Glutathione as a cerebral substrate in depressive behavior

Pal, Shanti N.; Dandiya, P. C.

doi:10.1016/0091-3057(94)90191-0

Cited by 47 publications

(29 citation statements)

References 26 publications

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“…In animal studies, antidepressants of different classes have been shown to replenish, to varying degrees, the glutathione depletion seen in the inescapable shock behavioural paradigm of depression (Pal and Dandiya, 1994). Venlafaxine was associated with the correction of several depression-specific oxidative markers in the rat cortex (Eren et al, 2007b).…”

Section: Preclinical Studiesmentioning

confidence: 99%

“…Data from animal models have demonstrated the depletion of glutathione (Pal and Dandiya, 1994), reduction of GSH-Px and vitamin C, and rise in lipid peroxidation and NO (Eren et al, 2007b) in association with stress-induced behavioural depression.…”

Section: Animal Studiesmentioning

confidence: 99%

“…As no clinical trials of antioxidant therapies have been published for major depressive disorder, the primary evidence for antioxidant efficacy at present is derived from the previously cited animal study, which demonstrated the prevention and reversal of shock-induced behavioural depression with glutathione (Pal and Dandiya, 1994).…”

Section: Preclinical Studiesmentioning

confidence: 99%

“…Findings of altered antioxidant enzyme levels have been mixed, with reports of elevated SOD (Bilici et al, 2001;Khanzode et al, 2003;Sarandol et al, 2007b), GSH-Px and GR (Bilici et al, 2001), diminished SOD (Herken et al, 2007), and no change (Srivastava et al, 2002). In one study of major depressive disorder patients who had been medication-free for at least 2 months, the plasma total antioxidant potential and (Bilici et al, 2001) Improved MDA, SOD and vitamin C levels with SSRIs for 3 months 62 (Khanzode et al, 2003) Improved SOD and NO levels after antidepressant treatment for 8 wk 36 (Herken et al, 2007) No significant changes in oxidative markers with 6 wk of antidepressant treatment 96 (Sarandol et al, 2007b) Preclinical studies Mice Replenish glutathione depletion ; prevent and/or reverse shockinduced behavioural depression Imipramine, maprotiline, fluvoxamine, trazodone (Pal and Dandiya, 1994) Rats Correction of GSH-Px, glutathione, vitamin C, and lipid peroxidation levels in the stress-induced depression model Venlafaxine (Eren et al, 2007b) Modulation of antioxidant proteins Venlafaxine, fluoxetine (Khawaja et al, 2004) Improvement of depression-related lipid peroxidation, and GSH-Px, glutathione and vitamin C depletion Lamotrigine, aripiprazole, escitalopram (Eren et al, 2007a) In-vitro cell studies…”

Section: Human Assays Of Oxidants Antioxidants and Oxidative Productsmentioning

confidence: 99%

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Oxidative stress in psychiatric disorders: evidence base and therapeutic implications

Berk

Dean

et al. 2008

Int. J. Neuropsychopharm.

865

569

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Oxidative stress has been implicated in the pathogenesis of diverse disease states, and may be a common pathogenic mechanism underlying many major psychiatric disorders, as the brain has comparatively greater vulnerability to oxidative damage. This review aims to examine the current evidence for the role of oxidative stress in psychiatric disorders, and its academic and clinical implications. A literature search was conducted using the Medline, Pubmed, PsycINFO, CINAHL PLUS, BIOSIS Previews, and Cochrane databases, with a time-frame extending to September 2007. The broadest data for oxidative stress mechanisms have been derived from studies conducted in schizophrenia, where evidence is available from different areas of oxidative research, including oxidative marker assays, psychopharmacology studies, and clinical trials of antioxidants. For bipolar disorder and depression, a solid foundation for oxidative stress hypotheses has been provided by biochemical, genetic, pharmacological, preclinical therapeutic studies and one clinical trial. Oxidative pathophysiology in anxiety disorders is strongly supported by animal models, and also by human biochemical data. Pilot studies have suggested efficacy of N-acetylcysteine in cocaine dependence, while early evidence is accumulating for oxidative mechanisms in autism and attention deficit hyperactivity disorder. In conclusion, multi-dimensional data support the role of oxidative stress in diverse psychiatric disorders. These data not only suggest that oxidative mechanisms may form unifying common pathogenic pathways in psychiatric disorders, but also introduce new targets for the development of therapeutic interventions.

