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Objective:To observethe changesof thecontentanddistributionof cochlearactiningrowingratsatdif-ferentperiodsof irondeficiency (ID)and to explorethepathogeneticmechanismof ID-inducedsensorineuralhear-ingloss.Methods:Actinof cochlearmembranoustissuewasseparatedanddeterminedwithSDS-PAGEandWest-ernblot.Therelativecontentanddistributionof cochlearactinin bothID andnormalratsin week8and12were studiedby TLC-densitometricdeterminationandimmunohistochemicalprocedures.Results:A markedreductionof relativecontentandimmunohistochemicalreactionproductof cochlearactinwasfoundinIDratswithsensorineural hearinglossincomparisonwithnormalcontrols.Therewasno significantdifferenceof cochleaactinamongdiffer-entgroupsof IDratswithhearingloss.Conclusion: ID-inducedsensorineuralhearinglossis probablyassociated withreductionof actininthecochlea.It is suggestedthattheexperimentalID periodof timehaveno considerable effecton therelativecontentanddistributionof cochlearactin.
Objective: To observethe changesof thecontentanddistributionof cochlearactiningrowingratsatdif-ferentperiodsof irondeficiency (ID) and to explorethepathogeneticmechanismof ID-inducedsensorineuralhear-ingloss.Methods: Actinof cochlearmembranoustissuewasseparatedanddeterminedwithSDS-PAGEandWest-ernblot.Therelativecontentanddistributionof cochlearactinin bothID andnormalratsin week8and12were studiedby TLC-densitometricdeterminationandimmunohistochemicalprocedures.Results: A markedreductionof relativecontentandimmunohistochemicalreactionproductof cochlearactinwasfoundinIDratswithsensorineural hearinglossincomparisonwithnormalcontrols.Therewasno significant difference of cochlea actin amongdiffer-entgroups of IDrats witharingloss. Conflusion: ID-induced seseural injuryaringossisassociatedwithreductionofactininthecochlea.Itis suggestedThisperiodIDperiodof timehaveno considerable effecton therelativecontentanddistributionofcochlearactin.