oxidat stress regard mediat nerv cell death sever neurodegen disord parkinson diseas sesamin lignan main found sesam oil current under studi it antioxid possibl neuroprotect properti use 1methyl4phenylpyridin mpp ion activ metabolit potent parkinsonismcaus toxin 1methyl4phenyl1256tetrahydropyridin produc oxid stress neurodegener neuron pc12 cell which express dopamin well neurofila our result show picomolar dose sesamin protect neuron pc12 cell from mpp induc cellular death reveal colorimetr measur product reactiv oxygen speci also demonstr sesamin act rescu tyrosin hydroxylas level from mpp induc deplet sesamin howev did modul dopamin transport level estrogen receptoralpha beta protein express examin sever paramet cell distress found sesamin also elicit strong increas superoxid dismutas activ well protein express decreas catalas activ mpp stimul induc nitric oxid synthas protein express neuron pc12 cell final sesamin possess signific antiinflammatori properti disclos it potenti reduc mpp induc interleukin6 mrna level microglia from studi determin import lignan sesamin neuroprotect molecul it possibl role complementari prevent therapi neurodegen diseas

Vicky Lahaie-Collins

Julie Bournival

Marilyn Plouffe

Julie Carange

Maria-Grazia Martinoli

Sesamin Modulates Tyrosine Hydroxylase, Superoxide Dismutase, Catalase, Inducible No Synthase and Interleukin-6 Expression in Dopaminergic Cells Under Mpp+-Induced Oxidative Stress

previous have shown window opportun nicotinamid nam therapi 50 follow cortic contus injuri cci extend 48 hrs postcci when administ over six day postcci interv the purpos present studi determin more chronic nam treatment protocol administ follow cci would extend current window opportun effect treatment onset group rat receiv either unilater cci sham procedur initiat nam therapi 50 began either 15min 4hrs 8hrs 24hrs postinjuri all group receiv daili system treatment 12 day postcci 24 interv behavior assess were conduct 28 day post injuri includ vibrissa forelimb place bilater tactil adhes remov forelimb asymmetri task locomotor place test behavior analysi both tactil remov locomotor place test show all namtreat group facilit recoveri function compar salin treatment howev vibrissaeforelimb place forelimb asymmetri test onli 4hr 8hr namtreat group were signific differ from salinetr group the lesion analysi show treatment nam out 8 hrs postcci signific reduc size injuri caviti the window opportun nam treatment taskdepend some situat can extend 24 hrs postcci these result suggest long term treatment regimen 50 nam start clinic relev time point may prove efficaci human tbi

Michael R Hoane

Jeremy L Pierce

Nicholas A. Kaufman

Jason E. Beare

Variation  in Chronic Nicotinamide Treatment after Traumatic Brain Injury Can Alter Components of Functional Recovery Independent of Histological Damage

arsenic natur occur element ubiquit present environ high concentr natur occur arsenic drink water major health problem differ part world despit arsenic be health hazard well document carcinogen safe effect specif prevent therapeut measur avail among various recent strategi adopt administr antioxid has been report most effect the present studi design evalu therapeut efficaci monoisoamyl dimercaptosuccin acid miadmsa administ either individu combin taurin post chronic arsenic exposur rat arsenic expos male rat 25 ppm sodium arsenit drink water 24 week were treat taurin 100 onc daili monoisoamyl dimercaptosuccin acid miadmsa 50 oral onc daili either individu combin 5 consecut day biochem variabl indic oxid stress alongwith arsenic concentr blood liver kidney were measur arsenic exposur signific reduc blood δaminolevulin acid dehydratas alad activ key enzym involv heme biosynthesi enhanc zinc protoporphyrin zpp level clinic hematolog variabl like white blood cell wbc mean cell hemoglobin mch mean cell hemoglobin concentr mchc show signific decreas signific elev platelet plt count these chang were accompani signific decreas superoxid dismutas sod activ increas catalas activ arsenic exposur caus signific decreas hepat renal glutathion gsh level increas oxid glutathion gssg these biochem chang were correl increas uptak arsenic blood liver kidney administr taurin signific reduc hepat oxid stress howev coadministr higher dose taurin 100 miadmsa provid more pronounc effect improv antioxid status liver kidney reduc bodi arsenic burden compar individu treatment miadmsa taurin the result suggest order achiev better effect chelat therapi coadministr taurin miadmsa might prefer

