Initiation of lipid peroxidation in submitochondrial particles: Effect of respiratory inhibitors

Glinn, Michele; Ernster, Lars; Lee, C.P.

doi:10.1016/0003-9861(91)90591-6

Cited by 25 publications

(15 citation statements)

References 25 publications

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“…These results are similar to our earlier findings with brain mitochondria derived from cerebral ischemia-injured rats (Sciamanna et al, 1992;Sciamanna and Lee, 1993) and suggest that Ca2+ plays an important role in both TBIand ischemia-induced damage. The fact that TBI-induced impairments in respiratory rates with succinate as substrate were less than those observed with NAD-linked substrates suggests that Complex I is more susceptible to the effects of TBI, in line with those observed with peroxidative damage (Glinn et al, 1991;Ernster, 1993).…”

Section: Discussionmentioning

confidence: 64%

Mitochondrial Dysfunction and Calcium Perturbation Induced by Traumatic Brain Injury

Xiong

Peterson

et al. 1997

Journal of Neurotrauma

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Traumatic brain injury (TBI) is associated with primary and secondary injury. A thorough understanding of secondary injury will help to develop effective treatments and improve patient outcome. In this study, the GM model of controlled cortical impact injury (CCII) of Lighthall (1988) was used with modification to induce lateral TBI in rats. Forebrain mitochondria isolated from ipsilateral (IH) and contralateral (CH) hemispheres to impact showed a distinct difference. With glutamate + malate as substrates, mitochondria from the IH showed a significant decrease in State 3 respiratory rates, respiratory control indices (RCI), and P/O ratios. This decrease occurred as early as 1 h and persisted for at least 14 days following TBI. The State 3 respiratory rates, RCI, and P/O ratios could be restored to sham values by the addition of EGTA to the assay mixture. A significant amount of Ca2+ was found to be adsorbed to the mitochondria of both the IH and the CH with higher values seen in the IH. The rate of energy-linked Ca2+ transport in the IH was significantly decreased at 6 and 12 h. These data indicate that CCII-induced TBI perturbs cellular Ca2+ homeostasis and results in excessive Ca2+ adsorption to the mitochondrial membrane, which subsequently inhibits the respiratory chain-linked electron transfer and energy transduction.

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Section: Discussionmentioning

confidence: 64%

Mitochondrial Dysfunction and Calcium Perturbation Induced by Traumatic Brain Injury

Xiong

Peterson

et al. 1997

Journal of Neurotrauma

Self Cite

400

244

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“…This result is in accordance with our earlier finding [10] that brain mitochondria can utilize both endogenous and externally added substrates for these enzymes. The present evidence for a differential distribution of GPx and PHGPx in relation to the mitochondrial inner membrane is of special interest, suggesting a strategic role of the two enzymes in eliminating, on one hand, HzO2 generated in the inner and outer rnitochondrial compartments by superoxide dismutase and by monoamme oxidase; and, on the other hand, phospholipid hydroperoxides formed in the inner membrane which is an important potential site of lipid peroxidation (27)(28)(29). The data reported here further underline the functional importance of the contact sites between the inner and outer mitochondrial membranes, including their role in the transport of proteins [30][31][32] and lipids [33,34], as well as various enzyme activities [26], ion conductance [35] and, in general, the metabolic interplay between mitochondria and the rest of the cell.…”

Section: Methodsmentioning

confidence: 80%

Distribution of glutathione peroxidases glutathione reductase in rat brain mitochondria

1991

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The distribution of glutathione reductase (GR), gtutathione peroxidase (GPx) and phosphotipid hydroperoxide giutathione peroxidase (PHGPx) in isolated rat brain mitochondria was investigated, using a fractionation procedure for the separation of inner and outer membranes, contact sites between the two membranes and a soluble Fraction mainly originating from the mitochondrial matrix. The data indicate that GW and GPx are concentrated in the soluble fraction, with a minor portion of the two enzymes being associated with the contact sites. PHGPx is localized largely in the inner membrane. The possible functional significance of these findings is discussed.

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“…In mitochondrial membranes, an electron transport chain is involved in enzymatic lipid peroxidation. It has been reported that NAD(P)H supports enzymatically-induced lipid peroxidation in submitochondrial particles in the presence of an iron chelate (Glinn et al 1991). Iso¯avans isolated from G. glabra showed potent inhibiton against mitochondrial lipid peroxidation induced by Fe 3 -ADPaNADH.…”

Section: Resultsmentioning

confidence: 97%

Protection of Mitochondrial Functions against Oxidative Stresses by Isoflavans from Glycyrrhiza glabra

Haraguchi

Yoshida

Ishikawa

et al. 2000

Journal of Pharmacy and Pharmacology

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Isoflavan derivatives, glabridin (1), hispaglabridin A (2), hispaglabridin B (3), 4'-Omethylglabridin (4) and 3'-hydroxy-4'-O-methylglabridin (5), isolated from Glycyrrhiza glabra, were investigated for their ability to protect liver mitochondria against oxidative stresses. Mitochondrial lipid peroxidation linked to respiratory electron transport and that induced non-enzymatically were inhibited by these isoflavans. Hispaglabridin A (2) strongly inhibited both peroxidations and 3'-hydroxy-4'-O-methylglabridin (5) was the most effective at preventing NADH-dependent peroxidation. 3'-Hydroxy-4'-O-methylglabridin (5) protected mitochondrial respiratory enzyme activities against NADPH-dependent peroxidation injury. Dihydroxyfumarate-induced mitochondrial peroxidation was also prevented by this isoflavan. Isoflavans from G. glabra were shown to be effective in protecting mitochondrial function against oxidative stresses.

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Initiation of lipid peroxidation in submitochondrial particles: Effect of respiratory inhibitors

Cited by 25 publications

References 25 publications

Mitochondrial Dysfunction and Calcium Perturbation Induced by Traumatic Brain Injury

Mitochondrial Dysfunction and Calcium Perturbation Induced by Traumatic Brain Injury

Distribution of glutathione peroxidases glutathione reductase in rat brain mitochondria

Protection of Mitochondrial Functions against Oxidative Stresses by Isoflavans from Glycyrrhiza glabra

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