ascorbic-acid and Retinal-Diseases

We investigated by means of a controlled prospective study, the effect of low dose oral colchicine (1.2 mg/day) on proliferative vitreoretinopathy (PVR) in humans. The PVR cases studied included ones associated with proliferative diabetic retinopathy, sickle retinopathy, trauma, and by venous occlusive disease. Applying Sandler's A statistic for correlated samples, we found no statistically significant difference between the results achieved in the colchicine group and those in the control group (vitamin C, 250 mg/day orally). We conclude that safe dosages of this drug do not significantly inhibit PVR.

Topics: Administration, Oral; Adult; Aged; Ascorbic Acid; Colchicine; Dose-Response Relationship, Drug; Humans; Male; Middle Aged; Pigment Epithelium of Eye; Prospective Studies; Retinal Diseases; Visual Acuity

We report a case of systemic oxalosis involving the eyes and joints due to long-term use of high-dose vitamin C in a patient receiving maintenance peritoneal dialysis (PD). This 76-year-old woman with autosomal dominant polycystic kidney disease underwent living unrelated kidney transplantation 10 years earlier. The transplant failed 6 months before presentation, and she initiated hemodialysis therapy before transitioning to PD therapy 4 months later. During the month before presentation, the patient noted worsening arthralgias and decreased vision. Ophthalmologic examination revealed proliferative retinopathy and calcium oxalate crystals. Plasma oxalate level was markedly elevated at 187 (reference range, <1.7) μmol/L, and urine oxalate-creatinine ratio was high (0.18mg/mg). The patient reported taking up to 4g of vitamin C per day for several years. Workup for causes of primary and secondary hyperoxaluria was otherwise negative. Vitamin C use was discontinued, and the patient transitioned to daily hemodialysis for 2 weeks. Plasma oxalate level before the dialysis session decreased but remained higher (30-53μmol/L) than typical for dialysis patients. Upon discharge, the patient remained on thrice-weekly hemodialysis therapy with stabilized vision and improved joint symptoms. This case highlights the risk of high-dose vitamin C use in patients with advanced chronic kidney disease, especially when maintained on PD therapy.

Topics: Aged; Ascorbic Acid; Calcium Oxalate; Dose-Response Relationship, Drug; Female; Humans; Hyperoxaluria; Kidney Failure, Chronic; Peritoneal Dialysis; Polycystic Kidney, Autosomal Dominant; Retinal Diseases; Treatment Outcome; Vitamins; Withholding Treatment

Spinal cord injury [SCI] leads to complex cellular and molecular interactions which affects various organ systems. The present study focused on determining the protection offered by Vitamin C against spinal injury-induced kidney damage in wistar rats. The experimental protocol was performed with three groups; Sham, SCI and Vitamin C [20 mg/kg/bw] followed by SCI. The kidney tissue was investigated for oxidative stress parameters [reactive oxygen species, protein carbonyl, sulphydryl content, thiobarbituric acid reactive species [TBARS], and myeloperoxidase activity] and antioxidant status [glutathione, superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase activity]. Further, inflammation studies were performed by analyzing expression of NF-κB, cycloxygenase-2, iNOS through western blot analysis and inflammatory cytokines by TNF-α and IL-1β levels. The present study shows clear evidence that Vitamin C treatment abrogated spinal injury-induced oxidative stress and inflammatory responses and enhanced the antioxidant status. Thus, the protection offered by Vitamin C against spinal cord injury-induced kidney damage is attributed to its anti-oxidant and anti-inflammatory effects.