Swaran J. S. Flora

Swapnila Chouhan

Gurusamy M. Kannan

Megha Mittal

Harimohan Swarnkar

Combined Administration of Taurine and Monoisoamyl Dmsa Protects Arsenic Induced Oxidative Injury in Rats

have develop evalu vitro cultur method assess ischem injuri primari mous renal tubular epitheli cell rtec which explor pathobiolog under acut kidney injuri rtec were predomin proxim tubul origin which most suscept ischem injuri compar other nephron segment oxidat stress induc chemic deplet atp use antimycin 2deoxydglucos expos cell 1 oxygen environ necrot injuri assess measur ldh releas cultur supernat optimal dose time exposur each injuri agent determin induct mild moder sever ischem injuri defin ldh releas 20 2149 50 abov baselin respect antimycin 2deoxydglucos produc progress increas ldh releas which time depend chemic concentr independ 1 oxygen environ also induc cell injuri over time onli glucos absent from cultur media antimycin most effect induc oxid stress caus mean ldh releas 61 48 compar 19 50 ldh releas induc 2deoxydglucos exposur 1 oxygen respect same 48 hour time pointth cell cultur method describ provid sever advantag includ use serum free media abil grow primari cell without matrix support the ldh assay injuri assess reproduc cost effect object minim background cell death simpl method cultur injuri primari mous renal tubular epitheli cell has therebi been establish provid use tool futur investig ischem kidney injuri

Anne C. Breggia

Jonathan Himmelfarb

Primary Mouse Renal Tubular Epithelial Cells Have Variable Injury Tolerance to Ischemic and Chemical Mediators of Oxidative Stress

spermatogenesi high complic process which function spermatozoa haploid generat from primit mitot spermatogonia diploid this process involv differenti transform sever type germ cell spermatocyt spermatid undergo meiosi differenti due it sophist complex testi possess intrins mechan modul regul differ stage germ cell develop under intim indirect cooper sertoli leydig cell respect furthermor develop germ cell must transloc from basal apic adlumin compart seminifer epithelium thus extens junction restructur must occur assist germ cell movement within seminifer tubul three princip type junction found name anchor junction tight junction gap junction other less studi junction desmosomelik junction hemidesmosom junction with varieti junction type test use differ regul monitor junction turnov among uncount junction modul nitric oxid promin candid due it versatil extens downstream network synthes nitric oxid synthas nos three tradit nos specifi endotheli nos enos induc nos inos neuron nos nnos one testisspecif nnos tnnos found testi for enos inos were recent shown have putat junction regul properti more import two noss like reli downstream solubl guanylyl cyclas cgmp protein kinas signal pathway regul structur compon tight junction adheren junction test apart from involv junction regul nos also particip control level cytokin hormon test other hand play uniqu role modul germ cell viabil develop indirect act some aspect male infertil testicular patholog condit thus nos bear irreplac role maintain homeostasi microenviron seminifer epithelium via it differ downstream signal pathway

Nikki P. Y. Lee

C. Yan Cheng

Nitric Oxide and Cyclic Nucleotides: Their Roles in Junction Dynamics and Spermatogenesis

R. John Aitken

Shaun D. Roman

Antioxidant Systems and Oxidative Stress in the Testes

for number diseas entiti oxid stress becom signific factor etiolog progress cell dysfunct injuri therapeut strategi can identifi novel signal transduct pathway amelior toxic effect oxid stress may lead new avenu treatment spectrum disord includ diabet alzheimer diseas parkinson diseas immun system dysfunct respect metabotrop glutam receptor mglur may offer excit prospect sever disord sinc receptor can limit prevent apoptot cell injuri well impact upon cellular develop function yet role mglur complex natur may requir specif mglur modul particular diseas entiti maxim clinic efficaci limit potenti disabl here discuss potenti clinic translat mglur highlight role novel signal transduct pathway metabotrop glutam system may vital clinic util mglur

Kenneth Maiese

Zhao Zhong Chong

Yan Chen Shang

Jinling Hou

Therapeutic Promise and Principles: Metabotropic Glutamate Receptors

About this journal

Oxidative Medicine and Cellular Longevity publishes research involving cellular and molecular mechanisms of oxidative stress in the nervous system and related organ systems in relation to aging, immune function, vascular biology, and metabolism.

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Chief Editor&nbsp;Dr Vasquez-Vivar has experience in free radical and redox biology research including the discovery of the role of tetrahydrobiopterin in the regulation of superoxide generation by endothelial and neuronal nitric oxide synthase.

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Oxidative Medicine and Cellular Longevity - Table of contents 2008

Oxidative Medicine and Cellular Longevity | Hindawi

title

Oxidative Medicine and Cellular Longevity publishes research involving cellular and molecular mechanisms of oxidative stress in the nervous system and related organ systems in relation to aging, immune function, vascular biology, and metabolism.

Oxidative Medicine and Cellular Longevity