Users Online: 917

Home Print this page Email this page Small font sizeDefault font sizeIncrease font size

Home | About us | Editorial board | Search | Ahead of print | Current issue | Archives | Submit article | Instructions | Subscribe | Contacts | Login 
     

   Table of Contents      
ORIGINAL ARTICLE
Year : 2018  |  Volume : 8  |  Issue : 2  |  Page : 41-46

Morin Inhibiting Photocarcinogenesis by Targeting Ultraviolet-B-Induced Oxidative Stress and Inflammatory Cytokines Expression in Swiss Albino Mice


1 Department of Biochemistry, Vinayaka Mission’s Kirupananda Variyar Medical College and Hospitals, Salem, Tamil Nadu, India
2 Department of Biotechnology, Vinayaka Mission’s Kirupanada Variyar Engineering College, Vinayaka Mission’s Research Foundation (Deemed to be University) Salem, Tamil Nadu, India

Date of Web Publication26-Apr-2018

Correspondence Address:
Sridevi Muruhan
Vinayaka Mission’s Kirupanada Variyar Engineering College, Vinayaka Mission’s Research Foundation (Deemed to be University), Periyaseeragapadi – 636 301, Salem, Tamil Nadu
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijnpnd.ijnpnd_5_18

Rights and Permissions
   Abstract 

Aim: To evaluate the effect of morin in ultraviolet-B (UV-B)-induced oxidative stress and inflammatory cytokines expression in the skin of Swiss albino mice. Materials and Methods: Swiss albino mice were divided into six treatment groups, and each group consisted of eight mice based on their exposure to UV-B radiation (180 mJ/cm2) and their respective treatment with morin (15 mg/kg). Morin was administered both intraperitoneally and topically thrice in a week for 30 weeks before UV-B exposure. After the treatment period, the mice were sacrificed, and the effect of morin on UV-B radiation-induced lipid peroxidation and enzymatic and nonenzymatic antioxidant levels was estimated on skin tissues spectrophotometrically. Western blot analysis was used to estimate the inflammatory cytokines. Results: This study revealed that the intraperitoneal and topical administration of morin significantly lowered the incidence of UV-B-induced tumor size in the skin of Swiss albino mice. Further, morin significantly reduced (P < 0.05) lipid peroxidation and increased the antioxidant levels in Swiss albino mice. It was also observed that morin reduced the expression of tumor necrosis factor-α and interleukin-6. Conclusion: Morin has a stimulative effect on endogenous antioxidant defense mechanisms. It can prevent the photo damage of macromolecules such as lipids and the oxidation of proteins, thereby reducing oxidative stress and inflammation.

Keywords: Antioxidants, lipid peroxidation, morin, UV-B radiation


How to cite this article:
Chandrakesan A, Muruhan S, Sayanam RR. Morin Inhibiting Photocarcinogenesis by Targeting Ultraviolet-B-Induced Oxidative Stress and Inflammatory Cytokines Expression in Swiss Albino Mice. Int J Nutr Pharmacol Neurol Dis 2018;8:41-6

How to cite this URL:
Chandrakesan A, Muruhan S, Sayanam RR. Morin Inhibiting Photocarcinogenesis by Targeting Ultraviolet-B-Induced Oxidative Stress and Inflammatory Cytokines Expression in Swiss Albino Mice. Int J Nutr Pharmacol Neurol Dis [serial online] 2018 [cited 2018 Oct 20];8:41-6. Available from: http://www.ijnpnd.com/text.asp?2018/8/2/41/231271


