Increase in the adp/atp exchange in rat liver mitochondria irradiated in vitro by helium-neon laser

Passarella, Salvatore; Ostuni, Angela; Atlante, Anna; Quagliariello, Ernesto

doi:10.1016/s0006-291x(88)80940-9

Cited by 119 publications

(75 citation statements)

References 8 publications

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“…A similar increase in ATP production has been found in rat liver mitochondria after photostimulation with He-Ne laser in vitro [44,45] These metabolic effects result in increased tensile strength of healing skin wounds, as demonstrated by Lam et al [46] and Kovacs et al [47].…”

Section: Effects Of Laser Photostimulationmentioning

confidence: 52%

The Biological Effects of Laser Therapy and Other Physical Modalities on Connective Tissue Repair Processes

Enwemeka

Reddy

2000

LASER THERAPY

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Connective tissue injuries, such as tendon rupture and ligamentous strains, are common. Unlike most soft tissues that require 7-10 days to heal, primary healing of tendons and other dense connective tissues take as much as 6 -8 weeks during which they are inevitably protected in immobilization casts to avoid re-injury. Such long periods of immobilization impair functional rehabilitation and predispose a multitude of complications that could be minimized if healing is quickened and the duration of cast immobilization reduced. In separate studies, we tested the hypothesis that early function, ultrasound, 632.8 nm He-Ne laser, and 904 nm Ga-As laser, when used singly or in combination, promote healing of experimentally severed and repaired rabbit Achilles tendons as evidenced by biochemical, biomechanical, and morphological indices of healing. Our results demonstrate that: (1) appropriate doses of each modality, i.e., early functional activities, ultrasound, He-Ne and Ga-As laser therapy augment collagen synthesis, modulate maturation of newly synthesized collagen, and overall, enhance the biomechanical characteristics of the repaired tendons. (2) Combinations of either of the two lasers with early function and either ultrasound or electrical stimulation further promote collagen synthesis when compared to functional activities alone. However, the biomechanical effects measured in tendons receiving the multi-therapy were similar, i.e., not better than the earlier single modality trials. Although tissue repair processes in humans may differ from that of rabbits, these findings suggest that human cases of connective tissue injuries, e.g., Achilles tendon rupture, may benefit from appropriate doses of He-Ne laser, Ga-As laser, and other therapeutic modalities, when used singly or in combination. Our recent meta-analysis of the laser therapy literature further corroborate these findings.

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Section: Effects Of Laser Photostimulationmentioning

confidence: 52%

The Biological Effects of Laser Therapy and Other Physical Modalities on Connective Tissue Repair Processes

Enwemeka

Reddy

2000

LASER THERAPY

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“…Measurement of ADP/ATP exchange was performed fluorometrically in control and photosensitized mitochondria as described by Passarella et al (12).…”

Section: Methodsmentioning

confidence: 99%

Singlet Oxygen Produced by Photodynamic Action Causes Inactivation of the Mitochondrial Permeability Transition Pore

