Next Article in Journal
Safety Evaluation of Cosmetic Ingredients: In Vitro Opportunities for the Identification of Contact Allergens
Next Article in Special Issue
The Efficiency and Safety of Leuphasyl—A Botox-Like Peptide
Previous Article in Journal / Special Issue
Tenskinmetric Evaluation of Surface Energy Changes in Adult Skin: Evidence from 834 Normal Subjects Monitored in Controlled Conditions
 
 
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Communication

l-Ergothioneine Protects Skin Cells against UV-Induced Damage—A Preliminary Study

1
Dr. Irena Eris Cosmetic Laboratories, Centre for Science and Research, Pulawska 107a, Warsaw 02-595, Poland
2
Institute of Genetics and Biotechnology, Faculty of Biology, University of Warsaw and Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Pawinskiego 5a, Warsaw 02-106, Poland
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Cosmetics 2014, 1(1), 51-60; https://doi.org/10.3390/cosmetics1010051
Submission received: 31 December 2013 / Revised: 10 March 2014 / Accepted: 11 March 2014 / Published: 20 March 2014
(This article belongs to the Special Issue Selected Papers from ISBS/SICC 1st Joint International Congress)

Abstract

:
Many changes related to aging at the cellular level may be due to the physiological condition of mitochondria. One of the most common types of damage of mtDNA is the so-called “common deletion” referring to a deletion of 4977 base pairs. In the skin cells this phenomenon probably is caused by oxidative damage of mtDNA induced by UV. The present study was aimed at evaluating the effect of the antioxidant l-ergothioneine on UV-induced damage in skin cells. The effect of l-ergothioneine on the reduced glutathione level was studied. The presence of the “common deletion” in human fibroblasts irradiated with UVA and treated with l-ergothioneine was evaluated by a polymerase chain reaction. We have demonstrated that l-ergothioneine enhanced the level of reduced glutathione and protected cells from the induction of a photoaging-associated mtDNA “common deletion”. In view of our results, l-ergothioneine could be an effective skin care and anti-photoaging ingredient.

Graphical Abstract

1. Introduction

Ultraviolet irradiation is one of the most important environmental factors in the development of a number of skin conditions, ranging from photoaging to cancer. UVA/B rays penetrate into the skin, reach cells and are absorbed by proteins, lipids, and nuclear and mitochondrial DNA, causing a cascade of oxidative events that can result in progressive deterioration of cellular structure and function [1,2,3].
There are many theories of aging and a number of them encompass the role of mitochondria in this process. Mitochondria are responsible for producing approximately 90% of the cellular energy in the process of oxidative phosphorylation where electrons from NADH and FADH2 are transferred to oxygen. This generates a significant amount of reactive oxygen species (ROS). Mitochondria are able to counteract the production of ROS with antioxidant defense systems which can detoxify the amount of ROS produced, however, some ROS do evade these processes and are able to damage mitochondrial DNA (mtDNA) as well as proteins and lipids.
Mitochondria contain their own DNA (mtDNA), which is distinct from nuclear DNA and more susceptible to damage. Mitochondrial DNA mutations and deletions have been shown to accumulate in many tissues in mammals during aging. mtDNA mutations are thought to arise due to the close proximity to the inner membrane where reactive oxygen species are continually produced in the electron transport chain. This, along with the absence of protective histones and impaired DNA photoproduct repair makes mtDNA a sensitive marker of UV-induced DNA damage [4,5].
It has been shown that photoaged skin is characterized by increased mutations in the mitochondrial (mt) genome [6]. The most frequently reported deletion is a large-scale (4977 bp) deletion also called the “common deletion” (CD). In human skin CD has been shown to occur more frequently with increasing sun exposure and thus appears to be a useful marker rather for UVA induced alterations than for chronological aging [7,8,9,10].
The use of antioxidants is an effective approach to prevent symptoms related to photo-induced aging of the skin. Many antioxidants have long been used in cosmetology. l-Ergothioneine (EGT) is an unusual sulphur-containing derivative of an amino acid, histidine, which is acquired by mammals exclusively in their diet. l-Ergothioneine has two functional groups: l-thiol (SH) group and quaternary ammonium group N–(CH3)3 (Figure 1). EGT’s thiol group implies an antioxidant role. The quaternary group EGT resembles carnitine and transfers fatty acids into the mitochondria, therefore increasing the ATP level in cells. EGT is concentrated in cells and tissues frequently exposed to oxidative stress. Numerous in vitro assays have demonstrated the antioxidant and cytoprotective capabilities of EGT against a wide range of cellular stressors [11,12,13].
Figure 1. Chemical structure of l-ergothioneine.
Figure 1. Chemical structure of l-ergothioneine.
Cosmetics 01 00051 g001
On the basis of these data on the antioxidant activity of l-ergothioneine we found it interesting to study the effect of this substance on UV-induced alterations in skin cell cultures, particularly on mtDNA damage.

