scholarly journals Melatonin and Its Metabolites Ameliorate UVR-Induced Mitochondrial Oxidative Stress in Human MNT-1 Melanoma Cells

2018 ◽  
Vol 19 (12) ◽  
pp. 3786 ◽  
Author(s):  
Konrad Kleszczyński ◽  
Bernadetta Bilska ◽  
Agatha Stegemann ◽  
Damian Flis ◽  
Wieslaw Ziolkowski ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Phosphorylation ◽  
Melanoma Cells ◽  
Ultraviolet B ◽  
Melatonin Receptors ◽  
Biologically Active ◽  
Uvb Radiation ◽  
Mitochondrial Oxidative Stress ◽  
Uncoupling Of Oxidative Phosphorylation ◽  
Uvb Exposure

Melatonin (Mel) is the major biologically active molecule secreted by the pineal gland. Mel and its metabolites, 6-hydroxymelatonin (6(OH)Mel) and 5-methoxytryptamine (5-MT), possess a variety of functions, including the scavenging of free radicals and the induction of protective or reparative mechanisms in the cell. Their amphiphilic character allows them to cross cellular membranes and reach subcellular organelles, including the mitochondria. Herein, the action of Mel, 6(OH)Mel, and 5-MT in human MNT-1 melanoma cells against ultraviolet B (UVB) radiation was investigated. The dose of 50 mJ/cm2 caused a significant reduction of cell viability up to 48%, while investigated compounds counteracted this deleterious effect. UVB exposure increased catalase activity and led to a simultaneous Ca++ influx (16%), while tested compounds prevented these disturbances. Additional analysis focused on mitochondrial respiration performed in isolated mitochondria from the liver of BALB/cJ mice where Mel, 6(OH)Mel, and 5-MT significantly enhanced the oxidative phosphorylation at the dose of 10−6 M with lower effects seen at 10−9 or 10−4 M. In conclusion, Mel, 6(OH)Mel and 5-MT protect MNT-1 cells, which express melatonin receptors (MT1 and MT2) against UVB-induced oxidative stress and mitochondrial dysfunction, including the uncoupling of oxidative phosphorylation.

scholarly journals Laminarin Attenuates Ultraviolet-Induced Skin Damage by Reducing Superoxide Anion Levels and Increasing Endogenous Antioxidants in the Dorsal Skin of Mice

Marine Drugs ◽  
2020 ◽  
Vol 18 (7) ◽  
pp. 345 ◽  
Author(s):  
Ji Hyeon Ahn ◽  
Dae Won Kim ◽  
Cheol Woo Park ◽  
Bora Kim ◽  
Hyejin Sim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Anion ◽  
Collagen Fibers ◽  
Ultraviolet B ◽  
Control Group ◽  
Dorsal Skin ◽  
Skin Damage ◽  
Superoxide Anion Production ◽  
Uvb Exposure ◽  
Immunohistochemical Studies

A number of studies have demonstrated that marine carbohydrates display anti-oxidant, anti-melanogenic, and anti-aging activities in the skin. Laminarin (LA), a low-molecular-weight polysaccharide, is found in brown algae. The benefits of LA in ultraviolet B (UVB) induced photodamage of the skin have not been reported. The aim of this study was to investigate the effects of pre-treated LA on histopathological changes and oxidative damage in mouse dorsal skin on day 5, following repeated UVB exposure. Histopathology, Western blot analysis and immunohistochemical studies showed that epidermal thickness in the UVB group was significantly increased; however, the thickness in the UVB group treated with LA (LA/UVB group) was less compared with that of the UVB group. Collagen fibers in the dermis of the UVB group were significantly decreased and destroyed, whereas, in the LA/UVB group, the density of collagen fibers was significantly increased compared with that of the UVB group. Oxidative stress due to superoxide anion production measured via dihydroethidium fluorescence staining was dramatically increased in the UVB group, whereas in the LA/UVB group, the oxidative stress was significantly decreased. Expressions of SOD1, glutathione peroxidase and catalase were markedly reduced in the UVB group, whereas in the LA/UVB group, they were significantly higher along with SOD2 than in the control group. Taken together, our results indicate that LA pretreatment prevents or attenuates skin damage, by decreasing oxidative stress and increasing antioxidant enzymes in mouse dorsal skin.

