Transplasma membrane electron transport: enzymes involved and biological function

Ly, Jennifer; Lawen, Alfons

doi:10.1179/135100003125001198

Cited by 76 publications

(51 citation statements)

References 159 publications

(155 reference statements)

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“…Analogous to the mitochondrial inner membrane, the PM contains enzymes involved in electron transport and energy metabolism ( Fig. 1) (25). Cells respond to oxidative stress by transferring electrons from NAD(P)H and ascorbate to extracellular free radicals and/or oxidants (26,27).…”

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confidence: 99%

Calorie restriction up-regulates the plasma membrane redox system in brain cells and suppresses oxidative stress during aging

Hyun

Emerson

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

249

160

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The plasma membrane (PM) contains redox enzymes that provide electrons for energy metabolism and recycling of antioxidants such as coenzyme Q and ␣-tocopherol. Brain aging and neurodegenerative disorders involve impaired energy metabolism and oxidative damage, but the involvement of the PM redox system (PMRS) in these processes is unknown. Caloric restriction (CR), a manipulation that protects the brain against aging and disease, increased activities of PMRS enzymes (NADH-ascorbate free radical reductase, NADH-quinone oxidoreductase 1, NADH-ferrocyanide reductase, NADH-coenzyme Q10 reductase, and NADH-cytochrome c reductase) and antioxidant levels (␣-tocopherol and coenzyme Q10) in brain PM during aging. Age-related increases in PM lipid peroxidation, protein carbonyls, and nitrotyrosine were attenuated by CR, levels of PMRS enzyme activities were higher, and markers of oxidative stress were lower in cultured neuronal cells treated with CR serum compared with those treated with ad libitum serum. These findings suggest important roles for the PMRS in protecting brain cells against age-related increases in oxidative and metabolic stress.Alzheimer's disease ͉ reactive oxygen species ͉ coenzyme Q10 ͉ oxidoreductase

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mentioning

confidence: 99%

Calorie restriction up-regulates the plasma membrane redox system in brain cells and suppresses oxidative stress during aging

Hyun

Emerson

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

249

160

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“…The PMRS acts to maintain the redox status of important antioxidants such as coenzyme Q ([CoQ] ubiquinone), ␣-tocopherol, and ascorbate (35,61,74), which are thought to protect cells from exogenous oxidative stress, in particular, by protecting membranes from lipid peroxidation chain reactions (33). The PMRS may also have a function in cellular communication via reactive oxygen species (18, 37) and in maintaining cellular redox status via NAD(P)H recycling (4).…”

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confidence: 99%

Nrf2 Signaling, a Mechanism for Cellular Stress Resistance in Long-Lived Mice

Leiser

Miller

2010

Molecular and Cellular Biology

128

117

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Transcriptional regulation of the antioxidant response element (ARE) by Nrf2 is important for the cellular adaptive response to toxic insults. New data show that primary skin-derived fibroblasts from the long-lived Snell dwarf mutant mouse, previously shown to be resistant to many toxic stresses, have elevated levels of Nrf2 and of multiple Nrf2-sensitive ARE genes. Dwarf-derived fibroblasts exhibit many of the traits associated with enhanced activity of Nrf2/ARE, including higher levels of glutathione and resistance to plasma membrane lipid peroxidation. Treatment of control cells with arsenite, an inducer of Nrf2 activity, increases their resistance to paraquat, hydrogen peroxide, cadmium, and UV light, rendering these cells as stress resistant as untreated cells from dwarf mice. Furthermore, mRNA levels for some Nrf2-sensitive genes are elevated in at least some tissues of Snell dwarf mice, suggesting that the phenotypes observed in culture may be mirrored in vivo. Augmented activity of Nrf2 and ARE-responsive genes may coordinate many of the stress resistance traits seen in cells from these long-lived mutant mice.The discovery of single gene mutations that extend life span, first in invertebrates (43,48,60) and then in mice (9, 14, 19), has provided new momentum for defining the molecular mechanisms that control the aging process. Since Harman first proposed the free radical theory of aging (23), many lines of evidence have suggested that oxidative stress plays an important role in aging. In roundworms (Caenorhabditis elegans) (44, 52) and fruit flies (Drosophila melanogaster) (7, 67, 109), mutations resulting in resistance to toxic stresses, both oxidative and otherwise, tend to result in increases in longevity. The relative importance of oxidation damage as a regulator of life span is more controversial. Longevity is often associated with resistance to oxidative injury within and among species, but most attempts to retard aging by antioxidant treatments have failed to show beneficial effects, and mutations that promote oxidative damage in mice have often had little impact on life span (25,72,81,86,96). Utilizing cells from the Snell dwarf mouse, a model of extended longevity, we are attempting to find the mechanism behind cellular stress resistance in hopes of relating this resistance to the delayed aging of the Snell dwarf animal.Snell dwarf mice are homozygous for a mutation at the Pit-1 locus which causes improper development of the anterior pituitary, leading to low levels of growth hormone, thyroid stimulating hormone, and prolactin in young and adult mice (10, 30). These pituitary defects lead to diminished circulating levels of insulin-like growth factor 1 (IGF-1) and thyroxine, which in turn result in reduced size and hypothermia. Snell dwarf mice, like the closely related Prop1 mutant Ames dwarf (9), live approximately 40% longer than littermate controls on several different background stocks (19,20) and show delay in many forms of aging-related pathologies (1,3,19).Previous work has shown that pr...

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“…Plasma membrane behavior may reflect health status of animal cells (Ly and Lawen 2003) and viral diseases cause alterations to membrane potential (Akeson et al 1992;Helenius et al 1985;Wiley and Skedel 1987). Similar consequences were also observed throughout early stages of recognition between microorganisms and plants (Elmore and Coaker 2011), whereas effects caused by viruses to membrane potential of the host are little investigated.…”

Section: Introductionmentioning

confidence: 87%

Early trans-plasma membrane responses to Tobacco mosaic virus infection

et al. 2017

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Early trans-plasma membrane behavior after in vivo mechanical inoculation of Nicotiana tabacum with Tobacco mosaic virus (TMV) was investigated and compared to virus quantification in leaf tissues. To identify early events related to virus/host interaction, the systemic virus TMV was used to infect lower leaves and tests were carried out on upper leaves which were not directly infected. Non-invasive microelectrodes were used to estimate trans-plasma membrane electron transport and membrane potential after artificial inoculum of virus, monitoring the plant for the following 15 days. Virus infection was assessed by ELISA and quantified by quantitative RT-PCR. Collected data showed that after 2-day post-inoculation (dpi), TMV was able to modify membrane parameters: transient hyperpolarization of trans-membrane potential was observed until 10 dpi, while redox activity in infected samples was higher compared to control until end of tests. Conversely, ELISA diagnostic test was not able to reveal the virus presence in tobacco leaves until 6 dpi, while leaf symptoms were manifested after 13 dpi.

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Transplasma membrane electron transport: enzymes involved and biological function

Cited by 76 publications

References 159 publications

Calorie restriction up-regulates the plasma membrane redox system in brain cells and suppresses oxidative stress during aging

Calorie restriction up-regulates the plasma membrane redox system in brain cells and suppresses oxidative stress during aging

Nrf2 Signaling, a Mechanism for Cellular Stress Resistance in Long-Lived Mice

Early trans-plasma membrane responses to Tobacco mosaic virus infection

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