The Cytotoxicity and Apoptosis Induced by 4-Tertiary Butylphenol in Human Melanocytes are Independent of Tyrosinase Activity

Yang, Fan; Sarangarajan, Rangaprasad; Poole, I. Caroline Le; Boissy, Raymond E.; Medrano, Estela E.

doi:10.1046/j.1523-1747.2000.00836.x

Cited by 69 publications

(62 citation statements)

References 38 publications

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“…To identify how MSH, ET-1, and MITF expression alter 4-TBP toxicity, we investigated the effects of MSH on the melanocyte and their contribution to sensitivity to 4-TBP. We have shown previously that neither proliferation rate 15 nor tyrosinase activity 14 has an effect on sensitivity to 4-TBP. We now demonstrate that despite the ability to remove ROS from the cellular environment, melanin content per se has no effect on melanocyte sensitivity to 4-TBP (Figures 4 and 7).…”

Section: -Tbp Inducedmentioning

confidence: 86%

“…11,12 Thus, 4-TBP, a competitive inhibitor of tyrosinase, 13 is metabolized in melanocytes and may generate reactive oxygen species capable of damaging these cells and inducing apoptosis. Ironically, expression levels of tyrosinase do not correlate with sensitivity to 4-TBP-induced apoptosis, 14 suggesting an alternative enzymatic mediator may be more critical.…”

mentioning

confidence: 99%

“…14 The percentage of cells that die following exposure to 4-TBP are unaffected by 12-O-tetradecanoylphorbol-13-acetate but can be reduced significantly by excluding ␣-melanocyte-stimulating hormone (MSH) 15 from the culture medium. MSH, a potent stimulator of melanogenesis, is a ligand for the melanocortin 1 receptor (MC1R).…”

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confidence: 99%

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A Role for Tyrosinase-Related Protein 1 in 4-tert-Butylphenol-Induced Toxicity in Melanocytes

Manga

Sheyn

Yang

et al. 2006

The American Journal of Pathology

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Vitiligo presents with depigmented cutaneous lesions following localized melanocyte death. Multiple factors contribute to cell death, including genetically determined susceptibility to trauma, and environmental factors, such as exposure to 4-tert-butylphenol (4-TBP). We demonstrate that 4-TBP induces oxidative stress that is more readily overcome by melanocytes from normally pigmented individuals than from two individuals with vitiligo. The antioxidant catalase selectively and significantly reduced death of melanocytes derived from two individuals with vitiligo, indicating a role for oxidative stress in vitiligo pathogenesis. In normal melanocytes, oxidative stress results in reduced expression of microphthalmia-associated transcription factor (MITF). Melanocyte-stimulating hormone-induced expression of MITF protein caused increased sensitivity to 4-TBP, whereas sensitivity of melanomas correlated with MITF expression. MITF stimulates melanin synthesis by up-regulating expression of melanogenic enzymes such as tyrosinase-related protein-1 (Tyrp1). Although melanin content per se did not affect sensitivity to 4-TBP, expression of Tyrp1 significantly increased sensitivity. Melanocytes and melanomas that express functional Tyrp1 were significantly more sensitive to 4-TBP than Tyrp1-null cells. Thus, normal melanocytes respond to 4-TBP by reducing expression of MITF and Tyrp1. We hypothesize that melanocytes in vitiligo demonstrate reduced ability to withstand oxidative stress due, partly, to a disruption in

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Section: -Tbp Inducedmentioning

confidence: 86%

mentioning

confidence: 99%

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A Role for Tyrosinase-Related Protein 1 in 4-tert-Butylphenol-Induced Toxicity in Melanocytes

Manga

Sheyn

Yang

et al. 2006

The American Journal of Pathology

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“…Flow-cytometric analysis of apoptosis An annexin V-fluorescein isothiocyanate (FITC) apoptosis detection kit (Oncogene Research Products, Boston, MA, USA) was used to detect apoptosis as previously described (Yang et al, 2000). All of the samples were assayed in triplicate.…”

Section: Cell Proliferation Assaymentioning

confidence: 99%

MicroRNA-451 functions as a tumor suppressor in human non-small cell lung cancer by targeting ras-related protein 14 (RAB14)

