Does Skin Lightening Cream Work
Introduction
Skin tone is branded every bit beauty, grace, and loftier social condition in many parts of the world, and this perception encourages, people, specially women to indulge in skin lightening products.1,2 Harmful products such every bit Hydroquinone, Kojic acid, and Mercury are present in many skin lightening products.two,3 Hydroquinone is considered as a primary topical ingredient for inhibiting melanin production considering information technology reduces the peel'due south production of melanin which is responsible for pare color.4 However, because of the carcinogenic nature of hydroquinone, it has been banned in some countries in a bid to reduce the risks of skin cancer.ane Apart from its furnishings on the skin, hydroquinone has been found to betrayal users to acute toxicity from oral exposure and information technology can also cause diseases such as thyroid disorder, leukemia, and liver damage.1,3 Chronic occupational exposure to hydroquinone grit had reportedly resulted in eye injuries, which varied from mild irritation and staining of conjunctivae and cornea to changes in the thickness and curvature of the cornea, loss of corneal luster, and impaired vision.five Prolonged exposure could lead to the development of severe ocular furnishings.iv College concentrations frequently irritate the skin, and if used for prolonged periods, information technology could crusade disfiguring effects including epidermal thickening.2 Oral ingestion of doses betwixt 5 g and 15 g doses caused convulsions and hemolytic anemia.6
Kojic acid on the other hand, known as Koji in Japan, is a fungal metabolic product which has the advantage of not beingness oxidized in skin lotions.one It is a chelation agent that is produced by several fungi including Aspergillus oryzae. It inhibits and prevents the formation of tyrosine and it contains some antimicrobial properties against several common bacterial stains even in small dilutions.7 A written reporteight had reported that 4% hydroquinone and 0.75% Kojic when combined for typical treatment were constructive in treating facial melasma. What might not have been adequately investigated would the possible effects of its prolonged or chronic employ on the skin.
Skin, the organ of study, is the largest organ of the human body which accounts for about 15% of the human trunk weight and its health could be afflicted by topical agents.9,10 The vital functions of the skin include protection, prevention of excess water loss from the torso and thermoregulation. The pare is equanimous of the superficial epidermis and the underlying dermis. The hypodermis lies beneath the dermis. Aloe vera, the institute that was used for the intervention is too known as Barbadensis miller. It is a shrubby or arborescent, perennial, xerophytic succulent, pea-green colour establish that has been known and used in centuries for its health, beauty, medicinal, and skin care properties.11 The high incidences of skin lightening using creams, which is otherwise chosen bleaching and the attendant potential consequences necessitated this study. Hence, this report also used aloe vera as a possible remedy for the furnishings of kojic acid and hydroquinone which are constitute in skin lightening creams.vi
Materials and Methods
Animal Treatment and Tissue Processing
Eighty adult [due north=80] female Wistar rats, with the average body weight of 120 g, were procured for the study from the institutional animate being holding facility. The standard procedures for fauna use and handling were followed according to Babcock University's Health Enquiry Ethical Committee which canonical the project (BUHREC 2018). The adult female Wistar rats were divided into 8 groups of ten each after the period of acclimatization every bit follows:
Group A: the control group; animals were treated with but olive oil every bit a placebo.
Grouping B: This grouping was treated with 2% hydroquinone and 98% olive oil during the period of the experiment.
Group C: This grouping was treated with ii% kojic acid and 98% olive oil.
Group D: This grouping was treated with iv% hydroquinone and 96% olive oil.
Group E: This group was treated with 4% kojic and 96% olive oil.
Grouping F: This group was treated 2% hydroquinone, 2% kojic acrid, and 96% olive oil.
Group G: This group was treated with iv% hydroquinone, 4% kojic acid, and 92% olive oil.
Group H: This group was treated with iv% hydroquinone, 4% kojic acid, aloe vera gel 4%, and 88% olive oil.
The required quantities of hydroquinone and kojic acid were dissolved in measured quantities of olive oil under mild rut [˂ 50°C]. The treatments lasted 28 days. The animals were sacrificed through the cervical dislocation. The tail skins were excised and preserved in 10% formal saline for immunohistochemical and histological procedures. The fixed tissues were processed following specific histological and histochemical protocols. Basic tissue processing included dehydration [using graded concentration of booze], clearing [using xylene], impregnation, and embedding [using molten wax]. The tissue samples were sectioned with a rotary microtome (~20 microns). The sections were mounted on glass slides for staining.