   Introduction Top


Clinical and epidemiological studies designate that ultraviolet (UV) radiation, mainly ultraviolet-B (UV-B) (290–320 nm), promotes the development of photocarcinogenesis.[1] Solar UV radiation exerts many effects on the skin including oxidative stress, inflammatory responses, and cell signaling pathway alterations, which lead to the development of skin cancer.[2] The skin possesses antioxidant substances to deal with oxidative stress. UV-B radiation exposure devastates the cutaneous antioxidants and leads to oxidative damage.[3] Dramatic rise in the lipid peroxidation products such as thiobarbituric acid (TBARS) and lipid hydroperoxides (LPH) occurs during chronic UV-B exposure.[4] The important targets of UV-B-induced reactive oxygen species (ROS) are stratum corneum lipids, yielding reactive squalene peroxides as byproducts[5] and hydroperoxy cholesterol species that may play a function in photocarcinogenesis and photosensitivity disorders.[6] Inflammatory responses that activated gene expression and cell proliferation were evoked by increased membrane lipid peroxidation.[7]

Enzymatic antioxidants such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) and nonenzymatic antioxidants such as glutathione (GSH) and vitamins E and C work synergistically and neutralize the radiation-induced ROS.[8] However, exposure to excessive amounts of UV-B light overcomes these antioxidant defense mechanisms and depletes cellular antioxidant status. The disproportion among the oxidants and antioxidants shifts the cellular redox-sensitive pathways. There are a number of evidences showing the decreased enzymatic antioxidant activities during UV-B exposure.[9]

In the skin, there is a conventional link between tissue damage, inflammation, and cancer development. A chronic inflammation of the skin resulted in the long-term production and accumulation of inflammatory factors associated with tumor development and progression.[10] Inflammatory response triggers a series of events that lead to the transmigration of leukocytes to the injured site. Activated leukocytes cause an abundant production of ROS leading to peroxidative impairment of the skin membranes and contributing to the exacerbation of lesions. Furthermore, these immune cells release growth factors, chemokines, and proinflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β, and IL-17, which interact as a network in the pathogenesis of various skin diseases.[11]

Treatment for skin cancer is tedious and causes various side effects. Therefore, preventive steps are necessary. Nowadays, herbal medicines are receiving much importance because of their effectiveness and negligible side effects. A variety of flavonoids and polyphenols derived from the plant have been reported to show antioxidant, anti-inflammatory, antimicrobial, antidiabetic, and anticancer effects.[12],[13],[14] Morin is a bioflavonoid largely isolated from the members of the Moraceae family. Morin present in several fruits and vegetables like osage orange, old fustic, guava leaves, apple, onion and in several beverages such as red wine, tea.[15] Morin exhibits several pharmacological properties such as anticancer, anti-inflammatory, and antioxidant.[16],[17],[18],[19] It has been proven that morin possess very strong inhibitory effect on lipid peroxidation in mouse liver homogenate.[20] It also showed a possible chemopreventive property against some cancers.[21] However, there are no studies on the role of morin in UV-B-induced antioxidant, lipid peroxidation, and inflammatory cytokines activities in an animal model. This study was undertaken to evaluate the same.


   Materials and Methods Top


Animals

The in-vivo experiments were conducted using male Swiss albino mice as an experimental model. The experiments were approved by (Ethical Clearance No. 244) the institutional animal ethical committee of K.M. College of Pharmacy, Madurai, Tamil Nadu, India (certified by CPCSEA, Reg. No. 161/02/CPCSEA). Normal healthy Swiss albino mouse weighing 17–20 g were chosen for this study. Thereafter, the mice were housed in well-ventilated rooms (temperature 65–85°F and humidity 60–70%) with a 13-h light/dark cycle. The mice were maintained on a standard laboratory diet of food and water during the experimental period.

Chemicals and reagents

Morin hydrate, sodium pyrophosphate buffer, phenazine methyl sulphate, dichromate acetic acid, sodium azide, two-dipyridyl solution, GSH reductase, hydrogen peroxide (H2O2), reduced nicotinamide adenine dinucleotide, reduced nicotinamide adenine dinucleotide phosphate, nitro blue tetrazolium, reduced GSH, 2-thiobarbituric acid, and citric acid were purchased from Sigma Chemical Company (St. Louis, MO, USA). All other reagents used were of analytical grade.

