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      Propolis Prevents the Effects of Chronic Alcohol Intake on Ocular Tissues


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          Aim: This study is designed to investigate the protective effects of propolis in ocular tissues against chronic alcohol exposure. Material and Method: Wistar albino rats were used in this study. Rats were divided into 4 groups, and each group was fed a special liquid diet which contained an equal amount of calories. The control group was fed the liquid special diet without alcohol and propolis. We added propolis (150 mg/kg) to the diet of the second group. The diet of the third group contained alcohol, the concentration of which was increased progressively. The fourth group was fed a diet including propolis and alcohol. To counterbalance caloric intake, we decreased the amount of glucose in the special liquid diet for groups 3 and 4. At the end of 30 days, the animals were sacrificed and samples were kept at –80°C until evaluation. Specimens were investigated by light microscopy for morphology and morphometry. Results: In the histological investigation of ocular tissues, alcohol caused an increase in thickness of the cornea and corneal epithelium compared to the control group (p < 0.05). This incremental tendency was significantly reduced by propolis, and values were very close to those of the control group (p > 0.05). Alcohol did not cause any significant alteration of rat retinal thickness. Conclusion: This study showed that propolis is highly effective against corneal edema secondary to chronic alcohol intake.

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          Most cited references16

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          Water extract of propolis and its main constituents, caffeoylquinic acid derivatives, exert neuroprotective effects via antioxidant actions.

          We investigated whether water extract of Brazilian green propolis (WEP) and its main constituents [caffeoylquinic acid derivatives (3,4-di-O-caffeoylquinic acid, 3,5-di-O-caffeoylquinic acid, chlorogenic acid) and cinnamic acid derivatives (p-coumaric acid, artepillin C, drupanin, baccharin)] exert neuroprotective effects against the retinal damage induced by oxidative stress. Additionally, their neuroprotective effects were compared with their antioxidant effects. WEP, 3,4-di-O-caffeoylquinic acid, 3,5-di-O-caffeoylquinic acid, chlorogenic acid, and p-coumaric acid (but not artepillin C, baccharin, or drupanin) concentration-dependently inhibited oxidative stress-induced neurotoxicity [achieved using L-buthionine-(S,R)-sulfoximine (BSO) to deplete glutathione in combination with glutamate to inhibit cystine uptake] in cultured retinal ganglion cells (RGC-5, a rat ganglion cell line transformed using E1A virus). At their effective concentrations against oxidative stress-induced retinal damage, WEP, 3,4-di-caffeoylquinic acid, 3,5-di-caffeoylquinic acid, and chlorogenic acid (but not cinnamic acid derivatives) inhibited lipid peroxidation (LPO) in mouse forebrain homogenates. Thus, the neuroprotective effects of WEP and caffeoylquinic acid derivatives paralleled those against LPO. These findings indicate that WEP and caffeoylquinic acid derivatives have neuroprotective effects against retinal damage in vitro, and that these effects may be partly mediated via antioxidant effects.
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            Taurine restores ethanol-induced depletion of antioxidants and attenuates oxidative stress in rat tissues.

            Ethanol by its property of generating free radicals during the course of its metabolism causes damage to cell structure and function. The study investigates the protective effects of the antioxidant aminoacid taurine on ethanol-induced lipid peroxidation and antioxidant status. Male Wistar rats of body weight 170-190 g were divided into 4 groups and maintained for 28 days as follows: a control group and taurine-supplemented control group, taurine supplemented and unsupplemented ethanol-fed group. Ethanol was administered to rats at a dosage of 3 g/kg body weight twice daily and taurine was provided in the diet (10 g/kg diet). Lipid peroxidation products and antioxidant potential were quantitated in plasma and in following tissues liver, brain, kidney and heart. Increased levels of thiobarbituric acid substances (TBARS) and lipid hydroperoxides (LHP) in plasma and tissues, decreased activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) were observed in hemolysate and tissues of ethanol-fed rats. The contents of reduced glutathione (GSH), alpha-tocopherol and ascorbic acid in plasma and tissues were significantly reduced in these animals as compared to control animals. Simultaneous administration of taurine along with ethanol attenuated the lipid peroxidation process and restored the levels of enzymatic and non-enzymatic antioxidants. We propose that taurine may have a bioprotective effect on ethanol-induced oxidative stress.
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              • Abstract: found
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              Alcohol-induced impairment of behavioral control: differential effects on engaging vs. disengaging responses.

              Model-based assessments of behavioral control have been used to study the acute effects of alcohol on the ability to execute and inhibit behavioral responses. Response inhibition appears more vulnerable to the impairing effects of alcohol than response execution. Current information processing models have yet to account for this observation. The present study used a reductionist approach to determine if the particular vulnerability of response inhibition to the effects of alcohol occurs at the level of the action (motor program). The study examined the effects of alcohol on the ability to execute and inhibit behavior in a context in which preliminary information signaled the likelihood that a response should be executed or suppressed. The engagement and disengagement of responses were directly compared under alcohol. Adults (N = 24) performed a cued go/no-go task that required quick responses to go targets and suppression of responses to no-go targets. Response requirements were manipulated by varying the nature of the action required whereby half of the participants made key press responses (response engagement) and the other half released ongoing key presses (response disengagement). Performance was tested under three doses of alcohol: 0.00, 0.45, and 0.65 g/kg. Dose-dependent increases in commission errors were only observed with response engagement and not with response disengagement. Reaction times were faster for response engagement than response disengagement. Response disengagement affords some protection against alcohol-induced impairment of inhibition, indicating that not all aspects of motor processing requiring inhibition are equally impaired by alcohol.

                Author and article information

                Ophthalmic Res
                Ophthalmic Research
                S. Karger AG
                November 2009
                23 July 2009
                : 42
                : 3
                : 147-151
                aResearch Hospital, Celal Bayar University Medical Faculty, Manisa, and Departments of bPhysiology and cHistology and Embryology, Faculty of Medicine, Inonu University, Malatya, Turkey
                229029 Ophthalmic Res 2009;42:147–151
                © 2009 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                : 06 July 2008
                : 28 August 2008
                Page count
                Figures: 6, Tables: 1, References: 20, Pages: 5
                Original Paper

                Vision sciences,Ophthalmology & Optometry,Pathology
                Chronic alcohol intake,Keratopathy,Propolis
                Vision sciences, Ophthalmology & Optometry, Pathology
                Chronic alcohol intake, Keratopathy, Propolis


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