2. Experimental Section

2.1. Cell Cultures

KB cells (epidermoid carcinoma cell line KB, American Type Culture Collection (ATCC), Manassas, VA, USA) were grown in standard RPMI medium (Invitrogen, Carlsbad, CA, USA), supplemented with 10% fetal calf serum, 2 mM l-glutamine and antibiotics (100 U/mL penicillin, 0.25 µg/mL streptomycin sulfate) at 37 °C in 5% CO2. The KB cell line was used as a model representing human keratinocytes.
Skin samples, obtained from donors undergoing cosmetic surgery, were treated with dispase II solution (5 mg/mL, Sigma-Aldrich, St. Louis, MO, USA) at 4 °C for 16 h, followed by separation of dermal and epidermal layers with tweezers. Next, the dermis was cut into ~1 mm2 fragments and treated with 2 mg/mL collagenase and 0.1 mg/mL DNase (Sigma-Aldrich, St. Louis, MO, USA) overnight. Liberated cells were seeded into cell culture flasks for culture. Primary human fibroblasts were grown in standard DMEM medium (Invitrogen, Carlsbad, CA, USA), supplemented with 10% fetal calf serum (Invitrogen, Carlsbad, CA, USA), 10 mM HEPES, 2 mM l-glutamine and antibiotics (100 U/mL penicillin, 0.25 µg/mL streptomycin sulfate) and 50 µg/mL uridine, with or without 20 µM l-ergothioneine (Barnet Products Corp.,Englewood Cliffs, NJ, USA), at 37 °C in 5% CO2. Confluent passages between 2 and 8 were used.

2.2. UVB Irradiation

Confluent KB cells (control and treated with 20 µM l-ergothioneine (Barnet Products Corp., Englewood Cliffs, NJ, USA)) were exposed to UVB (300 J/m2, fluorescent bulb TL12 Philips, emission peak at 313 nm) through phosphate buffered saline.

2.3. UVA Irradiation

The presence of the “common deletion” was evaluated in fibroblasts derived from 2 female donors aged 38 and 45 and from 2 male donors aged 30 and 42. Cells were grown in the presence of 50 µg/mL uridine (Sigma-Aldrich, St. Louis, MO, USA), with or without 20 µM l-ergothioneine and irradiated with 3 doses (8 J/cm2, fluorescent bulb GE F4T5/BLB, emission peak at 368 nm) of UVA per day, through phosphate buffered saline. This procedure was repeated for 4 consecutive days during 3 weeks.

2.4. Colorimetric Determination of Reduced Glutathione (GSH)

GSH level was measured using the GSH/GSSG-412 assay (OxisResearchTM, Portland, OR, USA)—colorimetric determination of reduced and oxidized glutathione. The method employs Ellmanʼs reagent (5,5'-dithiobis-2-nitrobenzoic acid—DTNB), which reacts with GSH to form a product which is spectrophotometrically detectable at 412 nm. The change in absorbance at 412 nm is a linear function of the GSH concentration in the reaction mixture [14]. The protein concentration was measured with Bradford Reagent (Sigma-Aldrich, St. Louis, MO, USA) [15]. Three independent experiments were performed. Comparisons between control and post-treatment measurements were performed using an unpaired Student’s t-test. Probability values of p < 0.05 were considered statistically significant.