scholarly journals Effect of Lactobacillus reuteri Administration on Wrinkle Formation and Type I Procollagen Levels in UVB-Exposed Male Balb/c Mice (Mus musculus)

2020 ◽  
Vol 4 (3) ◽  
pp. 113
Author(s):  
Ivanna Valentina ◽  
Achadiyani Achadiyani ◽  
Sunarjati Sudigdo Adi ◽  
Ronny Lesmana ◽  
Reni Farenia
Keyword(s):  
Oxidative Stress ◽  
Lactobacillus Reuteri ◽  
Ultraviolet B ◽  
Type I ◽  
Uvb Radiation ◽  
Dorsal Skin ◽  
Uvb Irradiation ◽  
Type I Procollagen ◽  
Group 3 ◽  
Group 1

Background: Chronic Ultraviolet B (UVB) exposure causes oxidative stress that may induce damages to the collagen matrix and thus plays a role in the wrinkle formation. Lactobacillus reuteri is a probiotic that may exerts antioxidant effects, thus helping to reduce damages caused by UVB-induced oxidative stress in the skin.Materials and Methods: Twenty-eight male Balb/c mice were divided equally into control group, UVB radiation only group, oral L. reuteri supplementation only group, and UVB radiation with oral L. reuteri supplementation group. UVB irradiation was given 3 times a week (100 seconds/exposure, within 3 cm distance) for 10 weeks, with a total dose of 166 mJ/cm2. Oral L. reuteri supplementation (0.2 mL, 108 CFU) was provided every morning after meal via orogastric feeding tube for 10 weeks. Wrinkle formation on the dorsal skin of the mice was evaluated in accordance with the Bissett method and type I procollagen levels was evaluated by western blotting.Results: In comparison with the group receiving only UVB irradiation, the group receiving probiotic and UVB irradiation showed significantly lower wrinkle scores (Group 1 vs. Group 3, 2.50±0.55 vs. 1.00±0,00; p<0.05) and significantly higher type I procollagen levels (Group 1 vs. Group 3, 0.88±0.36 vs. 1.92±0.46; p<0.05).Conclusion: Results of the current study showed that L. reuteri supplementation may reduce wrinkle formation and increase type I procollagen production in UVB-exposed dorsal skin of male Balb/c mice.Keywords: Lactobacillus reuteri, type I procollagen, photoaging, wrinkles, ultraviolet B

scholarly journals Echinacoside Alleviates UVB Irradiation-Mediated Skin Damage via Inhibition of Oxidative Stress, DNA Damage, and Apoptosis

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Di Zhang ◽  
Chengtao Lu ◽  
Zhe Yu ◽  
Xiayin Wang ◽  
Li Yan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Histopathological Examination ◽  
Ultraviolet B ◽  
Ros Generation ◽  
Antioxidant Enzyme Activities ◽  
Skin Damage ◽  
Uvb Irradiation ◽  
Uvb Exposure

Ultraviolet B (UVB) irradiation has been known to cause skin damage, which is associated with oxidative stress, DNA damage, and apoptosis. Echinacoside is a phenylethanoid glycoside isolated from Herba Cistanches, which exhibits strong antioxidant activity. In this study, we evaluate the photoprotective effect of echinacoside on UVB-induced skin damage and explore the potential molecular mechanism. BALB/c mice and HaCaT cells were treated with echinacoside before UVB exposure. Histopathological examination was used to evaluate the skin damage. Cell viability, lactate dehydrogenase (LDH) levels, antioxidant enzyme activities, reactive oxygen species (ROS) generation, DNA damage, and apoptosis were measured as well. Western blot was used to measure the expression of related proteins. The results revealed that pretreatment of echinacoside ameliorated the skin injury; attenuated oxidative stress, DNA damage, and apoptosis caused by UVB exposure; and normalized the protein levels of ATR, p53, PIAS3, hnRNP K, PARP, and XPA. To summarize, echinacoside is beneficial in the prevention of UVB-induced DNA damage and apoptosis of the skin in vivo and in vitro.