Salet

Moreno

Ricchelli³

et al. 1997

Journal of Biological Chemistry

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We have studied the effects of singlet oxygen produced by photodynamic action on the cyclosporin A-sensitive permeability transition (PT) in isolated rat liver mitochondria. Mitochondria were incubated with 3 M hematoporphyrin and irradiated at 365 nm with a fluence rate of 25 watts/m 2 . For short durations of irradiation (60 s) the adenine nucleotide translocase was inactivated, but mitochondria retained their ability to form a proton electrochemical gradient and accumulated Ca 2؉ and P i at the same rate as non-irradiated controls. Strikingly, however, the oxidative effects of photodynamic action prevented opening of the PT pore which is normally induced by Ca 2؉ plus P i or by treatment with diethyl pyrocarbonate (a histidine reagent) or diamide (a thiol oxidant). We show that the most likely targets for photodynamic action are critical histidines that undergo degradation. Irradiated, hematoporphyrinloaded mitochondria treated with diethyl pyrocarbonate or diamide still undergo the PT when treated with phenylarsine oxide, which reacts with a critical dithiol involved in pore modulation (Petronilli, V., Costantini, P., Scorrano, L., Colonna, R., Passamonti, S., and Bernardi, P. (1994) J. Biol. Chem. 269, 16638 -16642). These data suggest (i) that the dithiol cysteines are not oxidized by photodynamic action, but rather became inaccessible to oxidants; and (ii) that irradiation of hematoporphyrin-loaded mitochondria does not lead to pore denaturation, but rather to site-selective inactivation of discrete pore functional domains.When Ca 2ϩ -loaded mitochondria are treated with a variety of inducing agents, the opening of Ca 2ϩ -dependent pores leads to the so-called permeability transition of the inner membrane, which is specifically inhibited by nanomolar concentrations of cyclosporin A. Among Ca 2ϩ -dependent pore inducers, oxidizing agents have received considerable attention, and redox state changes of pyridine nucleotides, glutathione, or sulfhydryl groups have been shown to have a prominent role in the mechanism (or in the control) of Ca 2ϩ efflux following pore opening (for general reviews, see Refs. 1 and 2).In the present work, we have studied the effects of the very reactive species, singlet oxygen, 1 O 2 , on isolated rat liver mitochondria. The presence of 1 O 2 as a transient species able to damage cells, mainly at the mitochondrial level, can be observed in disease, such as in porphyria (3), and in the treatment of solid tumor by porphyrin photodynamic therapy (4). The effects of 1 O 2 on substrate transport, respiration, and phosphorylation are well documented, but few reports deal with those on the uptake and release of Ca 2ϩ from mitochondria (for a general review, see Ref. 5). In 1981 we have reported (6) that treatment with 1 O 2 produced by porphyrin photodynamic action can prevent Ca 2ϩ release due to membrane "damage" resulting from massive Ca 2ϩ loading. At that time, our interpretation was that such a release from Ca 2ϩ -overloaded mitochondria was probably of no physiological relevance....

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“…2.7.1.1), 0.5 E.U. glucose-6-phosphate-dehydrogenase (Roche/R-Biopharm), and 0.2 mmol/L NADPH (34). The influence of adenylate kinase (ADK)-dependent ATP synthesis was evaluated after treatment of isolated mitochondria with 10 Amol/L ADK-specific inhibitor P 1 P 5 -diadenosine-5 ¶-pentaphosphate, and no significant effect was observed (data not shown).…”

Section: Ant2 Knockdown Sensitizes Cells To Apoptotic Inductionmentioning

confidence: 99%

Chemosensitization by Knockdown of Adenine Nucleotide Translocase-2

Bras¹,

Borgne‐Sanchez

Touat³

et al. 2006

Cancer Research

102

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Mitochondrial membrane permeabilization (MMP) is a ratelimiting step of apoptosis, including in anticancer chemotherapy. Adenine nucleotide translocase (ANT) mediates the exchange of ADP and ATP on the inner mitochondrial membrane in healthy cells. In addition, ANT can cooperate with Bax to form a lethal pore during apoptosis. Humans possess four distinct ANT isoforms, encoded by four genes, whose transcription depends on the cell type, developmental stage, cell proliferation, and hormone status. Here, we show that the ANT2 gene is up-regulated in several hormonedependent cancers. Knockdown of ANT2 by RNA interference induced no major changes in the aspect of the mitochondrial network or cell cycle but provoked minor increase in mitochondrial transmembrane potential and reactive oxygen species level and reduced intracellular ATP concentration without affecting glycolysis. At expression and functional levels, ANT2 depletion was not compensated by other ANT isoforms. Most importantly, ANT2, but not ANT1, silencing facilitated MMP induction by lonidamine, a mitochondriontargeted antitumor compound already used in clinical studies for breast, ovarian, glioma, and lung cancer as well as prostate adenoma. The combination of ANT2 knockdown with lonidamine induced apoptosis irrespective of the Bcl-2 status. These data identify ANT2 as an endogenous inhibitor of MMP and suggest that its selective inhibition could constitute a promising strategy of chemosensitization. (Cancer Res 2006; 66(18): 9143-52)

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Increase in the adp/atp exchange in rat liver mitochondria irradiated in vitro by helium-neon laser

Cited by 119 publications

References 8 publications

The Biological Effects of Laser Therapy and Other Physical Modalities on Connective Tissue Repair Processes

The Biological Effects of Laser Therapy and Other Physical Modalities on Connective Tissue Repair Processes

Singlet Oxygen Produced by Photodynamic Action Causes Inactivation of the Mitochondrial Permeability Transition Pore

Chemosensitization by Knockdown of Adenine Nucleotide Translocase-2

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