2.5. “Common Deletion” (CD) PCR

Phenol-chloroform extraction of total DNA and PCR (Fermentas, Lithuania, Vilnius) were performed according to standard protocols. PCR reaction mixture, for both primer pairs, contained: F primer 2 μM; R primer 2 μM; dNTP 20 mM; Taq Buffer with (NH4)2SO4 and 20 mM MgCl2 1×; Taq polymerase 1 U; DNA 100 ng. All reactions were performed in 25 µL volume in the following conditions: the denaturation step was carried out at 94 °C for 3 min, 35 cycles of 94 °C for 30 s, 58 °C for 30 s, 72 °C for 1 min, and a final extension of 72 °C for 7 min. See Table 1 for primers used.
Table 1. PCR primers for detection of the “common deletion” in mtDNA.
Table 1. PCR primers for detection of the “common deletion” in mtDNA.
PCR primerOrientationPosition
MT1AF8224-8247
MT1CF13176-13198
MT2R13501-13477
PCR reaction with primers MT1AMT2 was carried out, amplifying a fragment 300 bp in length when the “common deletion” was present. In order to ensure that the absence of CD PCR product is caused by the absence of CD and not by an incorrect PCR reaction, PCR with primers MT1AMT2 was performed. A corresponding product 325 bp in length is obtained when the mitochondrial genome without the deletion is present and thus serves as a control for the PCR reaction. As a positive control of the PCR reaction, DNA isolated from a patient with a previously confirmed common deletion in mtDNA was used. PCR products were detected by electrophoresis on a 1.5% agarose gel with ethidium bromide against a DNA molecular-weight marker. The gel was photographed under UV transillumination. Three independent experiments were performed.

3. Results and Discussion

3.1. l-Ergothioneine Increases the Reduced Glutathione (GSH) Level

The tripeptide glutathione (GSH) is the most abundant intracellular non-protein thiol. It is present predominantly in a reduced form (GSH), which is the biologically active form. Over the years, a great deal of information has been gathered on the role of GSH in maintaining the intracellular reduction–oxidation (redox) environment including antioxidant defense via direct interaction with reactive oxygen/nitrogen species (ROS/RNS) or via activities of detoxification enzymes like GSH peroxidases and GSH-S-transferases [16]. In our study we tested the effect of l-ergothioneine on the reduced glutathione (GSH) level in the KB cell line using the GSH/GSSG-412 colorimetric assay. Our studies showed that l-ergothioneine at the 20 µM concentration (chosen according to our previous studies [17]) increased the reduced glutathione (GSH) level both in control and UVB irradiated KB cells (Table 2). Changes between GSH level in control compared with GSH level after treatment with l-ergothioneine, both in cells exposed and unexposed to UVB, were statistically significant. The UVB light was chosen for the irradiation of KB cells since it is the light of the UVB spectrum that is for the most part absorbed by the epidermis in vivo [18]. UVB may also damage epidermal cells both directly and indirectly by inducing the formation of reactive oxygen species, i.e., the superoxide anion [19]. Thus, it was deemed necessary to study the antioxidative effect of EGT on UVB irradiated epidermis.
Table 2. Quantitative determination of glutathione (GSH) level in KB cells.
Table 2. Quantitative determination of glutathione (GSH) level in KB cells.
KB cellsµmol GSH/µg protein
−UVB+UVB (300 J/m2)
control6.07 ± 0.153.03 ± 0.02
20 µM l-ergothioneine15.37 ± 0.134.65 ± 0.06
Our results are in line with numerous studies demonstrating that l-ergothioneine is an integral component of the cellular antioxidant defense system. It scavenges hydroxyl and peroxynitrite radicals as well as the superoxide anion radical and singlet oxygen. In vitro tests have also demonstrated that EGT also has strong copper chelating ability—it potentially inhibits tyrosinase activity [20,21,22].
Moreover, in vitro tests have demonstrated that in cultured fibroblasts EGT suppressed the tumor necrosis factor α (TNF α) up-regulation induced by UVB irradiation. In addition in fibroblasts exposed to UVA, EGT suppressed the expression of matrix metalloproteinase 1 (MMP 1) protein [23]. EGT also inhibited nuclear factor kβ (NF kβ) activation and limited the transcriptional activation of the gene for interleukin 8 (IL-8)—a chemotaxin which might account for neutrophil recruitment [24].
It has been demonstrated that EGT is a more powerful antioxidant than either coenzyme Q(10) or idebenone due to its relatively greater efficiency in directly scavenging free radicals and in protecting cells from UV-induced ROS [25].
Recently, a high specific transporter for EGT (ETT) was identified in mammalian tissues, which explains the high tissue levels of EGT and implies a physiological role. Depletion of ETT leads to augmented oxidative stress and cell death. ETT is highly concentrated in the plasma membrane and mitochondria [11].