scholarly journals Almond Consumption Increased UVB Resistance in Healthy Asian Women

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 319-319
Author(s):  
Susanne Henning ◽  
Jason Li ◽  
Gail Thames ◽  
Omar Bari ◽  
Patrick Tran ◽  
...  
Keyword(s):  
Skin Aging ◽  
Ultraviolet B ◽  
In Vivo Studies ◽  
Asian Women ◽  
Skin Extract ◽  
Uvb Radiation ◽  
Facial Skin ◽  
Uvb Exposure

Abstract Objectives Almonds are a rich source of phenolic and polyphenolic compounds, which have antioxidant activity. In vitro and in vivo studies have demonstrated that topical application of almond oil and almond skin extract reduces UVB-induced photoaging. Ultraviolet-B (UVB) protection by oral almond consumption has not been previously studied in humans. It was the objective to investigate whether oral almond consumption can increase resistance to UVB radiation and reduce skin aging in healthy Asian women. Methods Thirty-nine female participants (18–45 years) with Fitzpatrick skin type II-IV were randomly assigned to consume either 1.5 oz of almonds or 1.8 oz of pretzels daily for 12 weeks. Minimal erythema dose (MED) was determined using a standardized protocol, which determined the minimal radiation inducing erythema on the inner arm 24 hours following UVB exposure. Facial skin texture was evaluated by two dermatologists using the Clinician's Erythema Assessment scale and Allergan Roughness scale. Facial melanin index, hydration, sebum, and erythema were determined using a cutometer. Results Women who consumed almonds, experienced a significant increase in MED from 415 ± 64 to 487 ± 59 (18.7 ± 19.2%, P = 0.006) from baseline to week 12 compared to women in the pretzel group from 415 ± 67 to 421 ± 67 (1.8 ± 11.1%). The exposure time to reach minimal erythema was also increased significantly in the almond group from 160 ± 23 to 187 ± 25 (17.5 ± 22.2%) compared to the pretzel group from 165 ± 27 to 166 ± 25 (1.7 ± 14%) (p=0.026). There were no differences noted between the groups consuming almonds versus pretzels in Allergan roughness, melanin, hydration, or sebum on facial skin. Conclusions Our findings suggest that daily oral almond consumption may lead to enhanced protection from UVB photodamage by increasing the MED. Protection from other UV radiation was not tested and therefore almond consumption will not replace other methods of sun protection such as application of sunscreen or wearing protective closing. Funding Sources Almond Board of California.

scholarly journals Mitochondrial oxidative stress causes insulin resistance without disrupting oxidative phosphorylation

2018 ◽  
Vol 293 (19) ◽  
pp. 7315-7328 ◽  
Author(s):  
Daniel J. Fazakerley ◽  
Annabel Y. Minard ◽  
James R. Krycer ◽  
Kristen C. Thomas ◽  
Jacqueline Stöckli ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Oxidative Phosphorylation ◽  
Mitochondrial Oxidative Stress

Abstract B144: Elesclomol, an inducer of oxidative stress, targets oxidative phosphorylation (oxphos) in melanoma cells.