Preparation of morin and mode of administration

Morin (15 mg/kg body weight) was dissolved in 0.5% of dimethyl sulfoxide (DMSO) and administered intraperitoneally and topically at a volume of 0.2 ml/kg body weight.

Photocarcinogenesis protocol

Swiss albino mice were categorized into six treatment groups. Each group consisted of eight mice. The mice in Group 1 served as vehicle controls and were given 0.5% DMSO. The animals in Groups 2 and 5 were treated with morin (15 mg/kg body weight) intraperitoneally for 14 days. The animals in Groups 3 and 6 were treated with morin topically (abdomen and dorsal skin) for 14 days. After an interval of 14–31 days, morin treatment was given again thrice a week. Animals in Group 4 were not exposed to UV-B radiation for the first 14 days. Animals belonging to Groups 4–6 were exposed to UV-B irradiation (180 mJ/cm2/day) daily from the 15th to the 24th day. For Groups 5 and 6, morin treatment was performed 1 h before the exposure to UV-B irradiation. The mice were again UV-B irradiated (180 mJ/cm2) thrice in a week after a break of 25–31 days until the end of the experiments.

Ultraviolet-B exposure procedure and evaluation of tumor growth for Swiss albino mice

The skin in the dorsal portions of the Swiss albino mice was shaved using an electric clipper (Oster A2) minimum 2 days prior to the treatment with hair removing cream. The cream was cleaned with warm water and dipped in cotton sorbs. The mice to be used for the experiment were confirmed by ensuring that their skin had no signs of hair regrowth. The dorsal skin was exposed to UV-B radiation with a philips TL40W/12 RS lamp emitting 312 . The UV-B lamp was mounted 20 cm above the table where the mice were placed on. The photocarcinogenesis treatment procedure was performed thrice a week for 30 weeks (UV-B dose was 180 mJ/cm2). The appearance and development of tumors were checked weekly up to the end of the experiment.[22] Growths that were >1 mm in diameter and that persisted for at least 2 weeks were defined as tumors and recorded.

Skin tissue homogenization protocol

The mice were sacrificed by decapitation, and the dorsal skins were removed under anesthesia at various time points. Subcutaneous fat was removed, and the skins were stored at −80°C before use. Whole cell lysates were prepared in a radioimmunoprecipitation assay lysis buffer (120 mM NaCl, 40 mM Tris pH 8.0, 0.1% NP40) containing 1% β-mercaptoethanol, 0.1 M Na3VO4, 0.5 M NaF, and protease inhibitor cocktail and then centrifuged at 13,000×g for 15 min. Supernatants were collected, and they were used as total cell lysates.[23]

Estimation of lipid peroxidation and antioxidant status

The levels of TBARS in the skin tissue were assayed by the methods of Niehaus and Samuelsson.[24] The LPH were evaluated by the method of Jiang et al.[25] The activities of enzymatic antioxidants such as SOD, CAT, and GPx were assayed in the skin tissues by the method of Kakkar et al.; Sinha; and Rotruck et al., respectively.[26],[27],[28] The levels of nonenzymatic antioxidants such as GSH, vitamin C, and vitamin E were estimated on the skin tissues by the method of Ellman; Roe and Kuether; and Baker et al., respectively.[29],[30],[31]

Western blot analysis

An immunoblot (Western blot) analysis by the method of Towbin et al. was performed for TNF-α and IL-6 protein expressions in the skin tissue of mice treated with morin and UV-B irradiation.[32] The results were normalized to β-actin gene expression. Then the samples were subjected to sodium dodecyl sulfate polyacrylamide gel electrophoresis for the estimation of protein and were blotted on polyvinylidene fluoride (PVDF) membrane. The primary antibody was added to that and allowed to bind to the protein. Then, the PVDF membranes were washed with Tris-buffered saline with Tween 20 thrice with 10 min interval, and the protein expressions were detected by chemiluminescence substrate (LI-COR, USA). The images were attained by Image Studio software (LI-COR, USA).

