Skin inflammation induced by reactive oxygen species (ROS): an in-vivo model

Trenam, Charles W.; Dabbagh, Alya; Morris, Christopher J.; Blake, David R.

doi:10.1111/j.1365-2133.1991.tb14165.x

Cited by 56 publications

(33 citation statements)

References 25 publications

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“…A consequence of cholesterol deposition in membranes is a decrease in the permeability of oxygen (Subczynski et al, 1991 (Trenam et al, 1991;Kohler et al, 1999;Maziere et al, 1999;Fubini and Hubbard, 2003). Because perturbations in the permeability of the inner mitochondrial membrane may result in large-amplitude swelling of the mitochondria, rupture of the outer mitochondrial membrane, and release of proapoptotic proteins, we investigated whether CDDO-Me would induce this mPT in isolated mitochondria.…”

Section: Cddo-me Targets Mitochondrial Membrane Permeability 1191mentioning

confidence: 99%

“…is a highly reactive oxygen species (ROS) that can directly damage lipids and proteins and is a precursor to other ROS like H 2 O 2 . Curiously however, in addition to being an essential component of inflammation (Trenam et al, 1991;Fubini and Hubbard, 2003), mitochondrial-derived ROS have also been shown to be necessary for the activation of a variety of transcription factors, including NFB and activating protein 1 (Kohler et al, 1999;Maziere et al, 1999), and in fact, impairment of mitochondrial electron transport or increased antioxidant capacity have been shown to inhibit the activation of NFB by a variety of stimuli (Josse et al, 1998;Azevedo-Martins et al, 2003;Woo et al, 2004). These findings suggest that agents that affect mitochondrial electron transport could also have anti-inflammatory activity by modulating O 2 .…”

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confidence: 99%

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A Novel Mechanism of Action of Methyl-2-cyano-3,12 Dioxoolean-1,9 Diene-28-oate: Direct Permeabilization of the Inner Mitochondrial Membrane to Inhibit Electron Transport and Induce Apoptosis

Samudio

Konopleva²,

Pélicano

et al. 2006

Mol Pharmacol

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Methyl-2-cyano-3,12 dioxoolean-1,9 diene-28-oate (CDDOMe) is a synthetic oleanolic acid derivative that displays antitumorigenic and anti-inflammatory activities, and we have previously reported that this agent potently activates the intrinsic apoptotic pathway in leukemia cells. In this study, we demonstrate that mitochondrial dysfunction induced by CDDO-Me is mediated by direct permeabilization of the inner mitochondrial membrane, which results in the rapid depletion of mitochondrial glutathione (GSXm), loss of cardiolipin, and inhibition of mitochondrial respiration. More importantly, we demonstrate that in addition to activating the intrinsic apoptotic pathway, the mitochondrial effects of CDDO-Me may mediate its anti-inflammatory activity by modulating the generation of superoxide anion (O 2 . ). It is noteworthy that CDDO-Me did not increase the generation of O 2 . , and pretreatment of leukemia cells with CDDO-Me prevented the increase of this reactive oxygen species elicited by inhibition of complex I or III in the absence of de novo protein synthesis. CDDO-Me, but not other inhibitors of respiration, induced a time-and dose-dependent, cyclosporin A-independent permeability transition (PT) of isolated mitochondria that was sensitive to sulfhydryl antioxidants but not to EDTA. PT induced by CDDO-Me and Ca 2ϩ was accompanied by loss of GSXm, suggesting that the increased permeability of the inner mitochondrial membrane facilitates the loss of this antioxidant. Finally, transmission electron microscopy revealed that CDDO-Me rapidly induced caspase-independent mitochondrial swelling and loss of inner membrane structure before the release of cytochrome c. Taken together, our results indicate that CDDO-Me is a novel mitochondriotoxic agent that induces apoptosis and inhibits mitochondrial electron transport via perturbations in inner mitochondrial membrane integrity.2-Cyano-3,12-dioxooleana-1,9-diene-28-oic acid (CDDO) is a synthetic triterpenoid that displays potent anti-inflammatory and antitumorigenic activities in vitro and in vivo (Suh et al., 1999;Lapillonne et al., 2003;Konopleva et al., 2004). CDDO and its more potent methyl ester derivative, methyl-2-cyano-3,12-dioxooleana-1,9-diene-28-oate (CDDO-Me), induce apoptosis and differentiation in leukemia cells in culture, and we have demonstrated that apoptosis induced by these agents is initiated by the intrinsic apoptotic pathway possibly through direct perturbation of mitochondrial homeostasis (Konopleva et al., 2002(Konopleva et al., , 2004. As an anti-inflammatory agent, CDDO has been shown to potently prevent

