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Improvement in vehicle design may improve the delivery of drugs to the target site. A clinical trial was performed to evaluate an improved vehicle for topical benzoyl peroxide. Thirty-nine subjects participated in a split-face, double-blind trial of topical benzoyl peroxide 5 percent versus benzoyl peroxide 5 percent in 8 percent urea. All subjects had grade II or III acne as described by Pillsbury. Study solutions were randomly assigned to a selected side of the subject's face and applied twice a day to the appropriate side of the face for eight weeks. Total and inflammatory lesion counts were performed by the same investigator during the eight weeks of study at biweekly intervals. No overall differences in the response to the study preparations were observed when assessed objectively and subjectively.
Benzoyl peroxide, a powerful organic oxidizing agent, was applied topically according to a carefully developed technique to cutaneous ulcers of different types. The healing time was shortened greatly by the rapid development of healthy granulation tissue and the quick ingrowth of epithelium. Exceptionally large pressure ulcers with deep cavities, undercut edges and sinus tracts were sucessfully treated, as were stasis ulcers of long duration resistant to all other therapy. There were only 13 treatment failures among the 133 cases. The slow, sustained release of oxygen by benzoyl peroxide was though to be responsible for the success. The only complications were contact irritant dermatitis in 3% and contact allergic dermatitis in 2% of patients treated.
Benzoyl peroxide (BP) is shown to be a weak allergen. Of 25 guinea pigs, only 5 were sensitized in the TINA test. Before treatment, only 2 of 172 acne patients gave a positive patch test with 1% BP, but not with 0.1% BP. The following results suggest that BP is a strong irritant. The irritant potential ID50 in rabbits was 2.52%, and the IT50 was 2.31 days with 5% BP, 4.34 days with 1% and 8.35 days with 0.1% BP. 29% of acne patients and non-exposed controls had a positive patch test with 5% BP. However, only 11 of 155 acne patients had clinical signs of intolerance, which settled despite continued use in 10 cases. The possible reasons for this dichotomy are explored. Neither the irritant nor allergenic properties of BP impaired its clinical use.
Benzoyl peroxide (BzPO) is both a tumor promoter and progressor in mouse skin; however, BzPO is neither an initiator nor a complete carcinogen in this tissue. Although not mutagenic, BzPO has been observed to produce strand breaks in DNA of exposed cells. These actions are presumed to be mediated by free-radical derivatives of BzPO. Previous studies suggested that the metabolism of BzPO in keratinocytes proceeds via the initial cleavage of the peroxide bond, yielding benzoyloxy radicals which, in turn, can either fragment to form phenyl radicals and carbon dioxide or abstract H atoms from biomolecules to yield benzoic acid. Benzoic acid is the major stable metabolite of BzPO produced by keratinocytes. In the present study we have investigated the role of BzPO and its metabolites in the generation of strand scissions in a cell-free system using phi X-174 plasmid DNA. In this system BzPO produced DNA damage that was dose-dependent over a concentration range of 0.1-1 mM and required the presence of copper but not other transition metals. By contrast, benoic acid did not produce DNA damage in this system, either in the presence or in the absence of copper. The inclusion of spin trapping agents, such as N-tert-butyl-alpha-phenylnitrone (PBN), 3,5-dibromo-4-nitrosobenzenesulfonate, and nitrosobenzene, in incubations was found to significantly reduce the extent of DNA damage generated via the copper-mediated activation of BzPO. Electron paramagnetic resonance spectroscopy studies suggested that the primary radical trapped by PBN following copper-mediated decomposition of BzPO was the benzoyloxy radical.(ABSTRACT TRUNCATED AT 250 WORDS)
Benzoyl peroxide (BP), used widely in dermatologic therapy and by the food industry, is considered a tumor promoter in chemically induced skin. Tumor promoters of both the phorbol and non-phorbol type interact with protein kinase C (PKC). This enzyme, therefore, is regarded as the intracellular receptor for a number of tumor promoters. BP bears some structural resemblance to diacylglycerol (DAG) and thus may exert its action through the PKC system. Based on these observations, we have investigated the effect of BP on PKC from mouse skin. Our data show that unlike phorbol esters, which stimulate PKC (in vivo and in vitro), BP inhibits PKC. Concentration-dependent inhibition by BP is observed when PKC is stimulated by phorbol esters, diacylglycerol, phosphatidyl serine (PS), or a combination of the latter two. BP also inhibits PKC stimulated by (-) Indolactam V, a nonphorbol compound resembling the teleocidins. 3H-phorbol ester binding experiments reveal that inhibition by BP may be due to its interference with the phorbol ester binding site and consequently diacylglycerol binding. The binding data and the inability of BP to inhibit either cyclic AMP-dependent protein kinase I or II imply that BP interacts with PKC, and not with the histone substrate. Results presented here clearly indicate that unlike phorbol and certain non-phorbol type of tumor promoters BP does not stimulate PKC in vitro.
