Neurodegenerative diseases and oxidative stress

Emerit, J; Edeas, Marvin; Bricaire, François

doi:10.1016/j.biopha.2003.11.004

Cited by 915 publications

(528 citation statements)

References 63 publications

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“…There is evidence implicating oxidative stress as a central mechanism by which neuronal damage occurs. 25 There is also new evidence indicating that astrocytes expressing a mutated form of SOD1 may contribute to neuronal degeneration. 4 The mutated SOD1 has been suggested to induce the high production of reactive oxygen species and subsequent DNA damage in neurons.…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II and aldosterone-induced neuronal damage in neurons through an astrocyte-dependent mechanism

et al. 2011

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The contribution of the renin-angiotensin-aldosterone system (RAAS) to central nervous system (CNS) disorders is not yet fully understood. RAAS has been shown to be involved in the proliferation of astrocytes, which have a role in neuronal damage contributing to neurodegenerative diseases. However, the direct relationship between RAAS and neuronal damage is still unclear. We therefore examined the effect of angiotensin (Ang) II and aldosterone (Aldo) on damage to spinal ganglion neurons (SGNs) by regulating astrocytes. Ang II stimulation significantly increased DNA damage in SGNs in a time-dependent manner. This increase in DNA damage was further enhanced when SGNs were co-cultured with astrocytes. On the other hand, no significant increase was observed in SGNs co-cultured with astrocytes without Ang II stimulation. Moreover, the addition of conditioned medium from Ang II-treated astrocytes exacerbated SGN DNA damage. An Ang II type 1 receptor blocker, valsartan, inhibited Ang II-stimulated DNA damage but not DNA damage induced by conditioned medium prepared from astrocyte cultures. In contrast, an Aldo antagonist, eplerenone, significantly inhibited DNA damage induced by the culture medium from Ang II-treated astrocytes. Ang II-stimulated Aldo secretion in the conditioned medium from astrocytes. Furthermore, the administration of Aldo alone also enhanced DNA damage in SGNs. Finally, flow cytometric analysis showed that Ang II or Aldo treatment markedly increased the percentage of dead SGNs. In conclusion, Ang II-and Aldo-induced neuronal damage in SGNs through astrocytes regulation. Blocking Ang II and Aldo to target astrocytes might be useful for the treatment of CNS disorders.

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Section: Discussionmentioning

confidence: 99%

Angiotensin II and aldosterone-induced neuronal damage in neurons through an astrocyte-dependent mechanism

et al. 2011

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“…Superoxide anion generation, and the cellular damage resulting from it, is implicated in the pathophysiology of many conditions, including stroke, ischemia, asthma, atherosclerosis, and several neurodegenerative diseases [43], [44] and [45]. Increased superoxide anion generation due to paraquat and its contribution to paraquat toxicity have been catalogued over many years [8], [9], [46] and [47], and in this investigation, its role in the development of renal cytotoxicity has been confirmed in vitro.…”

Section: Discussionmentioning

confidence: 99%

Reduction of paraquat-induced renal cytotoxicity by manganese and copper complexes of EGTA and EHPG

Samai

Hague

Naughton

et al. 2008

Free Radical Biology and Medicine

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“…Consequently, inhibition of TYRO is important for the treatment of PD. On the other hand, oxidative stress occurring by different mechanisms is strongly connected with the neurodegenerative diseases including AD and PD [3].…”

Section: Introductionmentioning

confidence: 99%

Evaluation of possible in vitro neurobiological effects of two varieties of Cupressus sempervirens (Mediterranean cypress) through their antioxidant and enzyme inhibition actions

Tümen¹,

Şenol²,

Orhan

2012

Turk J Bioch

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Neurodegenerative diseases and oxidative stress

Cited by 915 publications

References 63 publications

Angiotensin II and aldosterone-induced neuronal damage in neurons through an astrocyte-dependent mechanism

Angiotensin II and aldosterone-induced neuronal damage in neurons through an astrocyte-dependent mechanism

Reduction of paraquat-induced renal cytotoxicity by manganese and copper complexes of EGTA and EHPG

Evaluation of possible in vitro neurobiological effects of two varieties of Cupressus sempervirens (Mediterranean cypress) through their antioxidant and enzyme inhibition actions

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