Effect of Monobenzyl Hydroquinone on Oxidase Systems In Vivo and In Vitro

Peck, Samuel M.; Sobotka, Harry

doi:10.1038/jid.1941.32

Cited by 34 publications

(13 citation statements)

References 5 publications

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“…It is a slow‐acting depigmenting agent inducing a type IV delayed hypersensitivity response . MBEH induces necrotic cell death in epidermal melanocytes . Similar to findings in mice , areas of human skin exposed to MBEH showed cytotoxic CD8 + T‐cell infiltrates, supporting that MBEH induces a cytotoxic T‐cell immune response that further contributes to depigmentation .…”

Section: Monobenzone Treatmentsupporting

confidence: 70%

“…The gradual effects, typically notable after four to twelve months of use, are undesirably slow for patients . Furthermore, although depigmentation is known to spread beyond the application site, MBEH treatment may not eliminate all melanocytes beyond the application site and carries a risk of repigmentation . Here, we propose to combine two synergistic mechanisms: the acceleration of autoimmunity and melanocyte death initiated by MBEH by amplifying T‐cell responses through immune adjuvants to induce effective, long‐lasting and universal depigmentation.…”

Section: Introductionmentioning

confidence: 99%

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Enhanced bleaching treatment: opportunities for immune‐assisted melanocyte suicide in vitiligo

Webb

Eby

Hariharan

et al. 2014

Experimental Dermatology

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Depigmentation in vitiligo occurs by progressive loss of melanocytes from the basal layer of the skin, and can be psychologically devastating to patients. T cell-mediated autoimmunity explains the progressive nature of this disease. Rather than being confronted with periods of rapid depigmentation and bouts of repigmentation, patients with long-standing, treatment-resistant vitiligo can undergo depigmentation treatment. The objective is to remove residual pigmentation in order to achieve a cosmetically acceptable result- that of skin with a uniform appearance. In the USA, only the use of mono-benzyl ether of hydroquinone (MBEH) is approved for this purpose. However, satisfactory results can take time to appear, and there is a risk of repigmentation. MBEH induces necrotic melanocyte death followed by a cytotoxic T cell response to remaining, distant melanocytes. As cytotoxic T cell responses are instrumental to depigmentation, we propose that combining MBEH with immune adjuvant therapies will accelerate immune-mediated melanocyte destruction to achieve faster, more definitive depigmentation than with MBEH alone. Since Toll-like Receptor (TLR) agonists-imiquimod, CpG, and Heat Shock Protein 70 (HSP 70)-all support powerful Th1 responses, we propose that using MBEH in combination with these agents can achieve superior depigmentation results for vitiligo patients.

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Section: Monobenzone Treatmentsupporting

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Enhanced bleaching treatment: opportunities for immune‐assisted melanocyte suicide in vitiligo

Webb

Eby

Hariharan

et al. 2014

Experimental Dermatology

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“…p-Benzyloxy-phenol is an inhibitor of melanogenesis (Lerner & Fitzpatrick, 1950;Peck & Sobotka, 1941). To investigate the effect of this inhibitor on Streptomyces lavendulae different concentrations of it were added to a complete medium containing 0.8 g. tyrosine/l.…”

Section: Inhibition Of Pigment Biosynthesismentioning

confidence: 99%

Melanin Biosynthesis by Streptomyces lavendulae

Mencher

Heim

1962

Journal of General Microbiology

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SUMMARYStreptomyces lavendulae was studied in a defined medium. When tyrosine was added to the medium a brown-black pigment was synthesized; without tyrosine, only a trace of this pigment was detected. Growth was the same with or without tyrosine. The addition of (2-14C) DL-tyrosine to the medium resulted in synthesis of a radioactive pigment, and tyrosinase activity was demonstrated in extracts of disrupted organisms. Of 15 amino acids added to the medium only tyrosine and tryptophan were used for pigment formation. Pigment production was inhibited by pbenzyloxy-phenol, an inhibitor of mammalian melanogenesis. In yeast + glucose medium a pH range of 6.8-8-2 was optimal for pigment synthesis; more pigment was formed at 20' than at 28' in spite of the fact that there was twice as much growth at the latter temperature. The pigment was precipitated from culture media by a method described for precipitating melanin from urine and in every way tested was identical with a synthetic dihydroxyphenylalanine-melanin. The data indicate that the brown-black pigment synthesized by S. lavendulae is melanin.

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“…If so, it could have serious implications for individuals who use future “skin-whitening candy” or other supplements, which appear to contain phenols 62, 63 . One study found that intramuscular injection of 4-TBP in black rabbits and dogs caused depigmentation 28 , while there are conflicting reports of depigmentation after feeding MBEH to guinea pigs 4, 64 .…”

Section: Household Products Thought To Induce Vitiligomentioning

confidence: 99%

Chemical-Induced Vitiligo

Harris

2017

Dermatologic Clinics

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Synopsis Chemical-induced depigmentation of the skin has been recognized for over 75 years, first as an occupational hazard but then extending to those using household commercial products as common as hair dyes. Since their discovery, these chemicals have been used therapeutically in patients with severe vitiligo to depigment their remaining skin and improve their appearance. The importance of recognizing this phenomenon was highlighted during an outbreak of vitiligo in Japan during the summer of 2013, when over 16,000 users of a new skin lightening cosmetic cream developed skin depigmentation at the site of contact with the cream and many in remote areas as well. Depigmenting chemicals appear to be analogs of the amino acid tyrosine that disrupt melanogenesis and result in autoimmunity and melanocyte destruction. Because chemical-induced depigmentation is clinically and histologically indistinguishable from non-chemically induced vitiligo, and because these chemicals appear to induce melanocyte autoimmunity, this phenomenon should be known as “chemical-induced vitiligo”, rather than less accurate terms that have been previously used.

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Effect of Monobenzyl Hydroquinone on Oxidase Systems In Vivo and In Vitro

Cited by 34 publications

References 5 publications

Enhanced bleaching treatment: opportunities for immune‐assisted melanocyte suicide in vitiligo

Enhanced bleaching treatment: opportunities for immune‐assisted melanocyte suicide in vitiligo

Melanin Biosynthesis by Streptomyces lavendulae

Chemical-Induced Vitiligo

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