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Section: Cddo-me Targets Mitochondrial Membrane Permeability 1191mentioning

confidence: 99%

mentioning

confidence: 99%

A Novel Mechanism of Action of Methyl-2-cyano-3,12 Dioxoolean-1,9 Diene-28-oate: Direct Permeabilization of the Inner Mitochondrial Membrane to Inhibit Electron Transport and Induce Apoptosis

Samudio

Konopleva²,

Pélicano

et al. 2006

Mol Pharmacol

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“…9,10) In these studies, skin injury was caused by glucose oxidase as a producer of H 2 O 2 or arachidonic acid. 9,10) Therefore, this is the first report on the effect of topical application of SOD on UVinduced skin damage.…”

Section: )mentioning

confidence: 99%

“…9) On the other hand, Simões et al studied topical application of SOD. 10) In this previous study, mouse ear edema model induced by arachidonic acid was used, and SOD reduced the edema.…”

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confidence: 99%

Efficient Intradermal Delivery of Superoxide Dismutase Using a Combination of Liposomes and Iontophoresis for Protection against UV-Induced Skin Damage

Kigasawa

Miyashita

Kajimoto

et al. 2012

Biological & Pharmaceutical Bulletin

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Superoxide dismutase (SOD) is a potent antioxidant agent that protects against UV-induced skin damage. However, its high molecular weight is a significant obstacle for efficient delivery into the skin through the stratum corneum and development of antioxidant activity. Recently, we developed a non-invasive transfollicular delivery system for macromolecules using a combination of liposomes and iontophoresis, that represents promising technology for enhancing transdermal administration of charged drugs (IJP, 403, 2011, Kajimoto et al.). In this study, in rats we attempted to apply this system to intradermal delivery of SOD for preventing UV-induced skin injury. SOD encapsulating in cationic liposomes was subjected to anodal iontophoresis. After iontophoretic treatment, the liposomes were diffused widely in the viable skin layer around hair follicles. In contrast, passive diffusion failed to transport liposomes efficiently into the skin. Iontophoretic delivery of liposomes encapsulating SOD caused a marked decrease in the production of oxidative products, such as malondialdehyde, hexanoyl lysine, and 8-hydroxi-2-deoxyguanosine, in UV-irradiated skin. These findings suggested that functional SOD can be delivered into the skin using a combination of iontophoresis and a liposomal system. In conclusion, we succeeded in developing an efficient intradermal SOD delivery system, that would be useful for delivery of other macromolecules. Key words superoxide dismutase; iontophoresis; liposome; transfollicular delivery; antioxidant activityThe skin is exposed constitutively to ultraviolet (UV) rays that cause the production of reactive oxygen species (ROS) in the skin, resulting in diverse skin disorders.1) It is well-known that the classes of UV that reach the ground are UVA and UVB. UVA readily penetrates deep layers of the skin, and causes production of melanin and wrinkling associated with destruction of collagen fiber, resulting in aging of the skin. 1)UVB causes skin inflammation and DNA damage that contribute to the pathogenesis of serious skin disorders, such as skin malignancy.1) ROS are also involved in the development of skin damage, and therefore elimination of ROS is essential for protecting the skin from UV-induced damage.Superoxide dismutase (SOD) may be used to prevent and treat ROS-induced disorders of various tissues as it has potent antioxidant activity.2) Because of its poor pharmacokinetic profile, systemic administration of free SOD does not result in induction of efficient in vivo antioxidant activity.3) In contrast, the skin is an available site for topical application of SOD due to its accessibility. Percutaneous delivery of SOD is therefore considered to be a promising method for prophylaxis or therapy of UV-induced skin damage. However, SOD are highly hydrophilic macromolecules and do not readily penetrate the deeper layers of the skin as the outer layer of the skin, the stratum corneum, functions as a significant barrier prohibiting penetration of drug molecules larger than 500 Da. 4)Iontophoresis...