Staining Techniques
The H&E staining technique was done post-obit the methods of Ref. 12 The slides, afterward dewaxing and rehydration, were placed in hematoxylin for 8–15 minutes for staining. The slides were so rinsed in tap h2o. The slides were farther dipped in a bluing agent for 3–5 long dips. They were stained with Eosin for a catamenia of xxx seconds and hematoxylin for ~2 minutes. They were also dehydrated in 95% and 100% alcohol, with iii changes each for two minutes. They were then cleared in three changes of xylene for 2 minutes each and later which the cover glass was mounted.
The Masson's Trichrome staining procedure for collagen fiber was done following the methods of.13 Tissues were deparaffinized and rehydrated through 100% alcohol, 95% alcohol, and 70% alcohol, so washed in distilled water. They were re-fixed in Bouin'south solution for 1 60 minutes at 56°C and rinsed under running tap water for five–ten minutes to remove the yellow color. They were and so stained in Weigert's fe hematoxylin working solution for x minutes and rinsed in running warm tap water for 10 minutes. Furthermore, they were washed in distilled water and stained again, in Biebrich red-acid Fuchsin solution for ten–15 minutes. They were washed again in distilled water and differentiated in phosphomolybdic-phosphotungstic acid solution for ten–15 minutes. Sections were transferred directly (without rinsing) to aniline blue solution and stained for v–10 minutes, then rinsed briefly in distilled water and differentiated in i% acerb acid solution for 2–5 minutes. They were again done in distilled water, and so dehydrated very quickly through 95% ethyl alcohol, absolute ethyl alcohol to wipe off Biebrich scarlet-acid Fuchsin staining, and cleared in xylene, afterwards which they were mounted with resinous mounting medium. The collagen fibers stained blue, the nuclei stained black, and the groundwork stained red.
The p65 immunohistochemistry technique protocol was carried out based on Abcam® specifications. Methane series sections were used for the immunohistochemistry study. Antigen retrieval was done though boiling before commencing with immunostaining. The slides were washed two x 5 min in TBS plus 0.025% Triton 10-100 with gentle agitation. The sections were blocked in ten% normal serum with 1% BSA in TBS for 2 hours at room temperature. Slides were drained for a few seconds. The primary antibody was diluted in TBS with i% BSA and practical. Sections were incubated overnight at four°C. Thereafter, sections were rinsed 2 x 5 min TBS 0.025% Triton with gentle agitation; and incubated in 0.3% HiiO2 in TBS for 15 minutes. The slides were mounted using albumin and observed nether the microscope. Suitably representative photomicrographs were captured.
Results
Results of the written report are presented (below) every bit photomicrographs of the skin sections as demonstrated using the H and East (Figure 1), Masson's trichrome technique (Figure 2) and the p65 immunohistochemistry technique (Effigy 3).
 | Figure 1 Photomicrograph of the skin of the experimental animals in Groups A–H, demonstrating the skin using H and E (H&Due east A-H; X400). The stratum corneum was disrupted in Groups B, D, and G (H&E B, D, and G). Note: Arrows betoken to specific features that are denoted past letters.Abbreviations: ED, Epidermis - (i) Stratum corneum (two) Stratum Granulosum (3) Stratum Spinosum (4) Stratum Basale; D, Dermis; One thousand, Gland; C, Connective tissue; Yard, Keratin. |
 | Figure 2 Photomicrograph of the skin of the experimental animals in Groups A–H demonstrating the skin using the Masson'southward trichrome technique (MT A-H; X400). The connective tissue was relatively more often than not preserved in the peel layers (MT A-H). Notation: Arrows bespeak to specific features that are denoted past letters.Abbreviations: ED, Epidermis - (1) Stratum corneum (2) Stratum Granulosum (three) Stratum Spinosum (4) Stratum Basale; D, Dermis; G, Gland; C, Connective tissue; Chiliad, Keratin. |
 | Figure 3 Photomicrograph of the skin of the experimental animals in Groups A–H demonstrating the skin using the p65 immunohistochemistry technique (p65 A-H). More cells in the groups B, D, F, and G expressed p65 which was used as an inflammation marker. Notation: Arrows point to specific features that are denoted by messages.Abbreviations: ED, Epidermis - (1) Stratum corneum (2) Stratum Granulosum (3) Stratum Spinosum (4) Stratum Basale; D, Dermis; G, Gland; C, Connective tissue; K, Keratin. |
Disruption of the Stratum Corneum Is Attributable to Hydroquinone Effects