et al. 2011

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Accumulating evidence suggests that microRNAs (miRNAs) are important gene regulators, which can have critical roles in diverse biological processes including tumorigenesis. In this study, we analyzed the miRNA expression profiles in non-small cell lung carcinoma (NSCLC) by use of a miRNA microarray platform and identified 40 differentially expressed miRNAs. We showed that miRNA (miR)-451 was the most downregulated in NSCLC tissues. The expression level of miR-451 was found to be significantly correlated with tumor differentiation, pathological stage and lymph-node metastasis. Moreover, low miR-451 expression level was also correlated with shorter overall survival of NSCLC patients (Po0.001). Ectopic miR-451 expression significantly suppressed the in vitro proliferation and colony formation of NSCLC cells and the development of tumors in nude mice by enhancing apoptosis, which might be associated with inactivation of Akt signaling pathway. Interestingly, ectopic miR-451 expression could significantly inhibit RAB14 protein expression and decrease a luciferasereporter activity containing the RAB14 3 0 -untranslated region (UTR). In addition,, RNA interference silencing of RAB14 gene could recapitulate the tumor suppressor function of miR-451, whereas restoration of RAB14 expression could partially attenuate the tumor suppressor function of miR-451 in NSCLC cells. Furthermore, we also showed that strong positive immunoreactivity of RAB14 protein was significantly associated with downregulation of miR-451 (P ¼ 0.01). These findings suggest that miR-451 regulates survival of NSCLC cells partially through the downregulation of RAB14. Therefore, targeting with the miR-451/RAB14 interaction might serve as a novel therapeutic application to treat NSCLC patients.

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“…4-tert-Butylphenol is widely distributed in aquatic environments, including river waters (20), seawaters (17), river sediments (17), marine sediments (23), and effluent samples from sewage treatment plants and wastewater treatment plants (22). Furthermore, 4-tert-butylphenol interacts with estrogen receptors (29,30,34,35,39) and exhibits other toxic effects on aquatic organisms and humans (4,15,16,25,26,42,43). Therefore, it is necessary to study the biodegradation of 4-tert-butylphenol to understand its fate in the aquatic environment, to establish technologies to treat the waters polluted by it, and to remove it from contaminated environments.…”

mentioning

confidence: 99%

Isolation and Characterization of 4- tert -Butylphenol-Utilizing Sphingobium fuliginis Strains from Phragmites australis Rhizosphere Sediment

Toyama

Momotani

Ogata

et al. 2010

Appl Environ Microbiol

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We isolated three Sphingobium fuliginis strains from Phragmites australis rhizosphere sediment that were capable of utilizing 4-tert-butylphenol as a sole carbon and energy source. These strains are the first 4-tertbutylphenol-utilizing bacteria. The strain designated TIK-1 completely degraded 1.0 mM 4-tert-butylphenol in basal salts medium within 12 h, with concomitant cell growth. We identified 4-tert-butylcatechol and 3,3-dimethyl-2-butanone as internal metabolites by gas chromatography-mass spectrometry. When 3-fluorocatechol was used as an inactivator of meta-cleavage enzymes, strain TIK-1 could not degrade 4-tert-butylcatechol and 3,3-dimethyl-2-butanone was not detected. We concluded that metabolism of 4-tert-butylphenol by strain TIK-1 is initiated by hydroxylation to 4-tert-butylcatechol, followed by a meta-cleavage pathway. Growth experiments with 20 other alkylphenols showed that 4-isopropylphenol, 4-sec-butylphenol, and 4-tert-pentylphenol, which have alkyl side chains of three to five carbon atoms with ␣-quaternary or ␣-tertiary carbons, supported cell growth but that 4-n-alkylphenols, 4-tert-octylphenol, technical nonylphenol, 2-alkylphenols, and 3-alkylphenols did not. The rate of growth on 4-tert-butylphenol was much higher than that of growth on the other alkylphenols. Degradation experiments with various alkylphenols showed that strain TIK-1 cells grown on 4-tert-butylphenol could degrade 4-alkylphenols with variously sized and branched side chains (ethyl, n-propyl, isopropyl, n-butyl, sec-butyl, tert-butyl, n-pentyl, tert-pentyl, n-hexyl, n-heptyl, n-octyl, tert-octyl, nnonyl, and branched nonyl) via a meta-cleavage pathway but not 2-or 3-alkylphenols. Along with the degradation of these alkylphenols, we detected methyl alkyl ketones that retained the structure of the original alkyl side chains. Strain TIK-1 may be useful in the bioremediation of environments polluted by 4-tert-butylphenol and various other 4-alkylphenols.

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The Cytotoxicity and Apoptosis Induced by 4-Tertiary Butylphenol in Human Melanocytes are Independent of Tyrosinase Activity

Cited by 69 publications

References 38 publications

A Role for Tyrosinase-Related Protein 1 in 4-tert-Butylphenol-Induced Toxicity in Melanocytes

A Role for Tyrosinase-Related Protein 1 in 4-tert-Butylphenol-Induced Toxicity in Melanocytes

MicroRNA-451 functions as a tumor suppressor in human non-small cell lung cancer by targeting ras-related protein 14 (RAB14)

Isolation and Characterization of 4- tert -Butylphenol-Utilizing Sphingobium fuliginis Strains from Phragmites australis Rhizosphere Sediment

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