3.2. l-Rrgothioneine Shows Protective Properties against the Induction of a Photoaging-Associated mtDNA “Common Deletion”

One of the best described mt deletions, the 4977 bp “common deletion”, is known to be involved in photoaging of the skin. Intraindividual comparison studies have revealed that the “common deletion” is increased up to 10-fold in photoaged skin, as compared with sun-protected skin of the same individuals [7]. The objective of our study was to evaluate the effect of l-ergothioneine on the occurrence of mtDNA “common deletion” in UV-irradiated human primary fibroblasts obtained from various donors. For the experiments on dermal cells only UVA irradiation was performed, since the great majority of UVB rays is absorbed by the epidermis and hence never reaches the dermal level [18]. UVA is known to cause mainly indirect damage to cellular structures and nucleic acids by inducing the formation of radical oxygen and nitrogen species but may also be responsible for single- and double-strands breaks in DNA [19]. Thus, exposure to UVA may be one of the main causes of mtDNA mutations including mtDNA deletions [26]. In our experiments, in fibroblasts which were not exposed to UVA we did not observe the “common deletion” after DNA isolation nor during 3 weeks of culture (Figure 2, lanes 9, 11 and 13). When we incubated fibroblasts with l-ergothioneine we also observed no “common deletion” PCR product (Figure 3, lanes 9, 11 and 13). To summarize this part of our study: first of all, cultured fibroblasts isolated from various donors did not initially show the “common deletion”. Secondly, l-ergothioneine, itself, had no influence on the presence of the “common deletion”.
Figure 2. Representative PCR analysis of the presence of the “common deletion” in a culture of human fibroblasts incubated with and without UVA exposure, without the presence of l-ergothioneine. M, molecular weight marker; C, control PCR reaction, confirming the presence of mtDNA; 1, fibroblasts after 1 week with UVA exposure; 3, fibroblasts after 2 weeks with UVA exposure; 5, fibroblasts after 3 weeks with UVA exposure; 7, positive control—DNA from a patient with a previously confirmed presence of “common deletion”; 9, fibroblasts after 1 week without UVA exposure; 11, fibroblasts after 2 weeks without UVA exposure; 13 fibroblasts after 3 weeks without UVA exposure.
Figure 2. Representative PCR analysis of the presence of the “common deletion” in a culture of human fibroblasts incubated with and without UVA exposure, without the presence of l-ergothioneine. M, molecular weight marker; C, control PCR reaction, confirming the presence of mtDNA; 1, fibroblasts after 1 week with UVA exposure; 3, fibroblasts after 2 weeks with UVA exposure; 5, fibroblasts after 3 weeks with UVA exposure; 7, positive control—DNA from a patient with a previously confirmed presence of “common deletion”; 9, fibroblasts after 1 week without UVA exposure; 11, fibroblasts after 2 weeks without UVA exposure; 13 fibroblasts after 3 weeks without UVA exposure.
Cosmetics 01 00051 g002
We were able to induce the “common deletion” using repetitive UVA irradiation in cultured human fibroblasts derived from two donors (Figure 2, lanes 1, 3 and 5) suggesting that there is an individual susceptibility to the induction of CD, at least in our in vitro model. Due to the fact that our “common deletion” analysis was performed on fibroblasts isolated from four donors, this requires further studies. When fibroblasts were irradiated and co-incubated with 20 µM l-ergothioneine we did not observe the “common deletion” even after 3 weeks with UVA exposure, suggesting that l-ergothioneine may prevent the formation of this particular damage in mtDNA (Figure 3, lanes 1, 3 and 5). Our results are in accordance with the previous studies where repetitive exposure of keratinocytes, fibroblasts or human skin to UVA at physiological doses was found to induce mutations of mtDNA [7,27,28,29]. Interestingly, it has been shown that in fibroblasts the level of CD is decreasing with prolonged culture, which can be counteracted with uridine supplementation of culture media [6,7,30]. For this reason, uridine supplementation was employed during all CD analyses in this study.
Figure 3. Representative PCR analysis of the presence of the “common deletion” in a culture of human fibroblasts incubated with and without UVA exposure, in the presence of 20 µM l-ergothioneine. M, molecular weight marker; C, control PCR reaction, confirming the presence of mtDNA; 1, fibroblasts after 1 week with UVA exposure; 3, fibroblasts after 2 weeks with UVA exposure; 5, fibroblasts after 3 weeks with UVA exposure; 7, positive control—DNA from a patient with a previously confirmed presence of “common deletion”; 9, fibroblasts after 1 week without UVA exposure; 11, fibroblasts after 2 weeks without UVA exposure; 13, fibroblasts after 3 weeks without UVA exposure.
Figure 3. Representative PCR analysis of the presence of the “common deletion” in a culture of human fibroblasts incubated with and without UVA exposure, in the presence of 20 µM l-ergothioneine. M, molecular weight marker; C, control PCR reaction, confirming the presence of mtDNA; 1, fibroblasts after 1 week with UVA exposure; 3, fibroblasts after 2 weeks with UVA exposure; 5, fibroblasts after 3 weeks with UVA exposure; 7, positive control—DNA from a patient with a previously confirmed presence of “common deletion”; 9, fibroblasts after 1 week without UVA exposure; 11, fibroblasts after 2 weeks without UVA exposure; 13, fibroblasts after 3 weeks without UVA exposure.
Cosmetics 01 00051 g003
Protection against the induction of a photoaging-associated mtDNA mutation has been also previously shown for two other widely applied cosmetic actives—β-carotene and genistein [31,32].
Our results demonstrated that l-ergothioneine may protect skin cells against some UV-induced damage; in particular against the occurrence of mitDNA “common deletion”. Further studies are required to assess the full-spectrum of l-ergothioneine’s protective activity. We conclude that l-ergothioneine, as an active compound of cosmetic products, shows considerable promise as an effective agent against the aging process. On the other hand, we have shown that in cosmetology, the detection of mtDNA deletions could be a useful tool to assess the effect of active ingredients on UV-irradiated human skin cells.