Topics: Animals; Antioxidants; Ascorbic Acid; Cyclooxygenase 2; Cytokines; Disease Models, Animal; Down-Regulation; Glutathione; Laminectomy; Male; NF-kappa B; Nitric Oxide Synthase Type II; Peroxidase; Protein Carbonylation; Rats; Rats, Wistar; Reactive Oxygen Species; Retinal Diseases; Spinal Cord Injuries

To investigate the rate and mechanism of oxygen consumption by the vitreous.. Oxygen consumption was measured with a microrespirometer. Vitreous ascorbate was measured spectrophotometrically and by gas chromatography-mass spectrometry. Vitreous degeneration was related to the rate of oxygen consumption and ascorbate concentration in samples obtained during vitrectomy.. Prolonged exposure to oxygen or treatment with ascorbate oxidase eliminated oxygen consumption by the vitreous. Adding ascorbate restored oxygen consumption. Oxygen consumption persisted after boiling or treating the vitreous with the chelating agents EDTA and deferoxamine. In patients undergoing retinal surgery, liquefaction of the vitreous and previous vitrectomy were associated with decreased ascorbate concentration and lower oxygen consumption.. Ascorbate in the vitreous decreases exposure of the lens to oxygen. The catalyst for this reaction is not known, although free iron may contribute. The gel state of the vitreous preserves ascorbate levels, thereby sustaining oxygen consumption. Vitrectomy or advanced vitreous degeneration may increase exposure of the lens to oxygen, promoting the progression of nuclear cataracts.. Determining how the eye is protected from nuclear cataracts should suggest treatments to reduce their incidence.

Topics: Ascorbate Oxidase; Ascorbic Acid; Cataract; Gas Chromatography-Mass Spectrometry; Gels; Humans; Oxygen; Oxygen Consumption; Retinal Diseases; Vitrectomy; Vitreous Body

Organophosphorus insecticide poisoning is widely investigated, and a growing number of evidence indicates its effects to cause ocular lesions, but the mechanisms of its ocular effects are not well elucidated. Here, effects of organophosphorus insecticide chlorpyrifos on mouse retina in vivo and protection of combination of vitamins C and E were reported. Cell apoptosis, lipid peroxidation and DNA damage were increased, and activities of antioxidant enzymes superoxide dismutase, catalase and glutathione peroxidase were decreased in retina of chlorpyrifos-administrated mice (63mg/kg, single treatment, via oral gavage). Pretreatment of combination of antioxidants vitamin C (250mg/kg) and vitamin E (150mg/kg) (once daily for 6 days, hypodermic injecting) significantly attenuated these effects of chlorpyrifos, demonstrating oxidative stress was involved in chlorpyrifos-induced cell apoptosis in mouse retina. Moreover, chlorpyrifos treatment inhibited acetylcholinesterase activity and promoted [Ca(2+)](i) level in mouse retinal cells, which were also attenuated by combination of vitamins C and E. These results may have implications for treatment of organophosphorus insecticide poisoning in retina with combination of vitamins C and E.

Topics: Acetylcholinesterase; Animals; Apoptosis; Ascorbic Acid; Calcium; Catalase; Chlorpyrifos; Comet Assay; DNA Damage; Drug Therapy, Combination; Glutathione Peroxidase; Insecticides; Male; Malondialdehyde; Mice; Mice, Inbred Strains; Microscopy, Confocal; Oxidative Stress; Retina; Retinal Diseases; Superoxide Dismutase; Vitamin E; Vitamins

Oxidative stress is thought to be involved in the pathogenesis of age-related diseases, such as atherosclerosis and retinal degeneration. The current study was conducted to examine vitreoretinal oxidative status in a model of porcine hypercholesterolemia to identify morphologic alterations and analyze the effect of dietary supplementation with vitamins C and E.. Adult miniature pigs were fed standard chow, cholesterol-rich chow, or a cholesterol-rich diet supplemented with vitamins C and E. Total cholesterol, triglycerides, high-density lipoproteins, lipid peroxidation, and tocopherol were measured in plasma. Lipid peroxidation and nitric oxide (NO) metabolites were measured in vitreous and retinal homogenates. Superoxide anion release in the retinal pigment epithelium (RPE) was analyzed by chemiluminescence. Retinal morphology was studied by transmission electron microscopy.. The high-cholesterol group, with increased retinal oxidative stress (P < 0.01) and NO metabolites in the retina (P < 0.05), had increased superoxide anion release (P < 0.05) and showed development of pyknosis, irregular nuclear membranes, and cytoplasmic accumulation of lipids and autophagocytic vacuoles in the RPE cells. Vitamins C and E prevented biochemical changes and most ultrastructural alterations in the RPE.. The results suggest an evolving role for hypercholesterolemia through increased retinal oxidative stress and NO synthesis that could be responsible for retinal ultrastructural alterations. The beneficial effects of vitamins C and E in the retinal tissue further support this hypothesis.

