Mitochondrial dysfunction and cellular stress progression after ultraviolet B irradiation in human keratinocytes

Paz, Mariela L.; Maglio, Daniel Horacio González; Weill, Federico S.; Bustamante, Juanita; Leoni, Juliana

doi:10.1111/j.1600-0781.2008.00348.x

Cited by 94 publications

(75 citation statements)

References 37 publications

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“…ROS and superoxide radical levels were highest 6 and 12 h after irradiation, respectively. 37) However, the NO levels of HaCaT cells remain unchanged at these periods, 37) an observation that is similar to the finding obtained with this work. Therefore, the cellular damage caused by UV-B irradiation seems to be mediated by the intracellular ROS level, but not by the NO level.…”

Section: Ros-scavenging Activitysupporting

confidence: 81%

Stereoselective Skin Anti-photoaging Properties of Ginsenoside Rg3 in UV-B-Irradiated Keratinocytes

Lim

Choi

Jung

2014

Biological & Pharmaceutical Bulletin

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Most UV-C radiation is absorbed by stratospheric ozone; very little reaches the Earth's surface. In contrast, UV-A and UV-B reach the Earth's surface and, subsequently, have the potential to harm humans. Although most biomolecules cannot absorb UV-A, UV-B is particularly harmful to living organisms. UV-A and UV-B contribute to detrimental effects via different molecular mechanisms, such as direct DNA damage, modulation of gene expression, and reactive oxygen species (ROS) generation.1) UV-B acts primarily on the epidermal basal cell layer of the skin. It initiates a photo-oxidation reaction that impairs the antioxidant status of the skin and increases the cellular ROS level, sequentially accelerating photoaging and the development of malignant diseases.2-5) UV-B is one of leading causes of skin changes, such as wrinkle formation, laxity, coarseness, mottled pigmentation, epidermal thickening, degradation of matrix macromolecules, vascularization, and immunosuppression. 6,7) Keratinocytes, the major cell population in the basal layer of the skin, are the primary targets of UV-B. In keratinocytes, UV-B induces the immediate generation of superoxide radical, which is sequentially converted to other ROS species, such as hydrogen peroxide and hydroxyl radical. Matrix metalloproteinases (MMPs) have been implicated in remodeling extracellular matrix (ECM) structures in wound healing, 9) dermal photoaging, 10) and severe pathologic states such as carcinogenesis.11) MMP-1 (interstitial collagenase) is produced by both dermal fibroblasts and epidermal keratinocytes. MMP-1 cleaves types I and III collagen into specific fragments that are further degraded by other MMPs, including MMP-2 (72 kDa gelatinase A/collagenase) and MMP-9 (92 kDa gelatinase B/type IV collagenase). UV radiation, including UV-B, induces the expression and secretion of MMP-1, -2, -3, -9, and/or -13 in the epidermis and dermis. 12,13) Destruction of collagen by UV irradiation, a cause of skin aging in both naturally aged and photoaged skin, is related to the enhanced induction of MMPs, which are secreted by epidermal keratinocytes and dermal fibroblasts. 14)Ginsenosides, also referred to as triterpenoid saponins, are the bioactive ingredients of ginseng, an herbal medication derived from the root of the Panax genus of plants that is widely used in traditional medicine. Ginsenosides are categorized into three groups on the basis of their aglycone (sapogenin) skeletons: the panaxadiol-type, including Rb1, Rb2, Rb3, Rc, Rd, Rg3, Rh2, and Rs1; the panaxatriol-type, including Re, Rf, Rg1, Rg2, and Rh1; and the oleanolic acid group, including Ro.Ginsenoside Rg3, one of the most effective ginsenosides, exerts a wide spectrum of pharmacological actions through anti-inflammatory, anti-tumor, anti-angiogenic, anti-metastatic, and anti-diabetic activities.15-21) Ginsenoside Rg3 exists in two stereoisomeric forms, 20(S)-Rg3 and 20(R)-Rg3 (Fig. 1), based on a chiral center at C-20 in its molecular structure. Of the two stereoisomers, 20(S)-Rg3 is the major constituen...