A major issue of the application of hydroquinone to the skin of the experimental animals is the disruption of the more superficial layers of the epidermis, the stratum corneum, which observable in Effigy 1 photomicrographs. This further showed that the cells in this layer were affected. While the mechanisms of the disruption could either be due to the removal of superficial cells as a result of the hydroquinone effects, it might also be due to retarded formation of the corneum layer cells due to alterations in the migration of cells from the deeper layers of the epidermis. Whichever of the ii possible mechanisms was responsible largely for this observation, the implications are numerous and might include the lesions of the skin, potential fragility of the skin and induced susceptibility to the ultraviolet (UV) rays and other environmental hazards. Information technology is also known that increased UV exposure is a major risk factor for skin cancer.14 By implication, reduced superficial protection means increased exposure of the deeper prison cell layers including the melanocytes to UV radiation15 This has serious implications because in that location are reports that this might increase the adventure of skin cancer.xvi
Loss of the superficial cells would mean that the treated peel was relatively thinner. This means a significant loss of the protective stratum corneum. This peel layer is very important to peel protection considering it is selectively permeable to chemicals and other agents.17 This also would imply that the mechanical strength of the skin to protect the body from mechanical trauma was reduced or compromised. One implication of this might be more frequent or serious pare trauma due to mechanical assaults. Hence, the skin that had been affected in such a manner by hydroquinone utilise might have reduced integrity against mechanical or physical assaults. Another consequence of such thinness of the skin might be compromised power to perform its function of homeostasis. There might include reduced power to conserve heat, because of the loss in the cells that account partly for the thickness of the skin. This might as well be extended to the reduced ability to conserve water as reduced superficial covering might lead to relatively increased skin vulnerability to losing water, especially when the environment is hot. A delicate skin is not only susceptible to mechanical trauma only also susceptible to penetrations that achieve to the deeper structures of the skin such equally bites from insects for instance. This might also make information technology easier for pathogens and toxins to admission the body through the skin.
Susceptibility to the UV rays and other environmental hazards is a major complication that might result from this effect. The skin normally has the correct thickness to protect the body from the furnishings of the sunday's ultraviolet [UV] rays. A significant loss of the stratum corneum might event in a major compromise of this ability. In addition to this, the inability of the pare to supplant the loss stratum corneum cells might as well exist extended to the melanocytes that are also largely required to protect the peel confronting the UV radiations. To this stop, the skin might be vulnerable to the UV radiation effects. The complications that can arise from this might therefore include cancer of the skin.15
It is worthy of annotation however that Kojic acid did non cause any observable disruption to the stratum corneum equally axiomatic in the photomicrographs in Effigy 1 and 2. On the other manus, its effects and interactions with the hydroquinone when both were practical appear to exist benign, by mildly ameliorating the effects of hydroquinone. This might explicate why it might oft be a co-ingredient of sure creams with hydroquinone. Its actions, notwithstanding, were not potent enough to totally improve the effects of hydroquinone. Thus, this report partly aligns with certain previous studies that kojic acrid at prescribed doses might not have deleterious effects when used for skin lightening or bleaching because at that place is no histological testify of a potentially deleterious result of kojic acid on the treated skins; all the same, it would not suffice to back up the acclaimed multiple health benefits of its uses in certain reports (eighteen; nineteen; 20).
Connective Tissue of the Skin
The agents that were used did non produce any extensive appreciable effects on the connective tissues of the skin. Thus, the underlying connective tissues were largely preserved and relatively undisrupted by all the agents that were administered [Figure ii].
