Elsevier

Brain Research

Volume 668, Issues 1–2, 30 December 1994, Pages 243-245
Brain Research

Trolox protects mitochondrial complex IV from nitric oxide-mediated damage in astrocytes

https://doi.org/10.1016/0006-8993(94)90530-4Get rights and content

Abstract

The efficacy of cystine, ascorbate and trolox, a vitamin E analogue, at protecting against nitric oxide-mediated mitochondrial complex IV damage has been investigated in cultured astrocytes. Of these compounds, only trolox afforded protection. It is suggested that lipid peroxidation is responsible for nitric oxide-mediated mitochondrial damage and that inhibitors of this process may be of therapeutic benefit in conditions where excessive nitric oxide production is implicated.

References (13)

There are more references available in the full text version of this article.

Cited by (53)

  • Glutamine-dependent effects of nitric oxide on cancer cells subjected to hypoxia-reoxygenation

    2023, Nitric Oxide - Biology and Chemistry
    Citation Excerpt :

    The concentrations of NO used in this study are in the higher range estimated to be released by tumor-associated macrophages [50,56]. Consistent with the literature, we demonstrated that NO inhibited oxidative metabolism and upregulated glycolysis during hypoxia in 3 diverse cancer cells lines which were highly dependent on L-Gln for their aerobic metabolism (Fig. 1, S1) [57–60]. Interestingly, the NO-dependent inhibition of respiration in an O2-dependent manner was largely independent of the presence of L-Gln suggesting that NO is capable of modulating cancer cell metabolism independently of glutaminolysis.

  • Protective effects of phenelzine administration on synaptic and non-synaptic cortical mitochondrial function and lipid peroxidation-mediated oxidative damage following TBI in young adult male rats

    2020, Experimental Neurology
    Citation Excerpt :

    Interestingly, astrocytes also have greater antioxidant capacity compared to neurons (Makar et al., 1994; Raps et al., 1989; Sagara et al., 1993); therefore, they are more equipped to handle elevated levels of reactive species (ROS/RNS). Astrocytic induction of NOS has been shown to inhibit the mitochondrial respiratory chain, with cytochrome c oxidase being the most susceptible component (Bolanos et al., 1994; Heales et al., 1994). Since astrocytes are more resistant to oxidative damage (Naga et al., 2007), astrocyte-derived NOS could be responsible for exacerbating the damage to their neighboring cells, neurons, and their mitochondria (Allaman et al., 2011; Belanger et al., 2011).

  • Synaptic Mitochondria are More Susceptible to Traumatic Brain Injury-induced Oxidative Damage and Respiratory Dysfunction than Non-synaptic Mitochondria

    2018, Neuroscience
    Citation Excerpt :

    Interestingly, astrocytes also have greater antioxidant capacity compared to neurons (Raps et al., 1989; Sagara et al., 1993; Makar et al., 1994); therefore, they are more equipped to handle elevated levels of ROS/RNS. Astrocytic induction of NOS has been shown to inhibit the mitochondrial respiratory chain, with cytochrome c oxidase being the most susceptible component (Bolanos et al., 1994; Heales et al., 1994). Since astrocytes are more resistant to oxidative damage (Naga et al., 2007), after TBI, astrocyte-derived NOS would be more damaging to their neighboring cells, neurons, and the damage to neuronal mitochondria is exacerbated (Allaman et al., 2011; Belanger et al., 2011).

  • Inhibition of neuronal mitochondrial complex I or lysosomal glucocerebrosidase is associated with increased dopamine and serotonin turnover

    2017, Neurochemistry International
    Citation Excerpt :

    Although GSH levels in the pre-PD patients are decreased to comparable level to those seen in PD, it is of note that complex I activity was not decreased (Jenner et al., 1992). This raises the possibility that GSH loss precedes and contributes to the loss of complex I activity, a hypothesis that is supported by a number of observations in both cellular and animal models (Barker et al., 1996; Bolanos et al., 1996; Heales et al., 1994, 2011). Another potential mechanism implicated in PD pathogenesis is failure of lysosomal autophagy (Lynch-Day et al., 2012) leading to impaired protein processing, e.g. alpha-synuclein and formation of Lewy bodies that are characteristic of PD (Beyer, 2007).

View all citing articles on Scopus

This work was funded by the Worshipful Company of Pewterers, the European Community and the Brain Research Trust.

View full text