Parinaric acid as a sensitive fluorescent probe for the determination of lipid peroxidation

Kuypers, Frans A.; Berg, Jeroen J.M. van den; Schalkwijk, Casper G.; Roelofsen, B.; Kamp, J.A.F. Op den

doi:10.1016/0005-2760(87)90027-0

Cited by 142 publications

(76 citation statements)

References 20 publications

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“…3) have been used to assess lipid peroxidation. Two often-used lipid-soluble probes are cis-parinaric acid [70][71][72][73][74][75][76][77][78] and C11-BODIPY(581/591) [77,[79][80][81][82][83][84]. cis-Parinaric acid oxidation products are non-fluorescent, thus it is the loss of parent fluorescence intensity that is monitored, whereas C11-BODIPY(581/591) undergoes a green-shift in its fluorescence allowing ratio-based methods to track both the parent and oxidation product(s) [80,85].…”

Section: Do We Know Where Tocopherol Does Its Most Important Job?mentioning

confidence: 99%

The location and behavior of α‐tocopherol in membranes

Atkinson

Harroun

Wassall

et al. 2010

Molecular Nutrition Food Res

173

128

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Vitamin E (a-tocopherol) has long been recognized as the major antioxidant in biological membranes, and yet many structurally related questions persist of how the vitamin functions. For example, the very low levels of a-tocopherol reported for whole cell extracts question how this molecule can successfully protect the comparatively enormous quantities of PUFAcontaining phospholipids found in membranes that are highly susceptible to oxidative attack. The contemporary realization that membranes laterally segregate into regions of distinct lipid composition (domains), we propose, provides the answer. We hypothesize a-tocopherol partitions into domains that are enriched in polyunsaturated phospholipids, amplifying the concentration of the vitamin in the place where it is most needed. These highly disordered domains depleted in cholesterol are analogous, but organizationally antithetical, to the wellstudied lipid rafts. We review here the ideas that led to our hypothesis. Experimental evidence in support of the formation of PUFA-rich domains in model membranes is presented, focusing upon docosahexaenoic acid that is the most unsaturated fatty acid commonly found. Physical methodologies are then described to elucidate the nature of the interaction of a-tocopherol with PUFA and to establish that the vitamin and PUFA-containing phospholipids co-localize in non-raft domains.

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Section: Do We Know Where Tocopherol Does Its Most Important Job?mentioning

confidence: 99%

The location and behavior of α‐tocopherol in membranes

Atkinson

Harroun

Wassall

et al. 2010

Molecular Nutrition Food Res

173

128

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“…Lipid peroxidation is a deleterious consequence of oxidative stress. To determine whether the observed increase in the rate of ROS production in the HXC cell lines produced a higher lipid peroxidation of the membranes in these cells, the loss of cis-parinaric acid fluorescence was used to measure the chemical process of lipid peroxidation (26). In a whole cell assay, the time course of the fluorescence decrease showed no significant differences among cell lines (Fig.…”

Section: Effects Of CI Inhibition On Oxidative Stressmentioning

confidence: 99%

Titrating the Effects of Mitochondrial Complex I Impairment in the Cell Physiology

Barrientos

Moraes

1999

Journal of Biological Chemistry

356

217

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The mitochondrial oxidative phosphorylation system consists of five multimeric enzymes (complexes I-V). NADH dehydrogenase or complex I (CI) is affected in most of the mitochondrial diseases and in some neurodegenerative disorders. We have studied the physiological consequences of a partial CI inhibition at the cellular level. We used a genetic model (40% CI-inhibited human-ape xenomitochondrial cybrids) and a drug-induced model (0 -100% CI-inhibited cells using different concentrations of rotenone). We observed a quantitative correlation between the level of CI impairment and cell respiration, cell growth, free radical production, lipid peroxidation, mitochondrial membrane potential, and apoptosis. We showed that cell death was quantitatively associated with free radical production rather than with a decrease in respiratory chain function. The results obtained with human xenomitochondrial cybrid cells were compatible with those observed in rotenoneinduced 40% CI-inhibited cells. At high concentrations (5-6-fold higher than the concentration necessary for 100% CI inhibition), rotenone showed a second toxic effect at the level of microtubule assembly, which also led to apoptosis. The correlation found among all the parameters studied helped clarify the physiological consequences of partial CI inhibitions at the cellular level.

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“…Lipid peroxidation studies Lipid peroxidation was determined by measuring the loss of fluorescence due to peroxidation of the naturally fluorescent fatty acid, cis-parinaric acid (Molecular Probes; Kuypers et al 1987). Hippocampal cultures were incubated with 10 lM cis-parinaric acid or 90% EtOH vehicle for 1 h prior to addition of 10 lL insult or vehicle.…”

Section: Dcf Studiesmentioning

confidence: 99%

Neuroprotective effects of bcl‐2 overexpression in hippocampal cultures: interactions with pathways of oxidative damage

Howard

Bottino

Brooke

et al. 2002

Journal of Neurochemistry

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Overexpression of bcl-2 protects neurons from numerous necrotic insults, both in vitro and in vivo. While the bulk of such protection is thought to arise from Bcl-2 blocking cytochrome c release from mitochondria, thereby blocking apoptosis, the protein can target other steps in apoptosis, and can protect against necrotic cell death as well. There is evidence that these additional actions may be antioxidant in nature, in that Bcl-2 has been reported to protect against generators of reactive oxygen species (ROS), to increase antioxidant defenses and to decrease levels of ROS and of oxidative damage. Despite this, there are also reports arguing against either the occurrence, or the importance of these antioxidant actions. We have examined these issues in neuron-enriched primary hippocampal cultures, with overexpression of bcl-2 driven by a herpes simplex virus amplicon: (i) Bcl-2 protected strongly against glutamate, whose toxicity is at least partially ROS-dependent. Such protection involved reduction in mitochondrially derived superoxide. Despite that, Bcl-2 had no effect on levels of lipid peroxidation, which is thought to be the primary locus of glutamate-induced oxidative damage; (ii) Bcl-2 was also mildly protective against the pro-oxidant adriamycin. However, it did so without reducing levels of superoxide, hydrogen peroxide or lipid peroxidation; (iii) Bcl-2 protected against permanent anoxia, an insult likely to involve little to no ROS generation. These findings suggest that Bcl-2 can have antioxidant actions that may nonetheless not be central to its protective effects, can protect against an ROS generator without targeting steps specific to oxidative biochemistry, and can protect in the absence of ROS generation. Thus, the antioxidant actions of Bcl-2 are neither necessary nor sufficient to explain its protective actions against these insults in hippocampal neurons.

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Parinaric acid as a sensitive fluorescent probe for the determination of lipid peroxidation

Cited by 142 publications

References 20 publications

The location and behavior of α‐tocopherol in membranes

The location and behavior of α‐tocopherol in membranes

Titrating the Effects of Mitochondrial Complex I Impairment in the Cell Physiology

Neuroprotective effects of bcl‐2 overexpression in hippocampal cultures: interactions with pathways of oxidative damage

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