Prominent Expression of P56 Is Owing to Hydroquinone Effects
The immunohistochemistry method demonstrated p65 which is a REL-associated protein that served as a marker for jail cell proliferation, degeneration, and inflammation. The prominent demonstration or expression of p56 in the skin of the experimental animals was attributable to the furnishings of hydroquinone [Figure 3]. This also strongly suggests inflammations or a chemical irritation or assault on the cells or the basal layers of the epidermis likewise every bit cells surrounding the sebaceous glands and the hair follicles. This also implies that the effects of hydroquinone as associated with the expression of p56 were not limited to the superficial layers of the pare. This might take a number of implications including the inflammation of the skin every bit well as links to certain cancers of the skin and other disorders. The expression of p65 in the report skins has significant implications on skin health, especially, relative to inflammations and skin cancers. The affected skins, from existing evidences, have increased levels of hazard. From previous studies, epidermal p65/NF-κB signalling was essential for pare carcinogenesis.21 Its normal function is also associated to the maintenance of skin immune homeostasis; hence, it is protective against spontaneous dermatitis22. The complications that might ascend from its anomalies are therefore of serious skin health consequences. A previous study7 had also stated that increased NF-κB activity acquired hyper-proliferation and dysplasia of the mouse epidermis.
Aloe Vera Showed Potentials to Better Hydroquinone Deleterious Effects
The application of aloe vera gel to the already treated skin had observable furnishings as Aloe vera gel application showed potentials to ameliorate hydroquinone deleterious effects by persevering the stratum corneum which were generally disrupted in other groups that were administered hydroquinone [to the peel] [Figures 1 and 2]. Furthermore, the expression of p56 in these groups was relatively reduced [Effigy iii]. Thus, aloe-vera gel as used had protective effects and by extension might exist protecting the skin from the potential consequences associated with the effects of hydroquinone. Aloe vera has been reported to have significant protective effects on the skin.11 Such protective effects also reportedly include anti-inflammatory effects23 and ameliorative furnishings against skin damages and traumas.24
The current findings are similar to a previous work,25 in which it was reported that the epidermis of hydroquinone-treated rabbits showed inflammatory cells, infiltration mainlylymphocytes and eosinophils. It was besides reported to accept potential carcinogenic furnishings. Furthermore, researchers had, in their previous report, labelled hydroquinone and its analogs – in dermatology – as potential wellness risks.26 Previous reports also showed that hydroquinone caused histological alterations in the liver; mainly hydrophobic degeneration. It has as well been recommended that hydroquinone should be used with moderation (27; 28).
Conclusions and Recommendations
The results obtained from this research showed that hydroquinone disrupted the epidermis and acquired inflammation to the cells of the deeper skin layers and other cells surrounding sebaceous glands and hair follicles. The application of aloe vera gel ameliorated the effects of hydroquinone on the experimental animals' peel. The existing notion that the use of hydroquinone and kojic acrid might exist safe is not in agreement with the results of this work; hence, further piece of work is recommended especially on the chronic and systemic effects of hydroquinone and kojic acrid on the skin and body.
Disclosure
The authors report no conflicts of involvement in this work.
References
1. Al-Saleh IA. Mercury contenting pare lightening creams and potential hazards to the Wellness of Saudi Women. J Toxical Environ Wellness. 2010;5(1):123–130.
2. Dyall-Smith DA, Scurry JP. Mercury pigmentation and mercury levels from the employ of cosmetic creams. Med J Aust. 2014;153:409–415. doi:x.5694/j.1326-5377.1990.tb125501.x
3. Ferreira AO, Freire ES, Polonini HC, Candido da Silva PJL, Brandaio MAF, Raposo NRB. Anti-ageing effects of monomethylsilanetriol and maltodextrin-stabilized orthosilicic acid on nails, skin and hair. Cosmet J. 2018;5(iv):12–15.
4. Brigs AP. Principles of Biological Chemistry.
five. Considine GD. Van Nostrand'southward encyclopaedia of Chemistry, 5th Edition. New York: John Wiley & Sons; 2006.
half-dozen. Li Q, Geiselhart Fifty, Mittler JN, Mudzinski SP, Lawrence DA, Freed BM. Inhibition of human being T lymphoblast proliferation by hydroquinone. Toxicol Appl Pharmacol. 1996;139(2):317–323.
vii. Poligone B, Hayden MS, Chen L, Pentland AP, Jimi Eastward, Ghosh S. A role for NF-κB activity in skin hyperplasia and the evolution o keratoacanthomata in mice. PLoS One. 2013;eight(8):e71887. doi:10.1371/periodical.pone.0071887
eight. Rochelle MBN, Kishore B, Bhat R, Sukumar D, Martis J, Ganesh H. A comparative study of the efficacy of 4% hydroquinone vs 0.75% kojic acid cream in the treatment of facial melasma. Indian J Dermatol. 2013;58(2):157–161. doi:x.4103/0019-5154.108070
9. Yetunde MA. Complications of Chronic use of Skin Lightening Cosmetics. Int J Dermatol. 2008;seven:344–353.
10. Seyyed MA, Rashid FA, Rahul EI, Quadri KI. The review on backdrop of aloe vera in healing of cutaneous wounds. PMC. 2015;2015:714216.
