AntiglycatingpotentialofZingiberofficinalisanddelayofdiabeticcataractinratsMeghaSaraswat,1PallaSuryanarayana,1PaduruYadagiriReddy,1MadhoosudanA.Patil,1NagallaBalakrishna,2GeereddyBhanuprakashReddy11BiochemistryDivision,NationalInstituteofNutrition,Hyderabad,India;2StatisticsDivision,NationalInstituteofNutrition,Hyderabad,IndiaPurpose:Advancedglycationendproducts(AGE)areassociatedinthedevelopmentofseveralpathophysiologiesincludingdiabeticcataract.Earlierwehavereportedthatsomecommondietaryagentshaveantiglycatingactivityandginger(Zingiberofficinalis)wasoneofthefewprominentagentsthateffectivelypreventedAGEformationinvitro.Inthisstudyweinvestigatedthepotentialofgingertopreventdiabeticcataractinrats.Methods:DiabeteswasinducedinWistar-NINratsbyintraperitonealinjectionofstreptozotocin(35mg/kgbodyweight)andthecontrolratsreceivedvehiclealone.WhileasetofdiabeticanimalsreceivedAIN-93diet,anothersetreceivedeither0.5or3%gingerintheirdietforaperiodoftwomonths.Cataractprogressionwasmonitoredbyslit-lampbiomicroscope.Attheendoftwomonths,theanimalsweresacrificedtoevaluatenon-enzymaticglycationandosmoticstressintheeyelens.Results:Slit-lampexaminationrevealedthatfeedingofgingernotonlydelayedtheonsetbutalsotheprogressionofcataractinrats.MolecularanalysesindicatedthatfeedingofgingersignificantlyinhibitedtheformationofvariousAGEproductsincludingcarboxymethyllysineintheeyelens.Inaddition,gingeralsocounteredhyperglycemia-inducedosmoticstressinthelens.Conclusions:Theresultsindicatedthatgingerwaseffectiveagainstthedevelopmentofdiabeticcataractinratsmainlythroughitsantiglycatingpotentialandtoalesserextentbyinhibitionofthepolyolpathway.Thus,ingredientsofdietarysources,suchasginger,maybeexploredforthepreventionordelayofdiabeticcomplications.Thestatisticalfactsindicatethattheworld,particularlySouth-EastAsiaincludingIndia,isfacingagrowingdiabetesepidemicofpotentiallydevastatingproportions[1,2].Prolongedexposuretochronichyperglycemia,withoutpropermanagement,canleadtovariousshort-termandlong-termsecondarycomplications,whichrepresentthemaincauseofmorbidityandmortalityindiabeticpatients.Cataract,characterizedbytheopacificationoftheeyelensthatinterfereswithtransmissionoflightontotheretina,isoneoftheearliestsecondarycomplicationsofdiabetes.Cataractistheleadingcauseofvisualimpairmentacrosstheworldandstudiesindicatethattheincidenceofcataractismuchhigherindiabeticthaninnon-diaeticindividuals[3,4].Considerableevidencesuggeststhatthelong-termpathologicalsequelofdiabetesisaresultoftheaccumulationoftissuemacromoleculesthathavebeenprogressivelymodifiedbynon-enzymaticglycation[5-7].Glycationisanon-enzymaticreactionbetweenreducingsugarandfreeaminogroupoftheprotein(predominantlytheε-aminogroupoflysineandtheguanidinegroupofarginine)forminganAmadoriproduct[5-7].ThelatterthenundergoesaseriesofCorrespondenceto:Dr.G.BhanuprakashReddy,NationalInstituteofNutrition,Jamai-Osmania,Tarnaka,Hyderabad-500604,India;Phone:91-40-27008921;FAX:91-40-27019074;email:geereddy@yahoo.comcomplexreactions(oxidativeandnonoxidative)resultingintheformationofadvancedglycationendproducts(AGE).Non-enzymaticglycationoflensproteinhasbeenconsideredtobeoneofthemajorfactorsresponsiblefordiabeticcataract[7-10],whichaltersproteinconformationandstability,inducesproteinaggregationandcross-linking,andleadstoproteininsolubilization[11-14].Studiesalsoshowthefo...
