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At least 19 recordsLinked to original sources
PubMed2000

An examination of the phenol-croton oil peel: part IV. Face peel results with different concentrations of phenol and croton oil.

In Part IV of this examination of the phenol-croton oil peel, the author presents peeling solutions using phenol in concentrations between 16% and 50% as the carrier for croton oil. Previously, in Part I, the author showed that phenol alone in concentrations of less than 50% has no significant peeling effect on the skin in the absence of taping. All of these formulas are dependent on the addition of croton oil for their peeling action. A topographic map of the face is presented that divides the face into the zones that the author believes are best treated with different strengths of croton oil. Five patients peeled between late 1992 and late 1995 were chosen as examples to illustrate the effect of different strengths of croton oil between 0.25% and 2.78%. The author has documented their immediate postoperative course photographically to show the effect of the different concentrations. It is clinically apparent that peels using croton oil between 0.25% and 0.5% generally heal within 7 days; peels between 0.6% and 1.0% usually heal within 9 or 10 days, and peels using concentrations higher than 1% heal later and have some risk of pigmentation loss. Peels using croton oil concentrations at 2% and above almost always have pigmentation loss and have healing delays in areas other than the thick skin of the lower nose and perioral area. The practical clinical formulas distributed at the time of the presentation of this article at the 1996 Annual Meeting of the American Society for Aesthetic Plastic Surgery in Orlando, Florida, entitled "Heresy Phenol Formulas--1996," are provided here. These have been used in both the United States and Europe over the past few years. A metric standard for drop size is suggested at 0.04 ml. This relates to the drop size used clinically over the years to measure croton oil. The adoption of this unit will make formulas around the world easier to calculate and compare. The author has produced a metric formula using the suggested standard size drop for croton oil. This uses 35% phenol as the carrier and provides the same range of treatment dilutions as the 1996 "Heresy Phenol Formulas." The need for research into "carriers" and solvents for croton oil is pointed out. Despite what is not known about how it works, the combination of croton seed extract and phenol has been a success story in providing facial rejuvenation from the 1920s to the present. The croton oil-phenol peel in its many formulas still sets the standard for facial rejuvenation.

Chemexfoliation↗
PubMed1996

Activation and degradation of benzoate, 3-phenylpropionate and crotonate by Syntrophus buswellii strain GA. Evidence for electron-transport phosphorylation during crotonate respiration.

A strictly anaerobic, benzoate-degrading bacterium, Syntrophus buswellii strain GA, was able to degrade benzoate or 3-phenylpropionate to acetate, CO2 and H2, if the hydrogen partial pressure was sufficiently low. The hydrogen was removed in syntrophic coculture by Methanospirillum hungatei or by Desulfovibrio sp. through interspecies hydrogen transfer or in pure culture by the use of crotonate as reducible cosubstrate. Alternatively, S. buswellii strain GA could grow in pure culture with crotonate. Activities of seven catabolic enzymes were measured in crude cell extracts of S. buswellii strain GA grown with various substrates and of crotonate-grown S. buswellii strain DSM 2612A. Benzoate, 3-phenylpropionate and crotonate were activated by CoA ligases. Glutaryl-CoA dehydrogenase was found to be involved in the degradation of aromatic compounds and enzymes catalysing beta-oxidation were involved in the reaction sequence from crotonyl-CoA to acetate. A c-type cytochrome was present in the cytoplasm, whereas b-type cytochromes were associated with the membranes of both S. buswellii strains grown on crotonate. These indicated the presence of an electron-transport system. A high growth yield of crotonate-grown S. buswellii strain GA might be explained by electron-transport phosphorylation in addition to substrate-level phosphorylation.

Bacteria, Anaerobic↗
PubMed2000

An examination of the phenol-croton oil peel: Part II. The lay peelers and their croton oil formulas.

From the turn of the century, lay face peelers, known as "skinners," ran "beautifier" salons. Beginning in the 1920s, lay peelers were using croton oil-phenol formulas in Hollywood. These persons were renowned, made a good living, and treated many, if not most, of the leading "stars" of the day. They had a treatment, a "secret," that physicians did not. Physicians brought their own wives to the peelers for their expertise. The leading lay peel personalities from the 1920s through to our time are presented. The lay peelers dominated the field until the 1960s, when legal attacks on them, often directly instigated by the newly educated physician peelers, put them at a legal disadvantage. Nevertheless, there was considerable interaction with many plastic surgeons along the way. Some plastic surgeons came into possession of the techniques and some also into knowledge of the ingredients in a formula. The author has presented the recipes of four of the renowned lay peelers, two from Hollywood, Gradé and Kelsen, and two from Miami, Coopersmith and Maschek. These recipes all have 80 to 90 percent less croton oil than the "classic" Baker formula and, therefore, wound less deeply. The Hollywood formulas were used on many celebrities both inside and outside the film world from the 1920s to the early 1990s. These lay recipes are cumbersome to prepare. The author has simplified the preparation of these lay recipes by using USP liquid phenol instead of crystals. These simple formulas are provided in a table and are as easy to prepare as the Baker formula.