Topics: Animals; Antioxidants; Ascorbic Acid; Cholesterol; Cholesterol, Dietary; Dietary Supplements; Hypercholesterolemia; Lipid Peroxidation; Male; Nitric Oxide; Oxidative Stress; Retina; Retinal Diseases; Superoxides; Swine; Swine, Miniature; Tocopherols; Triglycerides; Vitamin E; Vitreous Body

Antioxidants were administered to diabetic rats and experimentally galactosemic rats to evaluate the ability of these agents to inhibit the development of diabetic retinopathy. Alloxan diabetic rats and nondiabetic rats that were fed 30% galactose randomly received standard diets or the diets supplemented with ascorbic acid and alpha-tocopherol (vitamins C+E diet) or a more comprehensive mixture of antioxidants (multi-antioxidant diet), including Trolox, alpha-tocopherol, N-acetyl cysteine, ascorbic acid, beta-carotene, and selenium. Diabetes or galactose feeding of at least 12 months resulted in pericyte loss, acellular capillaries, and basement membrane thickening. Compared with diabetic controls, the development of acellular capillaries was inhibited by 50% (P < 0.05) in diabetic rats that received supplemental vitamins C+E, and the number of pericyte ghosts tended to be reduced. The vitamins C+E supplement had no beneficial effect in galactosemic rats, but these rats consumed only approximately half as much of the antioxidants as the diabetic rats. The multi-antioxidant diet significantly inhibited ( approximately 55-65%) formation of both pericyte ghosts and acellular capillaries in diabetic rats and galactosemic rats (P < 0.05 vs. controls), without affecting the severity of hyperglycemia. Parameters of retinal oxidative stress, protein kinase C activity, and nitric oxides remained elevated for at least 1 year of hyperglycemia, and these abnormalities were normalized by multi-antioxidant therapy. Thus, long-term administration of antioxidants can inhibit the development of the early stages of diabetic retinopathy, and the mechanism by which this action occurs warrants further investigation. Supplementation with antioxidants can offer an achievable and inexpensive adjunct therapy to help inhibit the development of retinopathy in diabetes.

Topics: Acetylcysteine; Animals; Antioxidants; Ascorbic Acid; beta Carotene; Chromans; Diabetes Mellitus, Experimental; Diabetic Retinopathy; Diet; Dietary Supplements; Galactosemias; Male; Pericytes; Rats; Rats, Sprague-Dawley; Retina; Retinal Diseases; Selenium; Vitamin E

