Hydroquinone and its analogues in dermatology – a potential health risk

@article{Westerhof2005HydroquinoneAI,
  title={Hydroquinone and its analogues in dermatology – a potential health risk},
  author={Wiete Westerhof and T J Kooyers},
  journal={Journal of Cosmetic Dermatology},
  year={2005},
  volume={4}
}
Hydroquinone has been used for decades as a skin lightening agent. Since January 1, 2001, its use in cosmetics has been banned. This ban is as a result of mid‐term effects such as leukoderma‐en‐confetti/occupational vitiligo and exogenous ochronosis. However, a recent literature search on hydroquinone as a skin lightening agent suggests that possible long‐term effects such as carcinogenesis may be expected as well. 

Hydroquinone and its analogues in dermatology – a risk‐benefit viewpoint

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Hydrolysis of arbutin to hydroquinone by human skin bacteria and its effect on antioxidant activity

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Normal skin microflora may increase the skin lightening effect of arbutin due to the antioxidant action of hydroquinone, which is more potent 1,1‐diphenyl‐2‐picrylhydrazyl radical scavenging activity and tyrosinase inhibition than arbuting.

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Efficacy and tolerability on melasma of a topical cosmetic product acting on melanocytes, fibroblasts and endothelial cells: a randomized comparative trial against 4% hydroquinone

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Topical use of hydroquinone as a depigmenting agent.

TLDR
Therapy with topically applied hydroquinone did not lead to complete disappearance of pathological hypermelanosis, but results were satisfactory enough to help most patients become less self-conscious about their pigmentary abnormalities.

A new formula for depigmenting human skin.

TLDR
The formula was therapeutically effective in treatment of melasma, ephelides, and postinflammatory hyperpigmentation and Senile lentigines were resistant to this therapy.

Hypothesis: Phenol and hydroquinone derived mainly from diet and gastrointestinal flora activity are causal factors in leukemia

TLDR
The hypothesis predicts that susceptibility to the disease would be related to diet, medicinal intake, genetics and gut-flora composition, and thus dietary modification and reduced use of medicines that elevate phenol levels may be the best intervention strategies for lowering leukemia risk.

Carcinogenicity of a nephrotoxic metabolite of the "nongenotoxic" carcinogen hydroquinone.

TLDR
Although HQ is generally considered a nongenotoxic carcinogen, the data suggest that HQ nephrocarcinogenesis is probably mediated by the formation of the quantitatively minor yet potent nephrotoxic metabolite TGHQ, which induces sustained regenerative hyperplasia, loss of tumor suppressor gene function, and the subsequent formation of renal adenomas and carcinomas.

Mechanism of depigmentation by hydroquinone.

TLDR
Findings indicate that HQ affects not only the formation, melanization, and degradation of melanosomes, but that it affects also the membraneous structures of melanocytes and eventually causes necrosis of whole melanocytes.

Human in vivo and in vitro hydroquinone topical bioavailability, metabolism, and disposition.

TLDR
Risk assessment should not only involve the bioavailability of intact topical hydroquinone, but also consider phase I and phase II metabolism in both humans and any animal for which toxicity potential was assessed.

Hydroquinone, a Bioreactive Metabolite of Benzene, Inhibits Apoptosis in Myeloblasts

TLDR
The ability of hydroquinone to induce a program of differentiation in the myeloblast that proceeds only to the myELocyte stage coupled with its ability to inhibit the CPP32 protease and, thereby, apoptosis of the proliferating myelocytes, may have important implications for benzene‐induced acute myeloid leukemia.

Development of a physiologically based pharmacokinetic model for hydroquinone.

TLDR
An initial physiologically based pharmacokinetic model was developed to characterize the role of kinetics in the strain differences observed in HQ-induced renal toxicity and tumorigenicity and represents the first stage in the development of a biologically based dose-response model for improving the scientific basis for human health risk assessments of HQ.

Hydroquinones cause specific mutations and lead to cellular transformation and in vivo tumorigenesis.

Benzo(a)pyrene and benzene are human carcinogens. The metabolic activation of these compounds into ultimate mutagenic and carcinogenic metabolites is prerequisite for their carcinogenic effects. In