Chemexfoliation↗
PubMed1984

Heat durability of Epstein-Barr virus-activating substances of plant origin: 12-O-tetradecanoylphorbol-13-acetate, 12-O-hexadecanoyl-16-hydrophorbol-13-acetate, croton oil, tung oil and Croton megalocarpus extract.

12-O-Tetradecanoyl-phorbol-13-acetate (TPA), 12-O-hexadecanoyl-16-hydrophorbol-13-acetate (HHPA), croton oil, tung oil and Croton megalocarpus ether extract, all of which are known to possess Epstein-Barr virus-activating potency, retained their capacity to induce Epstein-Barr virus early antigen complex in the viral genome-carrying human lymphoblastoid cells (Raji) even after heat treatment at 120 degrees C for 2 h or at 100 degrees C for 12 h. Such unusual heat resistance of the agents tested may contribute to the persistence and accumulation of the active principle(s) in soil under the plants which contain such substances, as we have previously reported.

Antigens, Viral↗
PubMed2000

An examination of the phenol-croton oil peel: Part I. Dissecting the formula.

This article investigates which ingredients are the active ones in the most popular peel formula. The benefits of the "phenol" peel have been attributed to the effects of phenol on the dermis. Baker published a simple peel formula in 1962 that became a classic that has been used since by almost all plastic surgeons and dermatologists. Brown et al., in 1960, passed along a set of dogmas: (1) phenol is the active ingredient; (2) phenol peels more deeply in lower concentrations; and (3) adding a surface tension-lowering agent increases the peel. This article seeks to dissect the Baker formula by removing the croton oil. A patient was peeled serially with 18% phenol, 35% phenol, and 50% phenol solutions containing Septisol (surface tension-lowering agent) but no croton oil. This showed that increasing concentrations of phenol caused more clinical tissue reaction as evidenced by edema and erythema, but no significant dermal injury was seen. USP 88% phenol without Septisol did cause injury to the dermis. To test the effect of croton oil in the formula, the patient's face was peeled with two variations: the perioral area was peeled with 50% phenol to which croton oil was added to a strength of 2.1% and the remainder with 50% phenol without croton oil. The perioral area showed vesiculation, slough, and dermal exposure characteristic of a deep peel requiring 11 days to heal. The remainder of the face treated with 50% phenol without croton oil showed only edema and erythema without significant dermal injury. This experiment shows that the main postulates of Brown et al.--that phenol in lesser concentrations peels more than in higher concentrations and that phenol is the sole agent--are not true. In a fourth peel, a 0.7% concentration of croton oil in 50% phenol was applied to the parts of the face not peeled with croton oil in the third peel. The areas peeled with 50% phenol with 0.7% croton oil healed in 7 days, whereas the treatment with 50% phenol with 2.1% croton oil required 11 days. Deconstructing the Baker formula reveals fallacies in the four-decade-long belief system regarding these peels. The serial peels performed in this study show that increasing concentrations of phenol without croton oil cause increasing skin reaction but insignificant peeling effect. The addition of croton oil to 50% phenol, however, causes a marked increase in the depth of peeling into the dermis. Lowering the concentration of croton oil caused a lesser burn, as evidenced by fewer days to heal. The depth of the peel, therefore, seems to be more dependent on the concentration of croton oil than phenol. This will be further explored in Parts II, III, and IV.

Aged↗
PubMed1976

Effects of croton oil on epidermal growth regulators (chalones).

Variations in epidermal chalones after a single surface application of methylcholanthrene have been described in previous papers. This paper reports a study of the effect of croton oil on epidermal growth regulators (G1 and G2 chalones). Hairless mice received a single topical application of 0.2 ml 0.25% acetone solution of croton oil. Control mice received only acetone. The short-term effect of croton oil on epidermal DNA synthesis and mitotic rate was studied. Other groups of croton oil-treated and acetone-treated mice were then killed at similar time intervals, and the treated area of skin was homogenized and extracted with water. The inhibitory effect of these extracts on normal epidermal DNA synthesis and mitotic rate was assayed in normal hairless mice. The resulting inhibition was interpreted as an expression of the concentration of G1 and G2 chalones, respectively, in the skin extracts. The first experiment confirmed that a single croton oil application provokes a short block in epidermal mitotic activity and probably also in DNA synthesis. This was followed by bimodal peaks of increased activity, the two maxima of mitotic rate on days 2 and 7. The concentration of the two chalones in the skins of treated animals varied in inverse proportion to the alterations in the DNA synthesis and the mitotic rate, with one exception. There was here initially a depression both of the mitotic rate and a low concentration of G2 chalone. This was interpreted as a short, initial direct effect of croton oil on the G2 chalone present at the time of application. It is concluded that croton oil application injures and kills epidermal cells, with subsequent alterations in the content of G1 and G2 chalones. This theory may explain the changes observed. The effects of croton oil on the amount of G1 and G2 chalones in the skin are probably related to the direct, toxic, cell-killing effect of croton oil, and not to its specific cancer promoting potency.

