Ultrastructural and biochemical observations on the effect of 4-hydroxyanisole plus tyrosinase on normal human melanocytes and keratocytes in tissue culture

Breathnach, A. S.; Robins, E J; Ethridge, Leslie; Bhasin, Y.; Gallagher, S.; Passi, S.; Nazzaro‐Porro, M.

doi:10.1038/bjc.1983.136

Cited by 11 publications

(2 citation statements)

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“…7). Since the toxic role of oxygen radicals persists for about 24 h (Table 2), it is evident that, subsequently, other mechanisms must be involved, such as the disappearance from the medium of essential growth factors, which may be destroyed, or inactivated, by quinones, semiquinones and oxygen radicals formed during the autoxidation of phenols, and/or the possible concomitant formation of toxic radical polymers (Breathnach et al, 1983;Naish, 1984).…”

Section: Discussionmentioning

confidence: 99%

Comparative cytotoxicity of phenols in vitro

Passi

Picardo

Nazzaro‐Porro

1987

Biochemical Journal

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Two melanotic human melanoma cell lines, IRE 1 and IRE 2, and the lymphoma-and leukaemia-derived cell lines Raji and K 562, were exposed to different concentrations (from 5 x 10-3 M to 10-5 M) of phenols, both substrates (s) and non-substrates (ns) of tyrosinase, in the presence or absence of the oxygenradical-scavenger enzymes superoxide dismutase, catalase and peroxidase. Monophenols were tyrosine (s), 4-hydroxyanisole (s) and butylated hydroxyanisole (ns); diphenols were L-3,4-dihydroxyphenylalanine (s), dopamine (3,4-dihydroxyphenethylamine) (s), terbutylcatechol (s), hydroquinone (s) and resorcinol (ns); triphenols were 6-hydroxydopa (3,4,6-trihydroxyphenylalanine) (s) and methyl gallate (s). Triphenols and oand p-diphenols underwent complete oxidation in culture medium within 24 h of incubation and were significantly more toxic than monophenols and the m-diphenol resorcinol, which, under the same cultural conditions, were much more stable. No significant differences in percentage survival were found among the different cell lines for each drug tested. The major component of toxicity up to 24 h of di-and tri-phenols is due to toxic oxygen species acting outside the cells and not to cellular uptake of these phenols as such.In fact the addition of oxygen-radical-scavenger enzymes significantly (P < 0.01) decreased the adverse effect of these drugs on all cell lines. The lower toxicity of monophenols and resorcinol as compared with that of di-and tri-phenols is due, in our opinion, to the fact that they are less oxidized under the conditions existing in the culture medium, and therefore do not produce sufficient levels of oxygen radicals. For these compounds, a primary intracellular action has to be taken into account to explain their cytotoxicity.

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Section: Discussionmentioning

confidence: 99%

Comparative cytotoxicity of phenols in vitro

Passi

Picardo

Nazzaro‐Porro

1987

Biochemical Journal

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“…The most active melanocytotoxic agent, to date, is an analog of tyrosine, 4-hydroxyanisole . Studies in vitro demonstrated its cytotoxicity against mammalian melanocytes (Riley et al, 1975;Breathnach et al, 1983), including human melanoma cells (Bleehen, 1976;Kanclerz & Aubert, 1984;Meyskens, 1984). Dewey et al (1977) observed 'regression' of Harding-Passey melanoma in 46% of the animals treated with intratumoural application of 4-OHA.…”

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confidence: 99%