4. Conclusions

Aging of human skin has been the subject of a profound interest for cosmetic industry which attempts to counteract this process. In our study we tested l-ergothioneine, one of the antioxidants used in cosmetology, and we found that l-ergothioneine enhanced the level of reduced glutathione and protected against the induction of a photoaging-associated mtDNA “common deletion”. l-Ergothioneine might be involved in the protection of mtDNA from ROS generated in the course of electron transport.
In view of these results l-ergothioneine could act as an effective skin care and anti-photo-aging ingredient. On the other hand, we have shown that in cosmetology, the detection of mtDNA deletions could be a useful tool to assess the effect of active ingredients on UV-irradiated human skin cells.

Acknowledgments

Aleksandra Solyga-Zurek was supported by Ministry of Science and Higher Education project grant ref N N302 119735.

Author Contributions

Study conception and design: Karolina Bazela, Aleksandra Solyga-Zurek, Renata Debowska, Katarzyna Rogiewicz, Irena Eris; Acquisition of data: Karolina Bazela, Aleksandra Solyga-Zurek; Analysis and interpretation of data: Karolina Bazela, Aleksandra Solyga-Zurek, Renata Debowska; Drafting of manuscript: Karolina Bazela, Aleksandra Solyga-Zurek; Critical revision: Ewa Bartnik.

Conflicts of Interest

The authors declare no conflict of interest.