Benzoyl peroxide (BzPO) is a free radical generating compound that acts as a tumor promoter and progressor in mouse skin. BzPO is cleaved in the presence of copper to produce benzoyloxyl and phenyl radicals. Treatment of mutation reporter plasmids with BzPO and copper yields predominantly single-strand breaks and G-->T transversion mutations. To explore the role of base modifications in the possible mammalian mutagenicity of BzPO the formation of 8-hydroxy-2'-deoxyguanosine (8-OHdG) within the DNA of cultured murine keratinocytes was investigated. Treatment with 10 microM BzPO produced a maximum 3-fold increase in levels of 8-OHdG versus vehicle controls within 1-2 h, with significant levels of 8-OHdG persisting 6 h after initial exposure to BzPO. Pretreatment with the copper chelator bathocuproine disulfonic acid reduced the levels of 8-OHdG generated by BzPO to near background. However, treatment with the iron chelator desferal did not. The stable metabolic product of BzPO benzoic acid was ineffective in producing 8-OHdG. Depletion of cellular glutathione with L-buthionine-(S,R)-sulfoximine increased the amount of BzPO-generated 8-OHdG, while supplementation with glutathione monoethyl ester reduced the number of 8-OHdG molecules formed. Collectively, these results suggest that BzPO at non-cytotoxic concentrations undergoes copper-dependent activation to a reactive product to generate 8-OHdG within cultured murine keratinocytes.
A double-blind, controlled clinical trial with 60 patients was employed in order to study the relative merits of two treatment schedules in acne vulgaris. One therapy comprised the topical application of a cream containing a combination of miconazole 2% and benzoylperoxide 5% (Acnidazil, Janssen) twice a day. In the other therapy, we applied a cream containing only benzoylperoxide 5%. Both groups of patients showed large and statistically significant reduction in the number of comedones, papules, and pustules during 12 weeks of therapy. Acnidazil, however, was found to have definitely better therapeutical results than benzoylperoxide alone: The lesions improved significantly faster, tolerance was better, and the patients overall evaluation clearly favored Acnidazil. 86,2% of the patients treated with Acnidazil rated the results good to very good, in contrast to 63% of the patients treated with benzoylperoxide only (p = 0.037).
62-65% reduction in the number of lesions was obtained in the treatment of 52 patients with acne vulgaris in this randomized single-blind study comparing a 5% benzoyl peroxide/2% miconazole cream (BPO-MCZ) with a 5% benzoyl peroxide gel (BPO). While BPO gel was equally effective in male and female patients (66 and 73% reduction of lesions), the BPO-MCZ cream was significantly more effective in the latter (50 vs. 74% mean reduction of lesions). Tolerance was significantly better with the BPO/MCZ cream preparation, particularly in females.
Alkaline elution was used to examine DNA single-strand breaks in cultured normal and carcinogen-altered mouse keratinocytes exposed to 12-O-tetradecanoyl phorbol-13-acetate and benzoyl peroxide. Seven cell lines derived from carcinogen-induced mouse skin papillomas and three cell lines derived from N-methyl-N'-nitro-N-nitrosoguanidine-treated non-tumor bearing mouse skin were resistant to phorbol ester-mediated DNA strand breaks after 6 or 24 h. Normal keratinocytes sustained strand breaks after 24 h but not after 6 h. Benzoyl peroxide induced extensive strand breaks in normal keratinocytes at both 6 and 24 h, and this was associated with marked cytotoxicity. In contrast, 9 of 10 cell lines showed complete or partial resistance to strand breaks following benzoyl peroxide exposure. It is proposed that differential resistance to DNA strand breaks and cytotoxicity among normal and carcinogen-altered keratinocytes provides the biological basis for the promoting action of benzoyl peroxide. Furthermore, sublethal DNA damage in preneoplastic or neoplastic keratinocytes may account for the potency of benzoyl peroxide in causing malignant conversion.
A double-blind, multi-centre general practice study was carried out to compare the effectiveness of benzoyl peroxide/potassium hydroxyquinoline sulphate cream, with or without hydrocortisone, its aqueous astringent cream base alone, and a benzoyl peroxide alcoholic gel in the treatment of 107 patients with acne vulgaris. Patients on entry were allocated at random to one of four treatment groups and instructed to apply the medication twice daily to all affected areas for 12 weeks. Assessments of the severity of acne on the face, chest and back, and response to treatment were made at 2, 4, 8 and 12 weeks. Acceptability of the treatment, i.e. 'greasiness', was also assessed by patients. The results showed that the combination cream preparation produced a greater reduction in acne scores than did the base or benzoyl peroxide alone. The addition of 1% hydrocortisone eliminated the flare reaction to benzoyl peroxide seen in patients in the other two active treatment groups. The majority of patients found the preparations cosmetically acceptable.
Benzoyl peroxide preparations have proven to be effective agents in the treatment of acne. In comparison to the numerous clinical communications, very few reports exist concerning the pharmacokinetics of benzoyl peroxide. The benzoyl peroxide content of abraded horny layers and its metabolite benzoic acid were investigated by high-pressure liquid chromatography after application (1-2 min) of emulsion containing benzoyl peroxide. It was found that benzoyl peroxide penetrates the stratum corneum very quickly where it is rapidly degraded to benzoic acid. No benzoyl peroxide depot in the stratum corneum could be demonstrated.