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Section: Preclinical Studiesmentioning

confidence: 99%

Section: Animal Studiesmentioning

confidence: 99%

Section: Preclinical Studiesmentioning

confidence: 99%

Section: Human Assays Of Oxidants Antioxidants and Oxidative Productsmentioning

confidence: 99%

See 2 more Smart Citations

Oxidative stress in psychiatric disorders: evidence base and therapeutic implications

Berk

Dean

et al. 2008

Int. J. Neuropsychopharm.

865

569

View full text Add to dashboard Cite

show abstract

“…Moreover, chronic stress may also affect levels of reduced glutathione (GSH), the non-enzymatic component of antioxidant defense (Madrigal et al 2001a;Ahmad et al 2010). Importantly, some mood disorders are characterized by GSH depletion in the brain and the accumulation of oxidative and nitrosative damage (Pal and Dandiya 1994).…”

Section: Resultsmentioning

confidence: 99%

Molecular mechanisms of regulation of antioxidant enzymes in the brain and liver of acutely and/or chronically stressed rats

Zlatković¹

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Najveću zahvalnost dugujem upravo mom mentoru, dr Dragani Filipović, koja me je uvela u metode naučnog rada i tokom godina usmeravala u profesionalnom razvoju. Hvala na prenetom znanju, stručnom vođenju, kao i na svim sugestijama i smernicama koje su me formirale kao istraživača.Veliko hvala za svo utrošeno vreme, savete i konstruktivne kritike koje su dovele do krajnjeg oblikovanja ove teze. Dr Nadeždi Nedeljković se zahvaljujem na ukazanom poverenju i korisnim savetima tokom doktorskih studija.Dr Siniši Đuraševiću se zahvaljujem na savetima i pomoći oko interpretacije pojedinih rezultata. Dr Snežani Pajović veliko hvala na omogućenim uslovima za eksperimentalni rad.Neizmerno hvala porodici i prijateljima, na svemu kroz šta su prošli zajedno sa mnom, na ljubavi i smehu, čineći da sve, pa i ova disertacija, dobije sasvim novu dimenziju. . REZIME Molekularni mehanizmi regulacije antioksidativnih enzima u mozgu i jetri akutno i/ili hronično stresiranih pacovaAktivacija hipolamo-hipofizo-adrenalne (HHA) ose predstavlja jedan od odgovora organizma na izlaganje stresnim uslovima. Dok aktivacija HHA ose uzrokovana kratkotrajnim stresorima ima adaptivni karakter, hroničan stres može dovesti do brojnih patoloških promena među kojima su i poremećaji raspoloženja. Uzrok deregulacije HHA ose u stresnim uslovima još uvek nije u potpunosti utvrđen, a smatra se da može biti povezan sa i pojavom oksidativnog stresa. Stoga je ispitana i okarakterisana aktivnost HHA ose, merenjem koncentracije kortikosterona (CORT) kao markera stresnog odgovora, kao i mehanizmi regulacije antioksidativnih enzima CuZnSOD iMnSOD, kao biomarkera oksidativnog stresa, u uslovima akutnog, hroničnog i kombinovanog stresa u hipokampusu i prečeonoj kori mozga i jetri mužjaka pacova Wistar soja. Cilj ove teze je bio bolje razumevanje biohemijskih i molekularnih mehanizama delovanja antioksidativnih enzima u moždanim strukturama i jetri pacova nakon izlaganja 21-dnevnoj socijalnoj izolaciji, koja predstavlja jedan od životinjskih modela depresije. Akutno izlaganje imobilizaciji ili niskoj temperaturi u trajanju od 2 sata korišćeno je kao pokazatelj "normalnog" odgovora na stres, dok je kombinacija hroničnog i akutnog stresa služila kao potvrda maladaptivnog efekta hroničnog stresa.Rezultati istraživanja su pokazali povećanu koncentraciju CORT-a u serumu životinja izloženih akutnim stresorima, dok su kod životinja izlaganih hroničnoj socijalnoj izolaciji vrednosti ostale nepromenjene. Međutim, značajno niža koncentracija CORT-a između životinja koje su izlagane kombinovanom i odgovarajućem akutnom stresu ukazala je na poremećaj u regulaciji HHA ose koji je izazvana hroničnom socijalnom izolacijom, a što je rezultovalo u neadekvatnm odgovoru na nove stresne situacije.Akutni stres imobilizacije doveo je do povećanja ekspresije MnSOD proteina u mitohondrijama obe moždane strukture, dok je kod životinja akutno izlaganih niskoj temperaturi ili hroničnom stresu izolacije nivo ovog proteina ostao nepromenjen. Međutim, aktivnostiCuZnSOD i MnSOD-a u prečeonoj kori n...

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