; Collery P
Magnesium. 1984. 3(4-6). P 315-23

Diabetes mellitus is the most common pathological state in which secondary magnesium deficiency occurs. Magnesium metabolism abnormalities vary according to the multiple clinical forms of diabetes: plasma magnesium is more often decreased than red blood cell magnesium. Plasma Mg levels are correlated mainly with the severity of the diabetic state, glucose disposal and endogenous insulin secretion. Various mechanisms are involved in the induction of Mg depletion in diabetes mellitus, i.e. insulin and epinephrine secretion, modifications of the vitamin D metabolism, decrease of blood P, vitamin B6 and taurine levels, increase of vitamin B5, C and glutathione turnover, treatment with high levels of insulin and biguanides. K depletion in diabetes mellitus is well known. Some of its mechanisms are concomitant to those of Mg depletion. But their hierarchic importance is not the same: i.e., insulin hyposecretion is more important versus K+ than versus Mg2+. Insulin increases the cellular inflow of K+ more than that of Mg2+ because there is more free K+ (87%) than Mg2+ (30%) in the cell. The consequences of the double Mg-K depletion are either antagonistic: i.e. versus insulin secretion (increased by K+, decreased by Mg2+) or agonistic i.e. on the membrane: (i.e. Na+K+ATPase), tolerance of glucose oral load, renal disturbances. The real importance of these disorders in the diabetic condition is still poorly understood. Retinopathy and microangiopathy are correlated with the drop of plasma and red blood cell Mg. K deficiency increases the noxious cardiorenal effects of Mg deficiency. The treatment should primarily insure diabetic control.

Click to go to the Life Extension Foundation Web Site

All Contents Copyright © 1995-2000 By The Life Extension Foundation