Statistical analysis

All the values were expressed as means of six (n = 6) determination. The data were statistically analyzed by the one-way analysis of variance method using the Statistical Package for the Social Sciences (SPSS) (SPSS Inc., Chicago, IL, United States) statistical software, and the group means were compared to Duncan’s multiple range test (DMRT). If the P value was <0.05, it was considered as statistically significant.


   Results Top


Effect of morin on lipid peroxidation products

[Figure 1] shows the effect of morin on TBARS and LPH levels in morin-treated and UV-B-exposed Swiss albino mice. UV-B-exposed animals showed elevated level of TBARS and LPH in the mice skin homogenate. The intraperitoneal and topical application of morin prior to each UV-B exposure resulted in significant reduction of TBARS and LPH levels.
Figure 1: Effect of morin on lipid peroxidation levels in ultraviolet-B-induced tumor-bearing skin tissue homogenate. Values are given as the mean ± standard deviation of six experiments in each group. Values not sharing a common superscript differ significantly at P < 0.05. TBARS = thiobarbituric acid; LPH = lipid hydroperoxides; DMRT = Duncan’s multiple range test

Click here to view


Preventive effect of morin on enzymatic antioxidant depletion

The data in this study demonstrated that UV-B irradiation resulted in a significant depletion of SOD, CAT, and GPx activities in the mice skin homogenate [Figure 2]. Intraperitoneal and topical treatment with morin significantly prevented the UV-B-induced depletion of enzymatic antioxidant activities and brought back the situation toward normalcy.
Figure 2: Effect of morin on enzymatic antioxidant activities in ultraviolet-B-induced tumor-bearing skin tissue homogenate. Values are given as the mean ± standard deviation of six experiments in each group. Values not sharing a common superscript differ significantly at P < 0.05. SOD = superoxide dismutase; CAT = catalase; GPx = glutathione peroxidase; DMRT = Duncan’s multiple range test

Click here to view


Preventive effect of morin on nonenzymatic antioxidant depletion

UV-B irradiation resulted in the reduction of intracellular GSH, vitamin C, and vitamin E levels in the mice skin homogenate [Figure 3]. Both, the intraperitoneal and topical application of morin, significantly restored the UV-B irradiation-induced depletion of nonenzymatic antioxidant levels.
Figure 3: Effect of morin on enzymatic antioxidant activities in ultraviolet-B-induced tumor-bearing skin tissue homogenate. Values are given as the mean ± standard deviation of six experiments in each group. Values not sharing a common superscript differ significantly at P < 0.05. GSH = glutathione; Vit-C = vitamin C; Vit-E = vitamin E; DMRT = Duncan’s multiple range test

Click here to view


Preventive effect of morin on inflammatory cytokines tumor necrosis factor-α and interleukin-6 expression in the skin of ultraviolet-B-induced tumor-bearing mice

UV-B-exposure resulted in the induction of inflammatory cytokine TNF-α and IL-6 in the skin of Swiss albino mice [Figure 4]. The immunoblots revealed that UV-B exposure increased the expression of IL-6 and TNF-α in the skin tissue of mice when compared to the nonirradiated skin of mice. Morin application 1 h before UV-B exposure decreased the expressions of IL-6 and TNF-α proteins when compared to the UV-B-irradiated skin of mice.
Figure 4: (a) Western blot analysis of IL-1 and TNF-α expression. (b) Histograms of densitometric analysis represent the mean intensity of IL-1 and TNF-α expression. Values are given as the mean ± SD of six experiments in each group. Values not sharing a common superscript differ significantly at P < 0.05 (DMRT)

Click here to view



   Discussion Top


UV radiation, specifically UV-B (280–320 nm) promotes skin cancer development by mutagenic, immunosuppressive, and oxidative stress inducing mechanisms; however, certain antioxidants may neutralize and prevent UV-B-induced photodamage.[33] Polyphenols and flavonoids are widely spread in plants. The flavonoids constitute a large group of compounds containing a number of phenolic hydroxyl groups attached to ring structures, and it possesses significant antioxidant activity.[34] A polyphenol, morin is known to be used as an antioxidant; it acts as a broad-spectrum antibiotic and is also nontoxic.[35]

