Mitochondrial Reactive Oxygen Species Generation and Calcium Increase Induced by Visible Light in Astrocytes

Jou, Mei‐Jie; Jou, Shuo-Bin; Guo, Mei-Jin; Wu, Hong-Yueh; Peng, Tsung-I

doi:10.1007/978-3-662-41088-2_5

Cited by 20 publications

(23 citation statements)

References 16 publications

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“…This ability of the mitochondria is of major pharmacological interest because it means that, after its exogenous administration in vivo, melatonin enters the mitochondria to exert its beneficial actions. Among these actions, melatonin antagonizes processes affecting Δψm such as calcium overload, either due to overexcitation, to protein misfolding or to damage by free radicals [53–55], counteracts the collapse of the Δψm induced by H 2 O 2 [53], doxorubicin [56] or oxygen/glucose deprivation [57], and inhibits the mitochondrial permeability transition pore, thereby rescuing cells from apoptosis [58]. In this regard, melatonin directly diminished permeability transition pore currents, with an IC 50 of 0.8 μ m [55], a concentration of melatonin compatible with our data here reported.…”

Section: Discussionmentioning

confidence: 99%

Melatonin protects the mitochondria from oxidative damage reducing oxygen consumption, membrane potential, and superoxide anion production

López

García

Escames

et al. 2009

Journal of Pineal Research

246

185

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The role of melatonin in improving mitochondrial respiratory chain activity and increasing ATP production in different experimental conditions has been widely reported. To date, however, the mechanism(s) involved are largely unknown. Using high-resolution respirometry, fluorometry and spectrophotometry we studied the effects of melatonin on normal mitochondrial functions. Mitochondria were recovered from mouse liver cells and incubated in vitro with melatonin at concentrations ranging from 1 nm to 1 mm. Melatonin decreased oxygen consumption concomitantly with its concentration, inhibited any increase in oxygen flux in the presence of an excess of ADP, reduced the membrane potential, and consequently inhibited the production of superoxide anion and hydrogen peroxide. At the same time it maintained the efficiency of oxidative phosphorylation and ATP synthesis while increasing the activity of the respiratory complexes (mainly complexes I, III, and IV). The effects of melatonin appeared to be due to its presence within the mitochondria, since kinetic experiments clearly showed its incorporation into these organelles. Our results support the hypothesis that melatonin, together with hormones such as triiodothyronine, participates in the physiological regulation of mitochondrial homeostasis.

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Section: Discussionmentioning

confidence: 99%

Melatonin protects the mitochondria from oxidative damage reducing oxygen consumption, membrane potential, and superoxide anion production

López

García

Escames

et al. 2009

Journal of Pineal Research

246

185

View full text Add to dashboard Cite

show abstract

“…On the other hand, several in vitro studies have demonstrated that some endogenous chromophores such as cytochromes and porphyrins can absorb the irradiation photons and produce reactive oxygen species (ROS) by photosensitization (32,33). These cellular ROS may react with channel proteins resulting in an increment of [Ca 2+ ] i at least partially via the L‐type calcium channel (34,35). In our case the activation of TRPV4 by ROS can not be excluded.…”

Section: Discussionmentioning

confidence: 99%

Effects of Low Power Laser Irradiation on Intracellular Calcium and Histamine Release in RBL‐2H3 Mast Cells

Yang

Chen

et al. 2007

Photochem & Photobiology

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Although laser irradiation has been reported to promote skin wound healing, the mechanism is still unclear. As mast cells are found to accumulate at the site of skin wounds we hypothesized that mast cells might be involved in the biological effects of laser irradiation. In this work the mast cells, RBL-2H3, were used in vitro to investigate the effects of laser irradiation on cellular responses. After laser irradiation, the amount of intracellular calcium ([Ca2+]i) was increased, followed by histamine release, as measured by confocal fluorescence microscopy with Fluo-3/AM staining and a fluorescence spectrometer with o-phthalaldehyde staining, respectively. The histamine release was mediated by the increment of [Ca2+]i from the influx of the extracellular buffer solution through the cation channel protein, transient receptor potential vanilloid 4 (TRPV4). The TRPV4 inhibitor, Ruthenium Red (RR) can effectively block such histamine release, indicating that TRPV4 was the key factor responding to laser irradiation. These induced responses of mast cells may provide an explanation for the biological effects of laser irradiation on promoting wound healing, as histamine is known to have multi-functions on accelerating wound healing.

