A Mode of Action for Butylated Hydroxytoluene-Mediated Photoprotection

Koone, Mark D.; Black, Homer S.

doi:10.1111/1523-1747.ep12524440

Cited by 21 publications

(13 citation statements)

References 15 publications

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“…It has been shown that systemically administered BHT results in diminished levels of UV radiation reaching potential epidermal target sites by increasing the photoprotective effect of the stratum corneum (Koone et al 1986). However, such an increased protective effect, as a result of a change in maturation of the stratum corneum, cannot account for the decrease of 8-MOP photobinding found with BHT, as the protective effect already occurred after one treatment, only 40 rain before irradiation (experiment 1, Table 1).…”

Section: C: By Changing the Optical Properties Of The Skinmentioning

confidence: 94%

Effect of alpha-tocopherol and di-butyl-hydroxytoluene (BHT) on UV-A-induced photobinding of 8-methoxypsoralen to Wistar rat epidermal biomacromolecules in vivo

1991

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The possible formation of singlet oxygen via photoexcited psoralens has been associated with the occurrence of, amongst others, erythema. Therefore it has been suggested to combine PUVA with the topical or systemic administration of antioxidants. However, the effect of these antioxidants on the photobinding of psoralens to DNA, which is held responsible for the anti-proliferative effect, should be taken into account. In the present study the effect of two phenolic antioxidants, alpha-tocopherol (AT) and butylated hydroxytoluene (BHT), on the in vivo photobinding of 8-methoxypsoralen (8-MOP) to not only epidermal DNA, but also proteins and lipids was determined. After topical application of an ethanolic antioxidant solution onto the shaven skin of Wistar rats, labeled 8-MOP was applied using the same solvent. After this the rats were exposed to UV-A. By separating epidermal lipids, DNA/RNA and proteins by a selective extraction method, irreversible binding of 8-MOP to each of these biomacromolecules was determined. Both AT and BHT caused a decrease in the photobinding of 8-MOP to epidermal DNA and proteins. To investigate the underlying mechanism of this protection, the effect of AT was compared with that of AT-acetate. It also proved helpful to study the effects of the antioxidants on the photobinding of another photosensitizer, namely chlorpromazine. From these experiments it was concluded that AT and BHT affect 8-MOP photobinding by quenching reactive 8-MOP intermediates, involving the phenolic hydroxyl group of the antioxidants. BHT offered protection against lipid binding of 8-MOP but AT, especially at high concentrations, enhanced the UV-A-induced binding of 8-MOP to lipids.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: C: By Changing the Optical Properties Of The Skinmentioning

confidence: 94%

Effect of alpha-tocopherol and di-butyl-hydroxytoluene (BHT) on UV-A-induced photobinding of 8-methoxypsoralen to Wistar rat epidermal biomacromolecules in vivo

1991

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“…The mechanism of action is not clearly known, but it is believed to decrease the dose of UVR reaching epidermal target sites by absorptive properties. 225 Dietary butylated hydroxytoluene has been shown to provide protective effect equivalent to SPF of 3.2. 226 The isoflavones that occur in many plants constitute a class of phytoestrogens and have modulating effects on estrogenic physiology; they are also effective antioxidants.…”

Section: Other Photoprotective Agentsmentioning

confidence: 99%

Photoprotection

Kullavanijaya

Lim

2005

Journal of the American Academy of Dermatology

343

265

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“…When stratum corneum, the nonliving outer layer of skin, was isolated and transmission of UV radiation through the stratum corneum measured, control animals exhibited 65% greater transmission than that from BHT-fed animals ( Figure 10). 48 This suggested that almost all of BHT's Significant comparisons of tumor latent period and tumor multiplicity, respectively: 4% corn oil versus 0.75% corn oil, P < .02, P = .004; 4% corn oil versus 4% menhaden oil, P = .002, P = .002; 4% corn oil versus 12% menhaden oil, P < .001, P < .001; 0.75% corn oil versus 12% menhaden oil, P < .004, nonsignificant (NS); 4% menhaden oil versus 12% menhaden oil, P < .02, NS. Other comparisons were not significantly different.…”

Section: Influence Of Butylated Hydroxytoluene (Bht) On Uv Carcinogenmentioning

confidence: 99%

“…Figure 10 Average transmission spectra for stratum corneum from animals prefed butylated hydroxytoluene (BHT)-supplemented and control diets. 48 Three scans on each of 8 samples of stratum corneum were averaged and areas under each curve calculated for the respective experimental and control groups. Closed circles = control; open circles= BHT supplemented.…”

Section: 56mentioning

confidence: 99%

Reassessment of a Free Radical Theory of Cancer With Emphasis on Ultraviolet Carcinogenesis

Black

2004

Integr Cancer Ther

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Pro-oxidants, reactive species and free radicals, are toxic substances that can cause oxidative damage to major constituents of biological systems. In contradistinction, antioxidants are defined as any substance that significantly prevents the pro-oxidant-initiated oxidation of a substrate. Consequently, it was suggested that it might be possible to reduce free radical damage and thus cancer risk through 3 dietary changes: (1) caloric reduction, that is, lowering the level of free radical reactions arising in the course of normal metabolism; (2) minimize dietary components that increase the level of free radical reactions (eg, polyunsaturated fats); and (3) supplement the diet with one or more free radical reaction inhibitors (antioxidants). Lipid peroxidation exemplifies the type of chain reaction initiated by free radicals in (2) and (3). Both the phenolic antioxidant butylated hydroxytoluene (BHT) and the carotenoid β-carotene can terminate such reactions and have been shown to influence ultraviolet (UV) carcinogenesis. However, there is a lack of cor relation between physicochemical and pathophysiological responses in both instances. Whereas the influence on UV carcinogenesis of both antioxidants has been reported to diminish as the level of dietary fat decreases, pointing to the involvement of lipid peroxidative reactions, the mode of BHT's action in inhibiting UV carcinogenesis appears to be related to UV dose diminution through increased spectral absorbance of the stratum corneum. β-carotene has no such effect and may actually exacerbate UV carcinogenesis under certain dietary conditions. This paradox points to the complex relationship between chemical mechanisms and biological mode of action of antioxidants. Recent clinical and experimental data suggest that antioxidant supplementation of the complex and intricately balanced natural antioxidant defense system as a cancer prevention strategy will demand extreme caution.

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A Mode of Action for Butylated Hydroxytoluene-Mediated Photoprotection

Cited by 21 publications

References 15 publications

Effect of alpha-tocopherol and di-butyl-hydroxytoluene (BHT) on UV-A-induced photobinding of 8-methoxypsoralen to Wistar rat epidermal biomacromolecules in vivo

Effect of alpha-tocopherol and di-butyl-hydroxytoluene (BHT) on UV-A-induced photobinding of 8-methoxypsoralen to Wistar rat epidermal biomacromolecules in vivo

Photoprotection

Reassessment of a Free Radical Theory of Cancer With Emphasis on Ultraviolet Carcinogenesis

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