References

  1. Glichrest, B.A. Photoaging. J. Invest. Dermatol. 2013, 133, E2–E6. [Google Scholar] [CrossRef]
  2. Bickers, D.R.; Athar, M. Oxidative stress in the pathogenesis of skin disease. J. Invest. Dermatol. 2006, 126, 2565–2575. [Google Scholar]
  3. Puizina-Ivic, N. Skin aging. Acta Derm. 2008, 17, 47–54. [Google Scholar]
  4. Tońska, K.; Sołyga, A.; Bartnik, E. Mitochondria and aging: Innocent bystanders or guilty parties? J. Appl. Genet. 2009, 50, 55–62. [Google Scholar] [CrossRef]
  5. Alexeyev, M.F.; LeDoux, S.P.; Wilson, G.L. Mitochondrial DNA and aging. Clin. Sci. 2004, 107, 355–364. [Google Scholar] [CrossRef]
  6. Krishnan, K.J.; Greaves, L.C.; Reeve, A.K.; Turnbull, D. The ageing mitochondrial genome. Nucleic Acids Res. 2007, 35, 7399–7405. [Google Scholar] [CrossRef]
  7. Birch-Machin, M.A.; Tindall, M.; Turner, R.; Haldane, F.; Rees, J.L. Mitochondrial DNA deletions in human skin reflect photo rather than chronologic aging. J. Invest. Dermatol. 1998, 110, 149–152. [Google Scholar] [CrossRef]
  8. Yang, J.H.; Lee, H.C.; Lin, K.J.; Wei, Y.H. A specific 4977-bp deletion of mitochondrial DNA in human ageing skin. Arch. Dermatol. Res. 1994, 286, 386–390. [Google Scholar] [CrossRef]
  9. Yang, J.H.; Lee, H.C.; Wei, Y.H. Photoageing-associated mitochondrial DNA length mutations in human skin. Arch. Dermatol. Res. 1995, 287, 641–648. [Google Scholar] [CrossRef]
  10. Ray, A.J.; Turner, R.; Nikaido, O.; Rees, J.L.; Birch-Machin, M.A. The spectrum of mitochondrial DNA deletions is a ubiquitous marker of ultraviolet radiation exposure in human skin. J. Invest. Dermatol. 2000, 115, 674–679. [Google Scholar] [CrossRef]
  11. Paul, B.D.; Snyder, S.H. The unusual amino acid l-ergothioneine is a physiologic cytoprotectant. Cell Death Differ. 2010, 17, 1134–1140. [Google Scholar] [CrossRef]
  12. Cheah, I.K.; Halliwell, B. Ergothioneine; antioxidant potential, physiological function and role in disease. Biochim. Biophys. Acta 2012, 1822, 784–793. [Google Scholar]
  13. Markova, N.G.; Karaman-Jurukovska, N.; Dong, K.K.; Damaghi, N.; Smiles, K.A.; Yarosh, D.B. Skin cells and tissue are capable of using l-ergothioneine as an integral component of their antioxidant defense system. Free Radic. Biol. Med. 2009, 46, 1168–1176. [Google Scholar] [CrossRef]
  14. Tietze, F. Enzymic method for quantitative determination of nanogram amounts of total and oxidized glutathione: Applications to mammalian blood and other tissues. Anal. Biochem. 1969, 27, 502–522. [Google Scholar] [CrossRef]
  15. Bradford, M.M. Rapid and sensitive method for quantitation of microgram quantities of protein utilising principle of protein dye binding. Anal. Biochem. 1976, 72, 248–254. [Google Scholar] [CrossRef]
  16. Dickinson, D.A.; Forman, H.J. Cellular glutathione and thiols metabolism. Biochem. Pharmacol. 2002, 64, 1019–1026. [Google Scholar] [CrossRef]
  17. Bazela, K.; Debowska, R.; Zielinska, A.; Jastrzebska-Brucka, E.; Kawczuga, D.; Eris, I. Protective role of Antioxidant Complex (AC) on human skin cells. In Proceedings of the 3rd International Conference on Oxidative Stress in Skin Medicine and Biology, Andros, Greece, 21–24 September 2006.
  18. Kligman, L.H. Photoaging. Manifestations, prevention, and treatment. Dermatol. Clin. 1986, 4, 517–528. [Google Scholar]
  19. Ichihashi, M.; Ueda, M.; Budiyanto, A.; Bito, T.; Oka, M.; Fukunaga, M.; Tsuru, K.; Horikawa, T. UV-induced skin damage. Toxicology 2003, 189, 21–39. [Google Scholar] [CrossRef]
  20. Aruoma, O.I.; Spencer, J.P.; Mahmood, N. Protection against oxidative damage and cell death by the natural antioxidant ergothioneine. Food Chem. Toxicol. 1999, 37, 1043–1053. [Google Scholar] [CrossRef]
  21. Laurenza, I.; Colognato, R.; Migliore, L.; Del Prato, S.; Benzi, L. Modulation of palmitic acid-induced cell death by ergothioneine: Evidence of an anti-inflammatory action. Biofactors 2008, 33, 237–247. [Google Scholar] [CrossRef]