Oxidative stress plays an important role in UV-B-induced skin carcinogenesis.[36] ROS play a main role in the UV-B-induced depletion of antioxidants.[37] UV-B radiation-induced ROS react with unsaturated fatty acids, proteins, and deoxyribo nucleic acid (DNA) that could result in the breakdown of lipid peroxides, protein–protein cross-links, and DNA strand, all of which can start radical chain reactions and finally enhance oxidative damage.[38] An increased level of lipid peroxidation products including TBARS and LPH in the UV-B-irradiated tumor-bearing skin is probably leads to overproduction of ROS. The intraperitoneal and topical application of morin diminished the lipid peroxidation status in UV-B-exposed skin tissues. This reduction may be due to the free radical scavenging property of the morin, which acts as an antilipoperoxidative agent.[39]

The epidermis layer of the skin contains antioxidant defenses including the enzymes SOD, CAT, and GPx, which remove ROS from the skin. Free radical scavengers such as vitamins C and E, carotenoids, and GSH are also present in the skin to reduce the damaging effects of ROS.[40] The most important mechanism played by SOD is that it helps in transforming ROS and nitrogen species into stable compounds, thereby protecting cells from UV-B damage.[41] CAT and GPx catalyses the conversion of H2O2 into H2O and molecular O2, thus decreasing the damaging effects of H2O2.[42],[43] The intraperitoneal and topical application of morin showed good improvement in the antioxidants status of UV-B-exposed skin tissues. Morin has been proven for its efficient protection of the skin against UVR exposure by elevating the endogenous CAT activity.[44]

UV-B radiation-generated ROS directly causes the depletion of the cellular antioxidant defense system. The intraperitoneal and topical application of morin completely restored the UV-B irradiation-induced depletion of nonenzymatic antioxidants such as GSH, vitamin E, and vitamin C. An earlier study reported that ferulic acid, a phenol, protects the skin form solar-stimulated sunburn cell formation and erythema when given along with α-tocopherol and ascorbic acid.[45] Another study showed that the topical application of sesamol, a polyphenolic compound, completely prevented the UV-B irradiation-induced depletion of GSH, vitamin E, and vitamin C levels,[46] which supports our present work.

Lee et al. examined the protective ability of morin in UV-B-irradiated human keratinocyte stem cells, thereby proving that morin attenuates the secretion of cytokines TNF-α and IL-6.[47] Another study revealed that ferulic acid possessed anticarcinogenic property. It acts against UV-B-induced epidermic tumor development by blocking the relevant cytokine secretion (TNF-α and IL-6) on human keratinocyte cells (HaCaT cells).[48] Thus, from this study, it can be acknowledged that morin decreases the expression of TNF-α and IL-6 in UV-B-irradiated skin of mice.


   Conclusion Top


We suggest that morin seizes photochemopreventive activity through the stimulation of endogenous antioxidant defense mechanisms and the prevention of photodamage to macromolecules such as lipids and the oxidation of proteins. This leads to the reduction in oxidative stress and provides protection against the depletion of the endogenous antioxidant system. The parameters of in-vivo anticancer evaluation and gene expression inhibition showed an enhanced anticancer potential of morin.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Ananthaswamy HN, Pierceall WE. Molecular mechanisms of ultraviolet radiation carcinogenesis. Photochem Photobiol 1990;52:1119-36.  Back to cited text no. 1
[PUBMED]    
2.
Katiyar SK, Matsui MS, Mukhtar H. Kinetics of UV light-induced cyclobutane pyrimidine dimers in human skin in vivo: An immunohistochemical analysis of both epidermis and dermis. Photochem Photobiol 2000;72:788-93.  Back to cited text no. 2
[PUBMED]    
3.
Sander CS, Chang H, Hamm F, Elsner P, Thiele JJ. Role of oxidative stress and the antioxidant network in cutaneous carcinogenesis. Int J Dermatol 2004;43:326-35.  Back to cited text no. 3
[PUBMED]    
4.
Prasad NR, Ramachandran S, Pugalendi KV, Menon VP. Ferulic acid inhibits UV-B induced oxidative stress in human lymphocytes. Nutr Res 2007;27:559-64.  Back to cited text no. 4
    
