Melatonin and nitric oxide

Melatonin is a product of the amino acid tryptophan in the pineal gland. Once synthesized, the specific mechanisms governing the release of melatonin from the pineal gland and its functions are largely unknown. Besides its regulatory role in circadian rhythms in mammals, because of its widespread subcellular distribution, melatonin contributes to the reduction of oxidative damage in both the lipid and the aqueous environments of the cell. This postulate is widely supported by the experimental observations showing that melatonin protects lipids in membranes, proteins in the cytosol, and DNA in the nucleus and mitochondria from free radical damage. Melatonin thus reduces the severity of disease conditions where free radicals are implicated. The direct free radical scavenging effects of melatonin are receptor independent. It has recently been shown that it has an ability to scavenge free radicals, including hydroxyl radicals, hydrogen peroxide, peroxyl radicals, singlet oxygen and nitric oxide (NO) and peroxynitrite anion. An excessive amount of NO, a free radical which is generated by the inducible form of NO synthase, is known to cause cytotoxic changes in cells. Hence, NO synthase is considered a pro-oxidative enzyme, and any factor that reduces its activity would be considered an antioxidant. Recent studies have shown that melatonin inhibits the activity of NO synthase, beside its NO and peroxynitrite scavenging activity. Thus, inhibition of NO production may be another means whereby melatonin reduces oxidative damage under conditions, such as ischemia-reperfusion, sepsis, etc, where NO seems to be important in terms of the resulting damage

Evaluation of foveal photoreceptor layer in eyes with macular edema associated with branch retinal vein occlusion after ozurdex treatment

The aim of this study was to evaluate the central retinal thickness (CRT), outer nuclear layer thickness (ONLT), photoreceptor layer thickness (PLT), photoreceptor layer integrity, and the correlation between visual acuity and PLT in eyes with branch retinal vein occlusion (BRVO) 2 months after treatment with intravitreal dexamethasone implant (Ozurdex; Allergan, Inc, Irvine, CA). In this prospective study, 32 eyes of 32 patients were enrolled. A single injection of Ozurdex was administered to all the patients. CRT, ONLT, and PLT were measured using spectral-domain optical coherence tomography before and 2 months after the injection. Best-corrected visual acuity (BCVA [logMAR]) and photoreceptor cell integrity were also evaluated. The average CRT, ONLT, PLT, and BCVA values for the sample group before the treatment were as follows: 707 +/- 261, 608 +/- 288, 70 +/- 25, and 0.96 +/- 0.22 A mu m, respectively. The average CRT, ONLT, PLT, and BCVA values for the sample group 2 months after the Ozurdex injection were as follows: 299 +/- 149, 211 +/- 138, 77 +/- 20, and 0.63 +/- 0.30 A mu m, respectively (p < 0.05). Two months after the Ozurdex injection, BCVA correlated with ONLT and PLT (r = 0.365, p = 0.048 and r = -0.488, p = 0.021, respectively), whereas BCVA was not correlated with CRT (r = 0.239, p = 0.189). Photoreceptor layer is associated with the visual function of eyes with macular edema secondary to BRVO. Also, ONLT seems to be more closely related to visual acuity improvement than CRT decrement

Posterior Ischaemic Optic Neuropathy after Uneventful Cataract Extraction

We report a case of posterior ischaemic optic neuropathy after cataract extraction. A 74-year-old man underwent uneventful phacoemulsification and posterior chamber intraocular lens implantation in left eye under peribulber anaesthesia. On the first postoperative day, the patient complained of vision loss in the in the left eye with a visual acuity of 1-m finger counting. After complete ocular, fluorescein angiographic, electrophysiological, systemic and laboratory evaluation, the diagnosis of posterior ischaemic optic neuropathy was made. This case highlights that posterior ischaemic optic neuropathy is a rare clinical entity and should be diagnosed only after exclusion of all other causes in differential diagnosis of postoperative visual loss

The Effect of Age on Dexamethasone Intravitreal Implant (Ozurdex (R)) Response in Macular Edema Secondary to Branch Retinal Vein Occlusion

Purpose: To investigate the effect of age on dexamethasone intravitreal implant (Ozurdex (R)) response in macular edema secondary to branch retinal vein occlusion (BRVO). Methods: Seventy-three eyes of 73 patients with macular edema secondary to BRVO were recruited in the study. The patients in the study were divided into the following four groups according to their ages: group 1 (= 80 years). Single-dose Ozurdex injection was applied to all patients. The effectiveness of Ozurdex treatment on macular edema is evaluated via optical coherence tomography (OCT) according to the age groups. Results: Two months after Ozurdex injection, mean reduction of central retinal thickness in groups 1, 2, 3, and 4 were -466.4 +/- 149.6, -379.7 +/- 238.7, -280.1 +/- 233.0, and -180.5 +/- 81.4 mu m, respectively. This reduction of central retinal thickness decreased with aging (p = 0.001). Also, ages of patients were negatively correlated with the mean reduction of central retinal thickness for the whole study group (r = -0.439, p < 0.001). Conclusion: Our study revealed that the effectiveness of Ozurdex treatment decreases with aging

Systemic Endothelial Function in Primary Open-Angle Glaucoma

Objective. We aimed to assess peripheral vascular endothelial function in open-angle glaucoma (POAG) by measuring flow-mediated dilatation (FMD). Materials and Methods. The study included 20 cases with POAG (group 1, mean age 58.68±13.3 years) and 30 healthy individuals (group 2, mean age 58.68±13.6 years). In all cases, responses of endothelial function were assessed by a cardiologist through measurement of FMD following brachial artery occlusion. Results. Mean percent of FMD, an indicator of endothelial function, was found to be 11.9±4.2% in group 1 and 12.3±4.4% in group 2 (P=0.86). Conclusion. No impairment in systemic vascular function of cases with POAG suggests that POAG could be a local disorder rather than being a component of systemic disease