Monobenzone

4-(Benzyloxy)phenol, or Monobenzone, is an organic chemical in the phenol family with chemical formula C13H12O2.

The nuclear factor (erythroid-derived 2)-like 2 (NRF2) antioxidant response promotes melanocyte viability and reduces toxicity of the vitiligo-inducing phenol monobenzone.[Pubmed:28370349]

Exp Dermatol. 2017 Jul;26(7):637-644.

Vitiligo, characterised by progressive melanocyte death, can be initiated by exposure to vitiligo-inducing phenols (VIPs). VIPs generate oxidative stress in melanocytes and activate the master antioxidant regulator NRF2. While NRF2-regulated antioxidants are reported to protect melanocytes from oxidative stress, the role of NRF2 in the melanocyte response to Monobenzone, a clinically relevant VIP, has not been characterised. We hypothesised that activation of NRF2 may protect melanocytes from Monobenzone-induced toxicity. We observed that knockdown of NRF2 or NRF2-regulated antioxidants NQO1 and PRDX6 reduced melanocyte viability, but not viability of keratinocytes and fibroblasts, suggesting that melanocytes were preferentially dependent upon NRF2 activity for growth compared to other cutaneous cells. Furthermore, melanocytes activated the NRF2 response following Monobenzone exposure and constitutive NRF2 activation reduced Monobenzone toxicity, supporting NRF2's role in the melanocyte stress response. In contrast, melanocytes from individuals with vitiligo (vitiligo melanocytes) did not activate the NRF2 response as efficiently. Dimethyl fumarate-mediated NRF2 activation protected normal and vitiligo melanocytes against Monobenzone-induced toxicity. Given the contribution of oxidant-antioxidant imbalance in vitiligo, modulation of this pathway may be of therapeutic interest.

Successful treatment of extensive vitiligo with monobenzone.[Pubmed:23277803]

J Clin Aesthet Dermatol. 2012 Dec;5(12):36-9.

Vitiligo is one of the most common dermatological disorders, appearing as one or more white macules or patches and affecting up to two percent of the population worldwide. The undesirable aesthetic properties of vitiligo, especially facial, may result in significant negative psychosocial effects, particularly a rate of depression twice that of the general population. While there is no cure, there are several treatment options, notably depigmentation in severe cases. Monobenzone is the most potent depigmenting agent. However, its use is limited due to the permanent and potent nature of the drug. This case presents an example of when timely and aggressive treatment with Monobenzone is warranted, demonstrating excellent clinical response, which resulted in a significant increase in the quality of life in a patient with severe vitiligo.

Different effects of five depigmentary compounds, rhododendrol, raspberry ketone, monobenzone, rucinol and AP736 on melanogenesis and viability of human epidermal melanocytes.[Pubmed:26440747]

Exp Dermatol. 2016 Jan;25(1):44-9.

Numerous medications are used to treat hyperpigmentation. However, several reports have indicated that repeated application of some agents, such as rhododendrol (RD), raspberry ketone (RK) and Monobenzone (MB), can be toxic to melanocytes. Although these agents had severe side effects in human trials, no current in vitro methods can predict the safety of such drugs. This study assessed the in vitro effects of five depigmentary compounds including leukoderma-inducing agents. In particular, we determined the effects of different concentrations and exposure times of different depigmentary agents on cell viability and melanogenesis in the presence and absence of ultraviolet B (UVB) radiation. Concentrations of RD, RK and MB that inhibit melanogenesis are similar to concentrations that are cytotoxic; however, concentrations of rucinol (RC) and AP736 that inhibit melanogenesis are much lower than concentrations that are cytotoxic. Furthermore, the concentrations that cause toxic effects depend on exposure duration, and prolonged exposure to RD, RK and MB had more cytotoxic effects than prolonged exposure to RC and AP736. The cytotoxic effects of RD and RK appear to be mediated by apoptosis due to increased expression of caspase-3 and caspase-8; UVB radiation increased the cytotoxicity of these agents and also increased caspase activity. Our results indicate that different leukoderma-inducing compounds have different effects on the viability of normal epidermal melanocytes and suggest that the in vitro assay used here can be used to predict whether an investigational compound that induces leukoderma may lead to adverse effects in human trials.

A mouse model of vitiligo induced by monobenzone.[Pubmed:23800067]

Exp Dermatol. 2013 Jul;22(7):499-501.

The paucity of vitiligo animal models limits the understanding of vitiligo pathogenesis and the development of therapies for the skin disorder. In this study, we developed a new mouse model of vitiligo by topically applying the skin-depigmenting agent Monobenzone on mice. We demonstrated that Monobenzone-induced skin depigmentation on the non-exposed sites and that the severity of lesions depended on drug dosage. The result of the histological examination of the depigmented skin indicated loss of epidermal melanocytes and perilesional accumulation of CD8(+) T cells. Furthermore, the Monobenzone-induced depigmentation of the Rag1 gene knockout did not appear on the non-exposed sites, supporting the involvement of infiltrating CD8(+) T cells in melanocyte destruction. Resemblance in histological characteristics and pathogenesis between Monobenzone-induced depigmentation and active human vitiligo suggests good potential of our mouse model for use in vitiligo research.

Monobenzone is a potent skin depigmenting agent. Monobenzone induces depigmentation and active human vitiligo and exhibits good potential for vitiligo research.

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