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“…The microtublin‐based movement machineries efficiently allow mitochondria to spatially and temporally deliver ATP that is crucial to cell survival especially during disrupted homeostasis of intracellular Ca 2+ [23–25]. Previously, we have demonstrated that mitochondrial movement is particularly sensitive to mitochondrial oxidative insults [5, 26–29]. During a specific mitochondrial oxidative stress induced by 490‐nm visible light irradiation [5, 27], cessation of mitochondrial movement associated with elevation of mitochondrial reactive oxygen species (mROS) was immediately observed during relative early time points (within 5–10 min) compared with the opening of the mitochondrial permeability transition (MPT), release of lethal proteins such as cytochrome c (>20–30 min), and final condensation and fragmentation of nuclear DNA (2–3 hr) [5, 27].…”

Section: Introductionmentioning

confidence: 99%

mtDNA T8993G mutation‐induced mitochondrial complex V inhibition augments cardiolipin‐dependent alterations in mitochondrial dynamics during oxidative, Ca²⁺, and lipid insults in NARP cybrids: a potential therapeutic target for melatonin

Peng

Hsiao

Reíter

et al. 2011

Journal of Pineal Research

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Mitochondrial dynamics including morphological fission and mitochondrial movement are essential to normal mitochondrial and cellular physiology. This study investigated how mtDNA T8993G (NARP)-induced inhibition of mitochondrial complex V altered mitochondrial dynamics in association with a protective mitochondrial phospholipid, cardiolipin (CL), as a potential therapeutic target. NARP cybrids harboring 98% of mtDNA T8993G genes and its parental osteosarcoma 143B cells were studied for comparison, and protection provided by melatonin, a potent mitochondrial protector, was explored. We demonstrate for the first time that NARP mutation significantly enhances apoptotic death as a result of three distinct lethal mitochondrial apoptotic insults including oxidative, Ca(2+), and lipid stress. In addition, NARP significantly augmented pathological depletion of CL. NARP-augmented depletion of CL results in enhanced retardation of mitochondrial movement and fission and later swelling of mitochondria during all insults. These results suggest that CL is a common and crucial pathological target for mitochondrial apoptotic insults. Furthermore, CL possibly plays a central role in regulating mitochondrial dynamics that are associated with NARP-augmented mitochondrial pathologies. Intriguingly, melatonin, by differentially preserving CL during various stresses (oxidation > Ca(2+) > lipid), rescues differentially CL-altered mitochondrial dynamics and cell death (oxidation > Ca(2+) > lipid). Thus, melatonin, in addition to being a mitochondrial antioxidant to antagonize mitochondrial oxidative stress, a mitochondrial permeability transition modulator to antagonize mitochondrial Ca(2+) stress, may stabilize directly CL to prevent its oxidization and/or depletion and, therefore, exerts great potential in rescuing CL-dependent mitochondrial dynamics-associated mitochondrial pathologies for treatment of NARP-induced pathologies and diseases.

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Mitochondrial Reactive Oxygen Species Generation and Calcium Increase Induced by Visible Light in Astrocytes

Cited by 20 publications

References 16 publications

Melatonin protects the mitochondria from oxidative damage reducing oxygen consumption, membrane potential, and superoxide anion production

Melatonin protects the mitochondria from oxidative damage reducing oxygen consumption, membrane potential, and superoxide anion production

Effects of Low Power Laser Irradiation on Intracellular Calcium and Histamine Release in RBL‐2H3 Mast Cells

mtDNA T8993G mutation‐induced mitochondrial complex V inhibition augments cardiolipin‐dependent alterations in mitochondrial dynamics during oxidative, Ca²⁺, and lipid insults in NARP cybrids: a potential therapeutic target for melatonin

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Mitochondrial Reactive Oxygen Species Generation and Calcium Increase Induced by Visible Light in Astrocytes

Cited by 20 publications

References 16 publications

Melatonin protects the mitochondria from oxidative damage reducing oxygen consumption, membrane potential, and superoxide anion production

Melatonin protects the mitochondria from oxidative damage reducing oxygen consumption, membrane potential, and superoxide anion production

Effects of Low Power Laser Irradiation on Intracellular Calcium and Histamine Release in RBL‐2H3 Mast Cells

mtDNA T8993G mutation‐induced mitochondrial complex V inhibition augments cardiolipin‐dependent alterations in mitochondrial dynamics during oxidative, Ca2+, and lipid insults in NARP cybrids: a potential therapeutic target for melatonin

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mtDNA T8993G mutation‐induced mitochondrial complex V inhibition augments cardiolipin‐dependent alterations in mitochondrial dynamics during oxidative, Ca²⁺, and lipid insults in NARP cybrids: a potential therapeutic target for melatonin