The stability of benzoyl peroxide in polyethylene glycol ointment base and some liquid vehicles (acetone, ethanol, propylene glycol, and their mixtures) was studied. Some solutions also contained an additional ingredient (acetanilide, benzoic acid, chlorhydroxyquinoline, and hydroxyquinoline) as a possible stabilizer. Benzoyl peroxide decomposed very fast (first-order K value 0.028 day-1 at 24 degrees) in polyethylene glycol ointment base. At 50 degrees, the potency of benzoyl peroxide in polyethylene glycol ointment base decreased to less than 1% in 5 days. Decomposition in solutions is complex. Considering acetone as a standard vehicle, ethanol improved the stability of benzoyl peroxide and propylene glycol had an adverse effect on the stability. Of the stabilizers studied, only chlorhydroxyquinoline improved the stability.
BACKGROUND: It has previously been shown that a combination of erythromycin and benzoyl peroxide is superior to either ingredient when used alone in the treatment of acne. A clindamycin/benzoyl peroxide combination gel might have an advantage over erythromycin/benzoyl peroxide gel because the former does not require refrigeration after it is dispensed. OBJECTIVE: Our purpose was to determine the efficacy and safety of a combination clindamycin/benzoyl peroxide gel when compared with benzoyl peroxide, clindamycin, or vehicle gels. METHODS: In two double-blind, randomized, parallel, vehicle-controlled trials, patients were treated for 11 weeks with once-nightly application of one of the above preparations. Evaluations were performed at 2, 5, 8, and 11 weeks and included lesion counts and assessment of global responses and irritant effects. RESULTS: A total of 334 patients completed the study. All three active preparations were significantly superior to the vehicle in global improvement and in reducing inflammatory lesions and noninflammatory lesions. The combination gel was significantly superior to the two individual agents in global improvement and reduction of inflammatory lesions and also to the clindamycin gel in reducing noninflammatory lesions. There was no significant difference in tolerance to the active gels versus the vehicle gel. CONCLUSION: In the treatment of acne, topical clindamycin/benzoyl peroxide combination gel is well tolerated and superior to either individual ingredient.
A lotion of benzoyl peroxide was applied postoperatively to chemosurgical wounds in a small group of patients. The technique of utilizing dressings of benzoyl peroxide is described and illustrated. Enhanced wound healing was observed in all cases. The effects appear to be due, at least in part, to antimicrobial activity, debriding activity, hyperbaric oxygenation, and stimulation of granulation.
The toxicity of composite resin on rabbit dental pulp was investigated biochemically. A microsomal fraction of rabbit dental pulp was incubated with each of the components of composite resins, and the formation of peroxide was determined by the thiobarbituric acid reaction. Benzoyl peroxide (BPO), the most widely used catalyst, was the most effective on peroxidation, but monomers were not. Cations such as Cu2+ or Fe2+ were required for acceleration of this reaction. Authentic polyunsaturated fatty acids and phospholipids were extensively converted into their peroxides by BPO, but amino acids and carbohydrates were not. Among the active oxygens, hydroxyl radicals were thought to be responsible for BPO-dependent peroxidation. The results presented in this paper indicate that the lipid portion of the cells may be attacked by hydroxyl radicals produced by BPO and copper or iron. Therefore, BPO is considered to be the major factor responsible for the toxicity of composite resins.
The mode of action of benzoyl peroxide in acne is three-fold, i.e. sebostatic, comedolytic and inhibitory to P. acnes in-vivo. Benzoyl peroxide is the topical treatment of choice in acne vulgaris. This agent is well tolerated by most patients. Primary irritant dermatitis can be avoided by less frequent application and the true incidence of contact sensitivity is low. The gel preparation has achieved a high degree of cosmetic acceptability. A synergistic effect with retinoic acid can be demonstrated. Tolerance to benzoyl peroxide develops in most subjects necessitating more vigorous therapy, usually after two or three weeks of treatment. Many acne sufferers with mild or moderate disease can avoid long-term oral antibiotic treatment by the judicious use of benzoyl peroxide topically.
The effectiveness of 10%, 20%, and 50% benzoyl peroxide in a lotion, 20% benzoyl peroxide in a gel, and the effect of the vehicles alone on wound reepithelialization were evaluated in young domestic pigs. Twenty percent benzoyl peroxide suspension in a lotion base substantially increased the rate of reepithelialization by 33% over a seven-day evaluation period. Twenty percent benzoyl peroxide suspension in a gel base and 10% benzoyl peroxide suspension in a lotion base slightly enhanced epidermal resurfacing, while 50% benzoyl peroxide suspension in a lotion base and the vehicle gel retarded healing. Variations in the rate of reepithelialization were observed when different lots of 20% benzoyl peroxide lotions were compared. Chemical analysis of each of the 20% benzoyl peroxide preparations tested disclosed great differences in zinc, magnesium, and sodium content.