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“…PEG, a well-known biomaterial (11), was covalently bonded to the fluorescent hydrogel fibers, thereby reducing inflammation (12,13). These PEG-bonded fluorescent hydrogel fibers maintained glucose responsiveness and transmitted fluorescent signals transdermally for an extended period.…”

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confidence: 99%

Long-term in vivo glucose monitoring using fluorescent hydrogel fibers

Heo

Shibata

Okitsu

et al. 2011

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

284

227

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The use of fluorescence-based sensors holds great promise for continuous glucose monitoring (CGM) in vivo, allowing wireless transdermal transmission and long-lasting functionality in vivo. The ability to monitor glucose concentrations in vivo over the long term enables the sensors to be implanted and replaced less often, thereby bringing CGM closer to practical implementation. However, the full potential of long-term in vivo glucose monitoring has yet to be realized because current fluorescence-based sensors cannot remain at an implantation site and respond to blood glucose concentrations over an extended period. Here, we present a long-term in vivo glucose monitoring method using glucose-responsive fluorescent hydrogel fibers. We fabricated glucose-responsive fluorescent hydrogels in a fibrous structure because this structure enables the sensors to remain at the implantation site for a long period. Moreover, these fibers allow easy control of the amount of fluorescent sensors implanted, simply by cutting the fibers to the desired length, and facilitate sensor removal from the implantation site after use. We found that the polyethylene glycol (PEG)-bonded polyacrylamide (PAM) hydrogel fibers reduced inflammation compared with PAM hydrogel fibers, transdermally glowed, and continuously responded to blood glucose concentration changes for up to 140 days, showing their potential application for long-term in vivo continuous glucose monitoring.glucose-responsive fluorescence | long-lasting implantable sensor | biocompatible interface | implantable glucose sensor | diabetes mellitus I n vivo glucose monitoring allows continuous glucose monitoring (CGM) and facilitates intensive control of blood glucose concentrations in diabetic patients. Long-lasting implantable sensors can reduce the frequency of implantation and replacement, resulting in long-term in vivo glucose monitoring with less effort by patients and less tissue damage. For decades, implantable sensors for long-term use have been developed using enzyme electrodes. However, these methods have several drawbacks for long-term use because these enzyme based sensors are insufficiently stable in vivo (1), they are poorly accurate in low glucose concentrations (2), and their activity is oxygen-dependent (3). In contrast, glucose-responsive fluorescence is a promising approach that maintains long-lasting functionality in vivo due to its enzyme-free and reversible reaction (4-9). We recently developed fluorescent hydrogel microbeads that are transdermally detectable, injectable, minimally invasive, and biocompatible (10). To bring this technology closer to long-term application, the fluorescent hydrogel sensors need to remain at the implantation site for a long period (over 3 mo) and be easily removable after use; despite their great potential for continuous glucose monitoring, the microbeads were not suitable for long-term monitoring in vivo because they dispersed from the implantation site and were difficult to remove. In addition, the biointerface of the fluoresce...

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Skin inflammation induced by reactive oxygen species (ROS): an in-vivo model

Cited by 56 publications

References 25 publications

A Novel Mechanism of Action of Methyl-2-cyano-3,12 Dioxoolean-1,9 Diene-28-oate: Direct Permeabilization of the Inner Mitochondrial Membrane to Inhibit Electron Transport and Induce Apoptosis

A Novel Mechanism of Action of Methyl-2-cyano-3,12 Dioxoolean-1,9 Diene-28-oate: Direct Permeabilization of the Inner Mitochondrial Membrane to Inhibit Electron Transport and Induce Apoptosis

Efficient Intradermal Delivery of Superoxide Dismutase Using a Combination of Liposomes and Iontophoresis for Protection against UV-Induced Skin Damage

Long-term in vivo glucose monitoring using fluorescent hydrogel fibers

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