11. Surjushe A, Vasani R, Saple DG. Aloe vera: a brusque review. Indian J Dermatol. 2008;53(iv):163–166. doi:10.4103/0019-5154.44785
12. Sheehan DC, Hrapchak BB. Theory and Practice of Histotechnology.
thirteen. Masson LE. Verhoeff; 2009. Stain.vetmed.vt.edu. Available from: http://education.vetmed.vt.edu/Curriculum/VM8054/Labs/.
fourteen. Gilchrest BA, Eller MS, Geller Ac, Yaar M. The pathogenesis of melanoma induced by ultraviolet radiation. Due north Engl J Med. 1999;340(17):1341–1348. doi:10.1056/NEJM199904293401707
fifteen. Watson Thou, Holman DM, Maguire-Eisen Grand. Ultraviolet radiation exposure and its impact on skin cancer adventure. Semin Oncol Nurs. 2016;32(3):241–254. doi:x.1016/j.soncn.2016.05.005
16. Sheehan JM, Potten CS, Immature AR. Tanning in human skin types two and three offers modest photo-protection confronting erythema. Photochem Photobiol. 1998;68(four):588–592. doi:10.1111/j.1751-1097.1998.tb02518.x
17. Bos D, Meinardi MM. The 500 dalton rule for the peel penetration of chemic compounds and drugs. Exp Dermatol. 2000;ix(3):165–169. doi:ten.1034/j.1600-0625.2000.009003165.x
xviii. Moon KY, Ahn KS, Lee J, Kim YS. Kojic acid, a potential inhibitor of nf-κb activation in transfectant man HaCaT and SCC-13 cells. Curvation Pharm Res. 2001;24(4):307–311.
xix. Ma DL, Xu T, Chan DS, Man Past, Fong WF, Leung CH. A highly selective, label-complimentary, homogenous luminescent switch-on probe for the detection of nanomolar transcription factor NF-kappaB. Nucleic Acids Res. 2011;39(10):e67. doi:10.1093/nar/gkr106
20. Saeedi M, Eslamifar Yard, Khezri 1000. Kojic acid applications in corrective and pharmaceutical preparations. Biomed Pharmacother. 2019;110:582–593. doi:x.1016/j.biopha.2018.12.006
21. Kim C, Pasparakis Chiliad. Epidermal p65/NF-κBsignalling is essential for skin carcinogenesis. EMBO Mol Med. 2014;6(7):970–983. doi:10.15252/emmm.201303541
22. Grinberg-Bleyer Y, Dainichi T, Oh H, et al. Genetic toxicology testing of 41 industrial chemicals, research. J Dermatol Sci. 2015;15:357–377.
23. Hutter JA, Salmon Chiliad, Stavinoha WB, Satsangi Northward, Williams RF, Streeper RT. Anti-Inflammatory C-glucosyl Chromone from Aloe Barbadensis. J National Prod. 1996;59:541–543.
24. Feily A, Namazi MR. Aloe vera in dermatology: a brief review. M Ital Dermatol Venereol. 2009;144(ane):85–91.
25. Kooyers TJ, Westerhof W. Toxicology and health risks of hydroquinone in skin lightening formulations. J Eur Acad Dermatol Venereology. 2006;20(vii):777–780. doi:x.1111/j.1468-3083.2005.01218.x
26. Westerhof W, Kooyers TJ. Hydroquinone and its analogues in dermatology - a potential health risk. J Cosmet Dermatol. 2005;4(2):55–59. doi:10.1111/j.1473-2165.2005.40202.x
27. Tse TW. Hydroquinone for skin lightening: rubber profile, elapsing of use and when should we finish?. J Dermatol Treat. 2010;21(five):272–275. doi:10.3109/09546630903341945
28. Al-Saleh I, Elkhatib R, Al-Rouqi R, Al-Enazi S, Shinwari Due north. The dangers of skin-lightening creams. Toxicol Environ Chem. 2012;94(1):195–219. doi:10.1080/02772248.2011.631925
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