  22. Franzoni, F.; Colognato, R.; Galetta, F.; Laurenza, I.; Barsotti, M.; Di Stefano, R.; Bocchetti, R.; Regoli, F.; Carpi, A.; Balbarini, A.; et al. An in vitro study on the free radical scavenging capacity of ergothioneine: Comparison with reduced glutathione, uric acid and trolox. Biomed. Pharmacother. 2006, 60, 453–457. [Google Scholar] [CrossRef]
  23. Obayashi, K.; Kurihara, K.; Okano, Y.; Masaki, H.; Yarosh, D.B. l-Ergothioneine scavenges superoxide and singlet oxygen and suppresses TNF-α and MMP-1 expression in UV-irradiated human dermal fibroblasts. J. Cosmet. Sci. 2005, 56, 17–27. [Google Scholar]
  24. Rahman, I.; Gilmour, P.S.; Jimenez, L.A.; Biswas, S.K.; Antonicelli, F.; Aruoma, O.I. Ergothioneine inhibits oxidative stress- and TNF-α-induced NF-κB activation and interleukin-8 release in alveolar epithelial cells. Biochem. Biophys. Res. Commun. 2003, 302, 860–864. [Google Scholar] [CrossRef]
  25. Dong, K.K.; Damaghi, N.; Kibitel, J.; Canning, M.T.; Smiles, K.A.; Yarosh, D.B. A comparison of the relative antioxidant potency of l-ergothioneine and idebenone. J. Cosmet. Dermatol. 2007, 6, 183–188. [Google Scholar] [CrossRef]
  26. Krishnan, K.J.; Reeve, A.K.; Samuels, D.C.; Chinnery, P.F.; Blackwood, J.K.; Taylor, R.W.; Wanrooij, S.; Spelbrink, J.N.; Lightowlers, R.N.; Turnbull, D.M. What causes mitochondrial DNA deletions in human cells? Nat. Genet. 2008, 40, 275–279. [Google Scholar] [CrossRef]
  27. Berneburg, M.; Plettenberg, H.; Medve-König, K.; Pfahlberg, A.; Gers-Barlag, H.; Gefeller, O.; Krutmann, J. Induction of the photoaging-associated mitochondrial common deletion in vivo in normal human skin. J. Invest. Dermatol. 2004, 122, 1277–1283. [Google Scholar] [CrossRef]
  28. Berneburg, M.; Gattermann, N.; Stege, H.; Grewe, M.; Vogelsang, K.; Ruzicka, T.; Krutmann, J. Chronically ultraviolet-exposed human skin shows a higher mutation frequency of mitochondrial DNA as compared to unexposed skin and the hematopoietic system. Photochem. Photobiol. 1997, 66, 271–275. [Google Scholar] [CrossRef]
  29. Koch, H.; Wittern, K.P.; Bergemann, J. In human keratinocytes the common deletion reflects donor variabilities rather than chronologic aging and can be induced by ultraviolet A radiation. J. Invest. Dermatol. 2001, 117, 892–897. [Google Scholar] [CrossRef]
  30. Bourgeron, T.; Chretien, D.; Rötig, A.; Munnich, A.; Rustin, P. Fate and expression of the deleted mitochondrial DNA differ between human heteroplasmic skin fibroblast and Epstein-Barr virus-transformed lymphocyte cultures. J. Biol. Chem. 1993, 26, 19369–19376. [Google Scholar]
  31. Wang, Y.N.; Wu, W.; Chen, H.C.; Fang, H. Genistein protects against UVB-induced senescence-like characteristics in human dermal fibroblast by p66Shc down-regulation. J. Dermatol. Sci. 2010, 58, 19–27. [Google Scholar] [CrossRef]
  32. Eicker, J.; Kürten, V.; Wild, S.; Riss, G.; Goralczyk, R.; Krutmann, J.; Berneburg, M. Betacarotene supplementation protects from photoaging-associated mitochondrial DNA mutation. Photochem. Photobiol. Sci. 2003, 2, 655–659. [Google Scholar] [CrossRef]

Share and Cite

MDPI and ACS Style

Bazela, K.; Solyga-Zurek, A.; Debowska, R.; Rogiewicz, K.; Bartnik, E.; Eris, I. l-Ergothioneine Protects Skin Cells against UV-Induced Damage—A Preliminary Study. Cosmetics 2014, 1, 51-60. https://doi.org/10.3390/cosmetics1010051

AMA Style

Bazela K, Solyga-Zurek A, Debowska R, Rogiewicz K, Bartnik E, Eris I. l-Ergothioneine Protects Skin Cells against UV-Induced Damage—A Preliminary Study. Cosmetics. 2014; 1(1):51-60. https://doi.org/10.3390/cosmetics1010051

Chicago/Turabian Style

Bazela, Karolina, Aleksandra Solyga-Zurek, Renata Debowska, Katarzyna Rogiewicz, Ewa Bartnik, and Irena Eris. 2014. "l-Ergothioneine Protects Skin Cells against UV-Induced Damage—A Preliminary Study" Cosmetics 1, no. 1: 51-60. https://doi.org/10.3390/cosmetics1010051

Article Metrics

Back to TopTop