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Section: Ros-scavenging Activitysupporting

confidence: 81%

Stereoselective Skin Anti-photoaging Properties of Ginsenoside Rg3 in UV-B-Irradiated Keratinocytes

Lim

Choi

Jung

2014

Biological & Pharmaceutical Bulletin

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“…In cell culture, UV-B-induced ROS affected mitochondrial membranes and thereby led to impaired ATP production (Shimmura and Tsubota, 1997;Gniadecki et al, 2001;Wallace, 2005;Paz et al, 2008). However, contrary to the results from cell culture studies, mitochondrial function was not affected by UV-B-induced ROS in our study.…”

Section: Discussioncontrasting

confidence: 56%

“…ROS damage to mitochondrial membranes can increase proton leak, which results in decreased membrane potential and ATP production (Skulachev, 1998;Brand et al, 2005). In addition, ROS can impair ATP production by disrupting substrate oxidation (Gniadecki et al, 2001;Paz et al, 2008). However, ADP phosphorylation (state 3 respiration) and (A) There was no effect of NAC or UV-B on SERCA activity (N=10-12 fish per treatment).…”

Section: Discussionmentioning

confidence: 99%

“…Increased ROS generation is a significant component of UV-B-induced damage to cells (Gniadecki et al, 2001;Ichihashi et al, 2003;Paz et al, 2008;Birch-Machin and Swalwell, 2010). Excess ROS can have detrimental effects on muscle function and metabolism, thereby impacting performance of animals under natural conditions (Kuwahara et al, 2010;Gram et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

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UV-B exposure reduces locomotor performance by impairing muscle function but not mitochondrial ATP production

Kazerouni

Franklin

Seebacher

2015

Journal of Experimental Biology

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Ultraviolet B radiation (UV-B) can reduce swimming performance by increasing reactive oxygen species (ROS) formation. High concentrations of ROS can damage mitochondria, resulting in reduced ATP production. ROS can also damage muscle proteins, thereby leading to impaired muscle contractile function. We have shown previously that UV-B exposure reduces locomotor performance in mosquitofish (Gambusia holbrooki) without affecting metabolic scope. Our aim was therefore to test whether UV-B influences swimming performance of mosquitofish by ROS-induced damage to muscle proteins without affecting mitochondrial function. In a fully factorial design, we exposed mosquitofish to UV-B and no-UV-B controls in combination with exposure to N-acetylcysteine (NAC) plus no-NAC controls. We used NAC, a precursor of glutathione, as an antioxidant to test whether any effects of UV-B on swimming performance were at least partly due to UV-B-induced ROS. UV-B significantly reduced critical sustained swimming performance and tail beat frequencies, and it increased ROS-induced damage (protein carbonyl concentrations and lipid peroxidation) in muscle. However, UV-B did not affect the activity of sarco-endoplasmic reticulum ATPase (SERCA), an enzyme associated with muscle calcium cycling and muscle relaxation. UV-B did not affect ADP phosphorylation (state 3) rates of mitochondrial respiration, and it did not alter the amount of ATP produced per atom of oxygen consumed (P:O ratio). However, UV-B reduced the mitochondrial respiratory control ratio. Under UV-B exposure, fish treated with NAC showed greater swimming performance and tail beat frequencies, higher glutathione concentrations, and lower protein carbonyl concentrations and lipid peroxidation than untreated fish. Tail beat amplitude was not affected by any treatment. Our results showed, firstly, that the effects of UV-B on locomotor performance were mediated by ROS and, secondly, that reduced swimming performance was not caused by impaired mitochondrial ATP production. Instead, reduced tail beat frequencies indicate that muscle of UV-B exposed fish were slower, which was likely to have been caused by slower contraction rates, because SERCA activities remained unaffected.

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“…However, this energy generation could trigger unwanted events such as the production of ROS. Under normal aerobic conditions the mitochondria produces 90% of the cellular energy through the electron transport chain (ETC) 7,8,9 . During this process about 2% of electrons leak out, causing a downstream of free radical reactions that, if unregulated, can interfere with mitochondrial function 7,10 .…”

mentioning

confidence: 99%

Synthetic Studies Toward a Novel Hydroxylamine of Potential Utility in the Preparation of Mitochondriotropic Nitrones

Perez¹

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Mitochondrial dysfunction and cellular stress progression after ultraviolet B irradiation in human keratinocytes

Cited by 94 publications

References 37 publications

Stereoselective Skin Anti-photoaging Properties of Ginsenoside Rg3 in UV-B-Irradiated Keratinocytes

Stereoselective Skin Anti-photoaging Properties of Ginsenoside Rg3 in UV-B-Irradiated Keratinocytes

UV-B exposure reduces locomotor performance by impairing muscle function but not mitochondrial ATP production

Synthetic Studies Toward a Novel Hydroxylamine of Potential Utility in the Preparation of Mitochondriotropic Nitrones

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