To measure the blood levels of oxygen and lipid-free radicals as lipid peroxidation products and of vitamins E, C and A, in order to explain intraocular inflammation, retinal neovascularization and detachment in Eales' disease.. Levels of the lipid peroxidation products produced by oxygen and lipid free radicals (estimated as thiobarbituric acid reactive substances-TBARS), vitamin E with ferric chloride, vitamin C with 2,6-dichlorophenol-indophenol and vitamin A with antimony trichloride were all evaluated in three groups of subjects between 20 and 40 years of age. Twenty three were patients with Eales' disease in the active perivasculitis stage (Group I), 19 were patients with Eales' disease in the healed-perivasculitis stage (Group II), and 46 were healthy volunteers (Group III), used as normal controls. Patients in each group were subdivided into two age groups, 20-30 and 31-40 years, each group containing both sexes.. The results showed a 4.6- and 5.6-fold increase in the levels of TBARS in erythrocytes of patients with Eales' disease in the active perivasculitis stage (Group I) and a 2-fold increase in patients with Eales' disease in the healed perivasculitis stage (Group II), when compared to levels in the controls (Group III). On the other hand, there was a decrease of 75 and 76.2% in the levels of vitamin E in serum, 34 and 40.9% of vitamin C in plasma and 72.8 and 67% of vitamin A in serum in patients with Eales' disease in the active perivasculitis stage (Group I), as compared to the controls (Group III). Also decreases of 56 and 43.5% of vitamin E in serum, 26.8 and 12.5% of vitamin C in plasma and 50.5 and 49.4% of vitamin A in serum were found in patients with Eales' disease in the healed perivasculitis stage (Group II) as compared to the healthy controls (Group III). The two values of variations between the patients and the normal control group given above for TBARS, vitamins E,C and A are for the two age groups, 20-30 and 31-40 respectively. The differences were statistically significant (P < 0.01 to 0.001).. Lowered levels of antioxidant vitamins E and C and consequent accumulation of oxygen and lipid free radicals, or vice versa, could explain the inflammation, neovascularization and retinal pathology in patients with Eales' disease. Also, vitamin A deficiency could aggravate retinal illness.

Topics: Adult; Antioxidants; Ascorbic Acid; Female; Humans; Lipid Peroxides; Male; Neovascularization, Pathologic; Reactive Oxygen Species; Retinal Diseases; Retinitis; Vasculitis; Vitamin A; Vitamin E

Topics: Ascorbic Acid; Exudates and Transudates; Humans; Male; Middle Aged; Retinal Diseases; Retinal Hemorrhage; Scurvy

Retinal light damage in dark-reared rats supplemented with ascorbic acid and exposed to multiple doses of intermittent light was studied and compared with damage in unsupplemented dark-reared and cyclic-light-reared rats. The extent of photoreceptor cell loss from intense light exposure was determined by whole-eye rhodopsin levels and retinal DNA measurements two weeks after light treatment. Two weeks after 3 or 8 hr of intermittent light, ascorbate-supplemented animals had rhodopsin and retinal DNA levels that were two to three times higher than in unsupplemented dark-reared rats. In both types of rats rhodopsin levels were influenced by the number of light doses, the duration of light exposure, and to a lesser extent, by the length of the dark period between exposures. Rhodopsin levels in the dark-reared ascorbate-supplemented rats were significantly higher than in unsupplemented dark-reared rats, and were similar to the levels in unsupplemented cyclic-light-reared animals. Ascorbate treatment had no effect on the rate of rhodopsin bleaching. However, regeneration was greater in supplemented rats after multiple 1-hr light exposures. Intermittent light also resulted in lower ascorbate levels in the retinas of supplemented and unsupplemented rats, with dramatic losses from the retinal pigment epithelium (RPE)-choroid in both types of animals. We conclude that ascorbic acid protects the eye by reducing the irreversible Type I form of light damage in dark-reared rats. Ascorbate appears to shift light damage to the Type II form typical of cyclic-light-reared animals.

Topics: Animals; Ascorbic Acid; Darkness; DNA; Dose-Response Relationship, Radiation; Eye; Light; Male; Periodicity; Photoreceptor Cells; Radiation-Protective Agents; Rats; Rats, Inbred Strains; Regeneration; Retina; Retinal Diseases; Rhodopsin

A 55-year-old woman with chronic renal failure treated with hemodialysis had severe bilateral visual loss develop due to retinal ischemia. Ophthalmoscopy showed crystals in the distribution of the retinal arteries, but not veins, and this led to a diagnosis of systemic oxalosis. Factors contributing to systemic oxalosis in addition to renal failure were ascorbic acid dietary supplementation, pyridoxine deficiency, and ileal resection. Histopathologic findings showed ocular calcium oxalate deposition limited nearly entirely to the walls of retinal blood vessels.