5.
Auffray B. Protection against singlet oxygen, the main actor of sebum squalene peroxidation during sun exposure, using commiphora myrrha essential oil. Int J Cosmet Sci 2007;29:23-9.  Back to cited text no. 5
[PUBMED]    
6.
Korytowski W, Schmitt JC, Girotti AW. Surprising inability of singlet oxygen-generated 6-hydroperoxycholesterol to induce damaging free radical lipid peroxidation in cell membranes. Photochem Photobiol 2010;86:747-51.  Back to cited text no. 6
[PUBMED]    
7.
Barrera G. Oxidative stress and lipid peroxidation products in cancer progression and therapy. ISRN Oncol 2012;2012:137289.  Back to cited text no. 7
[PUBMED]    
8.
Pinnell SR. Cutaneous photodamage, oxidative stress, and topical antioxidant protection. J Am Acad Dermatol 2003;48:1-22.  Back to cited text no. 8
[PUBMED]    
9.
Tomaino A, Cristani M, Cimino F, Speciale A, Trombetta D, Bonina F et al. In vitro protective effect of a Jacquez grapes wine extract on UVB-induced skin damage. Toxicol In Vitro 2006;20:1395-402.  Back to cited text no. 9
    
10.
Neagu M, Constantin C, Dumitrascu GR, Lupu AR, Caruntu C, Boda D et al. Inflammation markers in cutaneous melanoma-edgy biomarkers for prognosis. Discoveries 2015;3:e38.  Back to cited text no. 10
    
11.
Lowes MA, Bowcock AM, Krueger JG. Pathogenesis and therapy of psoriasis. Nature 2007;445:866-73.  Back to cited text no. 11
[PUBMED]    
12.
Vishu M, Mohankumar R, Srikalyani V, Ilango K. A study on phytochemical screening, antioxidant, antimicrobial and α-amylase inhibitory activities of crude extracts of the stem bark of pisonia grandis, R.BR. Asian J Pharm Clin Res 2017;10:129-32.  Back to cited text no. 12
    
13.
Deepankar G, Trishna D. Preliminary phytochemical screening and anti-inflammatory effect of the aqueous extract of tabernaemontana divaricata flower in wister rats. Int J Curr Pharm Res 2017;9:9-12.  Back to cited text no. 13
    
14.
Priyadarshni KC, Mahalingam PU. Antimicrobial and anticancer activity of silver nanoparticles from edible mushroom: A review. Asian J Pharm Clin Res 2017;10:37-40.  Back to cited text no. 14
    
15.
Nandhakumar R, Salini K, Devaraj SN. Morin augments anticarcinogenic and antiproliferative efficacy against 7, 12-dimethylbenz (a)-anthracene induced experimental mammary carcinogenesis. Mol Cell Biochem 2012;364:79-92.  Back to cited text no. 15
    
16.
Prahalathan P, Kumar S, Raja B. Morin attenuates blood pressure and oxidative stress in deoxycorticosterone acetate-salt hypertensive rats: A biochemical and histopathological evaluation. Metabol 2012;6:1087-99.  Back to cited text no. 16
    
17.
Merwid-Ląd A, Trocha M, Chlebda E, Sozański T, Magdalan J, Ksiądzyna D et al. Effects of morin-5′-sulfonic acid sodium salt (NaMSA) on cyclophosphamide-induced changes in oxido-redox state in rat liver and kidney. Hum Exp Toxicol 2012;31:812-9.  Back to cited text no. 17
    
