Chemically Induced Depigmentation of Skin and Hair

Searle, C. E.; Riley, Patrick A.

doi:10.1007/978-3-642-74612-3_38

Hair and Hair Diseases 1990

DOI: 10.1007/978-3-642-74612-3_38

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Chemically Induced Depigmentation of Skin and Hair

C. E. Searle¹,

Patrick A. Riley²

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1999

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“…In melasma, this treatment can correct focal hyperpigmentation by inhibition of melanin pigmentation (Grimes, 1995). Treatment with bleaching agents can also serve to depigment areas by destruction of melanocytes in individuals with systemic vitiligo exclusively in melanocytes (McGuire and Hendee, 1971; Searle when repigmentation is no longer a realistic treatment option and Riley, 1979; Naish-Byfield et al, 1991; Riley, 1998). Utilizing (Halder and Nordlund, 1998).this selective cytodestructive mechanism has been proposed as an Compounds with known bleaching effects include hydroxyantimelanoma therapy (Jimbow et al, 1989; Mascagna et al, 1992).…”

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confidence: 99%

Altered Gene Expression in Melanocytes Exposed to 4-Tertiary Butyl Phenol (4-TBP): Upregulation of the A2b Adenosine Receptor1

Yang

Brown

Cornelius³

et al. 1999

Journal of Investigative Dermatology

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Exposure to phenolic agents contributes to the development of occupational vitiligo. Proposed as a causative factor for leukoderma in vivo, the para-substituted phenol 4-tertiary butyl phenol was chosen to investigate early cellular events responsible for selective disappearance of melanocytes from the epidermis of individuals sensitive to such agents. To this end, differential display of melanocyte mRNA isolated from three separate cultures was performed following a 12 h exposure of cells to 250 microM 4-tertiary butyl phenol or to vehicle alone. Fragments of cDNA representing differentially expressed messages were cloned and subsequently confirmed by reverse dot blotting. Alignment analysis revealed that the L30 ribosomal protein was upregulated by the treatment, potentially reflecting altered levels of protein synthesis in response to stress. In addition, a gene sequence upregulated following exposure to 4-tertiary butyl phenol was identified as the A2b receptor (a P1 receptor for adenosine). Differential expression of this gene was confirmed in an RNase protection assay. By reverse transcription-polymerase chain reaction, the gene was shown to be expressed in keratinocytes and fibroblasts as well. Flow cytometry confirmed differential expression in melanocytes and fibroblasts, but not in keratinocytes. Interestingly, it has been reported that P1 purinoceptor stimulation can induce apoptosis. This is in concordance with results reported elsewhere demonstrating induction of apoptosis by 4-tertiary butyl phenol in human melanocytes, as well as with morphologic changes observed in this study in cells exposed to 250 microM 4-tertiary butyl phenol for 72 h. In conclusion, differential display is useful to establish melanocyte components involved in the cellular response to phenolic agents.

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mentioning

confidence: 99%

Altered Gene Expression in Melanocytes Exposed to 4-Tertiary Butyl Phenol (4-TBP): Upregulation of the A2b Adenosine Receptor1

Yang

Brown

Cornelius³

et al. 1999

Journal of Investigative Dermatology

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Chemically Induced Depigmentation of Skin and Hair

Cited by 1 publication

References 77 publications

Altered Gene Expression in Melanocytes Exposed to 4-Tertiary Butyl Phenol (4-TBP): Upregulation of the A2b Adenosine Receptor1

Altered Gene Expression in Melanocytes Exposed to 4-Tertiary Butyl Phenol (4-TBP): Upregulation of the A2b Adenosine Receptor1

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