Topics: Adult; Ascorbic Acid; Birefringence; Calcium Oxalate; Crystallization; Eye; Fluorescein Angiography; Graft Rejection; Humans; Kidney Failure, Chronic; Kidney Transplantation; Middle Aged; Renal Dialysis; Retinal Diseases

Mild and severe retinal photic injuries were inflicted on 22 eyes of seven monkeys fed a vitamin C-deficient diet and four monkeys given a vitamin C-enriched diet. The retinal lesions were studied by fundus examination, fluorescein angiography, and light and electron microscopy. While the general cellular response to photic injury in the retina of scorbutic animals was not different qualitatively from that in the normal animals, scurvy appeared to cause more severe tissue damage, an exaggerated repair response, and more advanced retinal degeneration. In the four groups of eyes, representing mild and severe photic injury in normal and scorbutic animals, a continuous spectrum of changes was produced. The least damage occurred from mild photic injury in the normal animals, and the most detrimental insult resulted from severe photic injury in the scorbutic animals. We propose that the basic mechanism by which ascorbate mitigates retinal photic injury depends on its redox properties. Ascorbate functions as an antioxidant in the retina. It scavenges superoxide radicals and hydroxyl radicals, quenches singlet oxygen, and reduces hydrogen peroxide, all of which are formed in retinal photic injury. This hypothesis provides an explanation for the high level of ascorbate in the retina. The pathogenetic mechanisms that correspond to the three distinct phases of pathologic changes observed in retinal photic injury are characterized. In phase 1, single oxygen is generated in a photodynamic reaction that damages the photoreceptor elements and pigment epithelium. In phase 2, macrophages attracted from the systemic circulation invade the subretinal space, and a photo-oxidative reaction generates superoxide radicals, hydrogen peroxide, and hydroxyl radicals. These free radicals attack the photoreceptor cells and pigment epithelium to cause further retinal damage. In phase 3, macrophages remain in the subretinal space for as long as 8 months after injury, causing persistent disruption of the blood-retinal barrier. The photo-oxidative reaction appears to linger, resulting in chronic retinal degeneration. It is hypothesized that in some forms of age-related macular degeneration, patients suffer from repeated mild photic insult throughout their lifetime. Aging has been associated with subclinical scurvy, which leads to even greater susceptibility to photic injury. Although ascorbate moderates many biochemical functions of the body and helps the retina ameliorate photo-oxidativ

Topics: Animals; Ascorbic Acid; Ascorbic Acid Deficiency; Light; Macaca fascicularis; Oxidation-Reduction; Retina; Retinal Diseases

Topics: Animals; Arteriosclerosis; Ascorbic Acid; Cattle; Endothelium; Female; Glycosaminoglycans; Insulin; Myocardium; Pregnancy; Retinal Diseases

Topics: Adult; Ascorbic Acid; Corneal Injuries; Epithelium; Foreign-Body Reaction; Glyoxylates; Humans; Hydrogen-Ion Concentration; Male; Melanins; Metabolic Diseases; Oxalates; Retinal Detachment; Retinal Diseases; Uveitis; X-Ray Diffraction

Topics: Adult; Ascorbic Acid; Blindness; Diabetes Complications; Female; Hemosiderosis; Humans; Male; Middle Aged; Oxalates; Retina; Retinal Detachment; Retinal Diseases

Topics: Adrenal Cortex Hormones; Adult; Aged; Arterial Occlusive Diseases; Ascorbic Acid; Cerebrovascular Disorders; Child; Chorioretinitis; Edema; Female; Humans; Ketones; Male; Middle Aged; Retinal Artery; Retinal Degeneration; Retinal Diseases; Retinal Vessels; Rutin; Vitamin B Complex; Xanthines