18.
Fang SH, Hou YC, Chang WC, Hsiu SL, Chao PD, Chiang BL. Morin Kuo Kuo Kuo sulfates/glucuronides exert anti-inflammatory activity on activated macrophages and decreased the incidence of septic shock. Life Sci 2003;74:743-56.  Back to cited text no. 18
[PUBMED]    
19.
Kuo HM, Chang LS, Lin YL, Lu HF, Yang JS, Lee JH et al. Morin inhibits the growth of human leukemia HL-60 cells via cell cycle arrest and induction of apoptosis through mitochondria dependent pathway. Anticancer Res 2007;27:395-405.  Back to cited text no. 19
    
20.
Yuting C, Rongliang Z, Zhongjian J, Yong J. Flavonoids as superoxide scavengers and antioxidants. Free Radic Biol Med 1990;9:19-21.  Back to cited text no. 20
    
21.
Sreedharan V, Venkatachalam KK, Namasivayam N. Effect of morin on tissue lipid peroxidation and antioxidant status in 1,2-dimethylhydrazine induced experimental colon carcinogenesis. Invest New Drugs 2009;27:21-30.  Back to cited text no. 21
[PUBMED]    
22.
Vaid M, Katiyar SK. Molecular mechanisms of inhibition of photocarcinogenesis by silymarin, a phytochemical from milk thistle (Silybum marianum L. Gaertn). Int J Oncol 2010;36:1053-60.  Back to cited text no. 22
[PUBMED]    
23.
Blalock TD, Varela JC, Gowda S, Tang Y, Chen C, Mast BA et al. Ischemic skin wound healing models in rats. Wounds 2001;13:35-44.  Back to cited text no. 23
    
24.
Niehaus WG, Samuelsson B. Formation of malonaldehyde from phospholipid arachidonate during microsomal lipid peroxidation. Eur J Biochem 1968;6:126-30.  Back to cited text no. 24
    
25.
Jiang ZY, Hunt JV, Wolff SP. Ferrous ion oxidation in the presence of xylenol orange for detection of lipid hydroperoxide in low density lipoprotein. Anal Biochem 1992;202:384-9.  Back to cited text no. 25
[PUBMED]    
26.
Kakkar P, Das B, Viswanathan PN. A modified spectrophotometric assay of superoxide dismutase. Ind J Biochem Biophys 1984;21:130-2.  Back to cited text no. 26
    
27.
Sinha AK. Colorimetric assay of catalase. Anal Biochem 1972;47:389-94.  Back to cited text no. 27
[PUBMED]    
28.
Rotruck JT, Pope AL, Ganther HE, Swanson AB, Hafeman DG, Hoekstra W. Selenium: Biochemical role as a component of glutathione peroxidase. Science 1973;179:588-90.  Back to cited text no. 28
    
29.
Ellman GL. Tissue sulfhydryl groups. Arch Biochem Biophys 1959;82:70-7.  Back to cited text no. 29
[PUBMED]    
30.
Roe JH, Kuether CA. The determination of ascorbic acid in whole blood and urine through the 2,4-dinitrophenylhydrazine derivative of dehydroascorbic acid. J Biol Chem 1943;11:145-64.  Back to cited text no. 30
    
31.
Baker H, Frank O, DeAngelis B, Feingold S. Plasma tocopherol in man at various times after ingesting free or acetylated tocopherol. Nutr Res 1980;21:531-6.  Back to cited text no. 31
    
32.
Towbin H, Staehelin T, Gordon J. Electrophoretic transfer of proteins from polyacrylamide gels to nitrocellulose sheets: Procedure and some applications. Proc Natl Acad Sci 1979;76:4350-4.  Back to cited text no. 32
[PUBMED]    
33.
Lee EH, Faulhaber D, Hanson KM, Ding W, Peters S, Kodali S et al. Dietary lutein reduces ultraviolet radiation-induced inflammation and immunosuppression. J Invest Dermatol 2004;122:510-7.  Back to cited text no. 33
    