2011 ◽  
Author(s):  
Stergios J. Moschos ◽  
Michelle Barbi de Moura ◽  
Shelley Fayewicz ◽  
Nicholas Bateman ◽  
Mai Sun ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Oxidative Phosphorylation ◽  
Melanoma Cells

scholarly journals Cyclobutane pyrimidine dimers from UVB exposure induce a hypermetabolic state in keratinocytes via mitochondrial oxidative stress

Redox Biology ◽  
2021 ◽  
Vol 38 ◽  
pp. 101808
Author(s):  
Csaba Hegedűs ◽  
Tamás Juhász ◽  
Eszter Fidrus ◽  
Eszter Anna Janka ◽  
Gábor Juhász ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cyclobutane Pyrimidine Dimers ◽  
Mitochondrial Oxidative Stress ◽  
Pyrimidine Dimers ◽  
Hypermetabolic State ◽  
Uvb Exposure

scholarly journals MORIN PREVENTS ULTRAVIOLET-B RADIATION-INDUCED PHOTOCARCINOGENESIS THROUGH ACTIVATING THROMBOSPONDIN-1 IN THE MOUSE SKIN

2018 ◽  
Vol 11 (3) ◽  
pp. 171
Author(s):  
Anjugam C ◽  
Sridevi M ◽  
Rajendra Prasad N ◽  
Agilan Balupillai
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Mouse Skin ◽  
Ultraviolet B ◽  
Uvb Radiation ◽  
Thrombospondin 1 ◽  
Radiation Induced ◽  
Cox 2 ◽  
Uvb Exposure

 Objective: In this study, we investigated whether morin, a natural flavonoid, could able to inhibit ultraviolet B (UVB)-induced carcinogenesis in the skin of Swiss albino mice.Methods: The mice were exposed to UVB radiation (180 mJ/cm2) on weekly thrice for 30 weeks, and morin was administered intraperitoneal and topical application 1 h before UVB exposure. UVB radiation induces the overexpression of cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), vascular endothelial growth factor (VEGF), transforming growth factor-beta (TGF-β), and Bcl-2 genes.Results: Morin significantly prevented UVB-induced activation of COX-2, iNOS, VEGF, TGF-β, and Bcl-2 expression in mouse skin. Thrombospondin-1 (TSP), a novel endogenous factor, inhibits angiogenesis and inflammation.Conclusion: The present study illustrates that the protective effect of morin against UVB-induced carcinogenesis may be modulated through activation of TSP-1 in UVB-exposed Swiss albino mice.

scholarly journals Horse Oil Mitigates Oxidative Damage to Human HaCaT Keratinocytes Caused by Ultraviolet B Irradiation

2019 ◽  
Vol 20 (6) ◽  
pp. 1490
Author(s):  
Mei Piao ◽  
Kyoung Kang ◽  
Ao Zhen ◽  
Hee Kang ◽  
Young Koh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Matrix Metalloproteinase ◽  
Oxidative Damage ◽  
Reactive Oxygen ◽  
Ultraviolet B ◽  
Electromagnetic Spectrum ◽  
Oxygen Species ◽  
Uvb Radiation ◽  
Hacat Keratinocytes

Horse oil products have been used in skin care for a long time in traditional medicine, but the biological effects of horse oil on the skin remain unclear. This study was conducted to evaluate the protective effect of horse oil on ultraviolet B (UVB)-induced oxidative stress in human HaCaT keratinocytes. Horse oil significantly reduced UVB-induced intracellular reactive oxygen species and intracellular oxidative damage to lipids, proteins, and DNA. Horse oil absorbed light in the UVB range of the electromagnetic spectrum and suppressed the generation of cyclobutane pyrimidine dimers, a photoproduct of UVB irradiation. Western blotting showed that horse oil increased the UVB-induced Bcl-2/Bax ratio, inhibited mitochondria-mediated apoptosis and matrix metalloproteinase expression, and altered mitogen-activated protein kinase signaling-related proteins. These effects were conferred by increased phosphorylation of extracellular signal-regulated kinase 1/2 and decreased phosphorylation of p38 and c-Jun N-terminal kinase 1/2. Additionally, horse oil reduced UVB-induced binding of activator protein 1 to the matrix metalloproteinase-1 promoter site. These results indicate that horse oil protects human HaCaT keratinocytes from UVB-induced oxidative stress by absorbing UVB radiation and removing reactive oxygen species, thereby protecting cells from structural damage and preventing cell death and aging. In conclusion, horse oil is a potential skin protectant against skin damage involving oxidative stress.

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