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Purpose: To investigate the effects of nicotine on retinal alterations in early-stage diabetes in an established rodent model. Materials and Methods: Sprague-Dawley rats were examined using a combination of confocal scanning laser ophthalmoscopy and spectral domain optical coherence tomography to determine changes in retinal structure in response to nicotine exposure, diabetes and the combined effects of nicotine and diabetes. Diabetes was induced by a single injection of 65 mg/kg streptozotocin and nicotine injections were administered subcutaneously daily. Retinal thickness in the superior, inferior, nasal and temporal quadrants were determined based on the spectral domain optical coherence tomography (SD-OCT) volume scans (20° × 20°) centered on the optic disc. Segmentation of discrete retinal layers was performed on a subset of SD-OCT cross-sections to further examine changes in each treatment group. Survival of neurons within the ganglion cell layer (GCL) was assessed by confocal morphometric imaging. Results: The control group did not experience any significant change throughout the study. The nicotine treatment group experienced an average decrease in total retinal thickness (TRT) of 9.4 µm with the majority of the loss localized within the outer nuclear layer (ONL) as determined by segmentation analysis ( p < 0.05). The diabetic group exhibited a trend toward decreased TRT while segmentation analysis of the diabetic retinopathy (DR) group revealed significant thinning within the ONL ( p < 0.05). The combination of nicotine and diabetes revealed a significant increase of 8.9 µm in the TRT ( p < 0.05) accompanied by a decrease in the number of GCL neurons. Conclusions: We demonstrated significant temporal changes in retinal morphology in response to nicotine exposure, diabetes and with the combined effects of nicotine and diabetes. These findings may have implications in determining treatment strategies for diabetic patients using products containing nicotine, such as cigarettes, smokeless tobacco, electronic cigarettes or smoking cessation products. [ABSTRACT FROM AUTHOR] more...

Purpose . To investigate the interrelationships between DNA damage,mitochondrial activity, and apoptosis in retinal pigment epithelial cells(RPE) after exposure to rod outer segments (ROS). Methods . After incubation of cultured human RPE with ROS, mitochondrialredox function was evaluated from MTT reduction. Mitochondrial (mt) and nuclear(n) DNA damage were determined by quantitative polymerase chain reactions(QPCR). Apoptotic RPE cells were detected by binding of annexin V to phosphatidylserine (PS) using fluorescence microscopy. The expression of the pro-apoptoticproteins, p53 and p21[sup waf-1] , and DNA repair enzymes, apurinic/apyrimidinicendonuclease (APE[sup ref-1] ) and DNA polymerase β (β-pol) werequantitatively determined by Western blotting analysis. Results . Mitochondrial function decreased by 20 ± 5% andannexin V immunofluorscent binding was enhanced after exposure of cells tophysiological levels of ROS (3.8 × 10[sup 6] cm[sup -2] )for 4 h. MtDNA was preferentially damaged after exposure to ROS with increasedlesion frequencies of 1.49 ± 0.37 and 2.2 ± 0.14 per 10 kb basepairs (bp), respectively after 5 and 7 h contact, compared to untreated controls(zero class damage). APE[sup ref-1] expression increased more than 340%above controls after exposure to ROS for 7 and 24 h. The expression of β-polin cultures increased 110% above controls after 24 h contact with the ROS.The expression of p53 and p21 in cells increased 100 and 38% above controlsafter 24 h exposure to the ROS. Conclusions . Exposure of ROS to ROS induced mtDNA damage and dysfunctionand activated nDNA repair pathways, which did not prevent apoptosis. [ABSTRACT FROM AUTHOR] more...

Reports on the medical case of an 18-year-old woman who underwent Nd:YAG laser photocoagulation to the preretinal hyaloid interface. History of a large red scotoma in the superior half of her vision in the left eye; Description of hemorrhagic retinopathy; Fundus findings. more...