34.
Ramachandran S, Rajendra Prasad N. Sesamol, a phenolic phytochemical present in Sesamum indicum, inhibits photocarcinogenesis by targeting UVB-induced lipid peroxidation and antioxidation depletion in Swiss albino mice. J Res Biochem 2011;1:1-8.  Back to cited text no. 34
    
35.
Panche AN, Diwan AD, Chandra SR. Flavonoids: An overview. J Nutr Sci 2016;5:e47.  Back to cited text no. 35
    
36.
Halliday GM. Inflammation, gene mutation and photoimmunosuppression in response to UVR-induced oxidative damage contributes to photocarcinogenesis. Mutat Res 2005;571:107-20.  Back to cited text no. 36
[PUBMED]    
37.
Merwald H, Klosner G, Kokesch C, Der-Petrossian M, Hönigsmann H, Trautinger F. UVA-induced oxidative damage and cytotoxicity depend on the mode of exposure. J Photochem Photobiol B 2005;79:197-207.  Back to cited text no. 37
    
38.
Fahlman BM. In vitro studies to assess the potential of quercetin as a topical sunscreen: Photooxidative properties, photostability and inhibition of UV radiation mediated skin damage. A thesis submitted to the College of Graduate Studies and Research; 2010.  Back to cited text no. 38
    
39.
Marković Z, Milenković D, Đorović J, Dimitrić Marković JM, Stepanić V, Lučić B et al. PM6 and DFT study of free radical scavenging activity of morin. Food Chem 2012;134:1754-60.  Back to cited text no. 39
    
40.
Addor FA. Antioxidants in dermatology. An Bras Dermatol 2017;92:356-62.  Back to cited text no. 40
    
41.
Shindo Y, Hashimoto T. Ultraviolet B-induced cell death in four cutaneous cell lines exhibiting different enzymatic antioxidant defences: Involvement of apoptosis. J Dermatol Sci 1998;17:140-50.  Back to cited text no. 41
[PUBMED]    
42.
Baehner RL, Murrmann SK, Davis J, Johnston RB Jr. The role of superoxide anion and hydrogen peroxide in phagocytosis-associated oxidative metabolic reactions. J Clin Invest 1975;56:571-6.  Back to cited text no. 42
[PUBMED]    
43.
Sharma P, Jha AB, Dubey RS, Pessarakli M. Reactive oxygen species, oxidative damage, and antioxidative defense mechanism in plants under stressful conditions. J Bot 2012;2012:217037.  Back to cited text no. 43
    
44.
Parihar VK, Prabhakar KR, Veerapur VP, Priyadarsini KI, Unnikrishnan MK, Rao CM. Anticlastogenic activity of morin against whole body gamma irradiation in Swiss albino mice. Eur J Pharmacol 2007;1:58-65.  Back to cited text no. 44
    
45.
Lin FH, Lin JY, Gupta RD, Tournas JA, Burch JA, Selim MA et al. Ferulic acid stabilizes a solution of vitamins C and E and doubles its photoprotection of skin. J Invest Dermatol 2005;125:826-32.  Back to cited text no. 45
    
46.
Rice-Evans C, Miller N, Paganga G. Antioxidant properties of phenolic compounds. Trends Plant Sci 1997;2:152-9.  Back to cited text no. 46
    
47.
Lee J, Shin YK, Song JY, Lee KW. Protective mechanism of morin against ultraviolet B-induced cellular senescence in human keratinocyte stem cells. Int J Radiat Biol 2014;90:20-8.  Back to cited text no. 47
[PUBMED]    
48.
Lin XF, Min W, Luo D. Anticarcinogenic effect of ferulic acid on ultraviolet-B irradiated human keratinocyte HaCaT cells.J Med Plants Res 2010;4:1686-94.  Back to cited text no. 48
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]



 

Top
 
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
    Abstract
   Introduction
    Materials and Me...
   Results
   Discussion
   Conclusion
    References
    Article Figures

 Article Access Statistics
    Viewed353    
    Printed42    
    Emailed0    
    PDF Downloaded45    
    Comments [Add]    

Recommend this journal