Mitochondrial dysfunction and lipid peroxidation in rat frontal cortex by chronic NMDA administration can be partially prevented by lithium treatment

Kim, Helena K.; Isaacs-Trepanier, Cameron; Elmi, Nika; Rapoport, Stanley I.; Andreazza, Ana Cristina

doi:10.1016/j.jpsychires.2016.02.001

Cited by 21 publications

(11 citation statements)

References 62 publications

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“…As OLZ treatment of macrophages increased superoxide and ROS, which includes hydrogen peroxide, these results indirectly suggest that this drug may cause mitochondrial dysfunction. Attenuation of ROS production by Li exposure may be possible as described in an investigation performed by Kim et al [51]. This study demonstrated that mitochondrial dysfunction and lipid peroxidation in rat frontal cortex triggered by chronic NMDA administration was partially reversed by Li treatment.…”

Section: Discussionsupporting

confidence: 63%

Lithium is able to minimize olanzapine oxidative-inflammatory induction on macrophage cells

et al. 2019

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BackgroundOlanzapine (OLZ) is a second-generation antipsychotic drug used for treatment of schizophrenia, bipolar disorder, and other neuropsychiatric conditions. Undesirable side effects of OLZ include metabolic alterations associated with chronic oxidative-inflammation events. It is possible that lithium (Li), a mood modulator that exhibits anti-inflammatory properties may attenuate OLZ-induced oxi-inflammatory effects.MethodologyTo test this hypothesis we activated RAW 264.7 immortalized macrophages with OLZ and evaluated oxidation and inflammation at the gene and protein levels. Li and OLZ concentrations were determined using estimated plasma therapeutic concentrations.ResultsOLZ triggered a significant increase in macrophage proliferation at 72 h. Higher levels of oxidative markers and proinflammatory cytokines, such as TNF-α, IL-1β, and IL-6, with a concomitant reduction in IL-10, were observed in OLZ-exposed macrophages. Lithium (Li) exposure triggered a short and attenuated inflammatory response demonstrated by elevation of superoxide anion (SA), reactive oxygen species (ROS), IL-1β, and cellular proliferation followed by elevation of anti-inflammatory IL-10 levels. Li treatment of OLZ-supplemented macrophages was able to reverse elevation of oxidative and inflammatory markers and increase IL-10 levels.ConclusionsDespite methodological limitations related to in vitro protocols, results suggested that Li may attenuate OLZ-induced oxidative and inflammatory responses that result from metabolic side effects associated with OLZ.

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Section: Discussionsupporting

confidence: 63%

Lithium is able to minimize olanzapine oxidative-inflammatory induction on macrophage cells

et al. 2019

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“…These data provide a causal link between LPO and mitochondrial dysfunction in HD (Lee et al 2011a). In rats, chronic injection of N-methyl-D-aspartate (NMDA) causes a decreased activity of mitochondrial complex I and II, as well as increased levels of LPO markers in brain tissue (Kim et al 2016), indicating a role of LPO in excitotoxic neuronal cell death. Similarly, excitotoxicity and LPO seem to be involved in ALS-associated cell death (Kruman et al 1999; Pedersen et al 1998; Shibata et al 2001; Ferrante et al 1997).…”

Section: Phospholipids and Mitochondrial Dynamics In Neurodegenerationmentioning

confidence: 99%

Mitochondrial lipids in neurodegeneration

et al. 2016

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Mitochondrial dysfunction is a common feature of many neurodegenerative diseases, including proteinopathies such as Alzheimer’s or Parkinson’s disease, which are characterized by the deposition of aggregated proteins in the form of insoluble fibrils or plaques. The distinct molecular processes that eventually result in mitochondrial dysfunction during neurodegeneration are well studied but still not fully understood. However, defects in mitochondrial fission and fusion, mitophagy, oxidative phosphorylation and mitochondrial bioenergetics have been linked to cellular demise. These processes are influenced by the lipid environment within mitochondrial membranes as, besides membrane structure and curvature, recruitment and activity of different proteins also largely depend on the respective lipid composition. Hence, the interaction of neurotoxic proteins with certain lipids and the modification of lipid composition in different cell compartments, in particular mitochondria, decisively impact cell death associated with neurodegeneration. Here, we discuss the relevance of mitochondrial lipids in the pathological alterations that result in neuronal demise, focussing on proteinopathies.

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“…Some investigators reported that oxidative inflammatory mechanisms have been hypothesized to perform a role in the onset of metabolic adverse effects related to olanzapine administration [24]. Olanzapine treatment of macrophages elevated superoxide and ROS, such as hydrogen peroxide, these findings suggest that olanzapine may lead to mitochondrial dysfunction [25].…”

Section: Discussionmentioning

confidence: 99%

Differential Expression of CD3, TNF-α, and VEGF Induced by Olanzapine on the Spleen of Adult Male Albino Rats and the Possible Protective Role of Vitamin C

Youssef

Salah

2019

Biomedicines

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Olanzapine is an antipsychotic drug effective in the treatment of stress-associated psychiatric illnesses, but its effect on the spleen remains unclear. Vitamin C is essential for the optimum function of the immune system. We aim to investigate the effect of Olanzapine on spleen structures and to assess the protective effect of vitamin C. Forty adult male albino rats were divided into four groups: group (I), a control; group (II), rats were given vitamin C at 40 mg/kg body weight; group (III), rats were given Olanzapine at 2 mg/kg body weight; and group (IV), rats were given vitamin C and Olanzapine at the same dose of group (II) and group (III) for one month. The hematoxylin and eosin (H&E) of the olanzapine treated group showed focal areas of cellular depletion and a decrease in the size of the white pulp. The red pulp was expanded and showed marked congestion and dilatation of blood sinusoids. Cluster of differentiation 3 (CD3) was significantly reduced, however both tumor necrosis factor alpha (TNF-α), and vascular endothelial growth factor (VEGF) were significantly higher. The administration of vitamin C repaired structural and immunohistochemical changes via increased CD3 and decreased TNF-α and VEGF. Therefore, the oxidative and the inflammatory pathways may be the possible mechanisms underlying olanzapine immunotoxicity. Vitamin C exerted immune modulator and antioxidant effects against olanzapine.

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Mitochondrial dysfunction and lipid peroxidation in rat frontal cortex by chronic NMDA administration can be partially prevented by lithium treatment

Cited by 21 publications

References 62 publications

Lithium is able to minimize olanzapine oxidative-inflammatory induction on macrophage cells

Lithium is able to minimize olanzapine oxidative-inflammatory induction on macrophage cells

Mitochondrial lipids in neurodegeneration

Differential Expression of CD3, TNF-α, and VEGF Induced by Olanzapine on the Spleen of Adult Male Albino Rats and the Possible Protective Role of Vitamin C

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