Animals↗
PubMed2000

An examination of the phenol-croton oil peel: Part III. The plastic surgeons' role.

In Part II, the author focused on the lay peelers' history and success using croton oil-containing phenol peeling recipes. In Part III, the author reviews what was known or should have been known about croton oil and phenol as physicians became keenly interested in face peeling in the mid-1950s. The lay peelers recognized that croton oil was a critical ingredient of the so-called phenol peel while physicians focused on phenol without recognizing the intense cytotoxic effect of croton resin. Physicians have persisted in this systematic error for 40 years. Both dermatology and plastic surgery have shown a remarkable credulity about phenol's action and lack of curiosity about croton oil's action. A hitherto unreferenced and unknown croton oil-containing formula of Adolph Brown, patented in 1959, has been unearthed, preceding Litton's and Baker's formulas in time. The recollections of Litton, Baker, Truppman, and Georgiade shed some light on the interaction between them and the lay peelers and how the formulas were transferred. Other plastic surgeons probably acquired the same knowledge, used it in their practices, but chose not to draw attention to it. None of the physicians credited the lay peelers. Brown, Litton, and Baker each could have published a complete formula, but only Baker did. However, his formula was vastly stronger than the lay formulas but, nevertheless, came to dominate medical peeling for the next 35 years because of its simplicity of preparation. A review of the peel literature reveals many oft-repeated but unsupported dogmas regarding the mode of action of phenol, which have obscured our understanding of the phenol-croton oil peel. Animal studies exist that refute these dogmas, e.g., (1) lesser concentrations of phenol wound more deeply; and (2) phenol has an all-or-nothing action. As well, studies from the early 1980s showed that the presence of croton oil caused much deeper burns than phenol alone. Suggested areas of research that could solve the conundrum of the phenol-croton oil peel are presented.

Chemexfoliation↗
PubMed2006

Cyclohexane carboxylate and benzoate formation from crotonate in Syntrophus aciditrophicus.

The anaerobic, syntrophic bacterium Syntrophus aciditrophicus grown in pure culture produced 1.4 +/- 0.24 mol of acetate and 0.16 +/- 0.02 mol of cyclohexane carboxylate per mole of crotonate metabolized. [U-13C]crotonate was metabolized to [1,2-(13)C]acetate and [1,2,3,4,5,7-(13)C]cyclohexane carboxylate. Cultures grown with unlabeled crotonate and [13C]sodium bicarbonate formed [6-(13)C]cyclohexane carboxylate. Trimethylsilyl (TMS) derivatives of cyclohexane carboxylate, cyclohex-1-ene carboxylate, benzoate, pimelate, glutarate, 3-hydroxybutyrate, and acetoacetate were detected as intermediates by comparison of retention times and mass spectral profiles to authentic standards. With [U-(13)C]crotonate, the m/z-15 ion of TMS-derivatized glutarate, 3-hydroxybutyrate, and acetoacetate each increased by +4 mass units, and the m/z-15 ion of TMS-derivatized pimelate, cyclohex-1-ene carboxylate, benzoate, and cyclohexane carboxylate each increased by +6 mass units. With [13C]sodium bicarbonate and unlabeled crotonate, the m/z-15 ion of TMS derivatives of glutarate, pimelate, cyclohex-1-ene carboxylate, benzoate, and cyclohexane carboxylate each increased by +1 mass unit, suggesting that carboxylation occurred after the synthesis of a four-carbon intermediate. With [1,2-(13)C]acetate and unlabeled crotonate, the m/z-15 ion of TMS-derivatized 3-hydroxybutyrate, acetoacetate, and glutarate each increased by +0, +2, and +4 mass units, respectively, and the m/z-15 ion of TMS-derivatized pimelate, cyclohex-1-ene carboxylate, benzoate, cyclohexane carboxylate, and 2-hydroxycyclohexane carboxylate each increased by +0, +2, +4, and +6 mass units. The data are consistent with a pathway for cyclohexane carboxylate formation involving the condensation of two-carbon units derived from crotonate degradation with CO2 addition, rather than the use of the intact four-carbon skeleton of crotonate.

Benzoates↗
PubMed1987

Suppressing effect of croton oil on intestinal carcinogenesis induced by methylazoxymethanol acetate in rats.

The effect of croton oil on intestinal carcinogenesis by methylazoxymethanol acetate (MAM) was examined in ACI/N rats. Twenty seven male and 28 female ACI/N rats were given a single intragastric intubation of MAM at a dose of 25 mg/kg body weight, followed by croton oil at 0.25 ml/kg body weight, 3 times a week, by gastric intubation until the termination of this experiment (365 days). The animals had diarrhea with administration of the croton oil, but the diarrhea had no effect on their gain in weight. Rats from all groups surviving more than 216 days were counted as effective animals. Seventeen out of 54 effective rats which were treated with MAM and croton oil developed intestinal tumors and the incidence of the intestinal tumors was significantly less than that of the group treated with MAM alone (30 out of 50 rats, P less than 0.01). The average number of tumors per rat in the experimental group which was treated with MAM and croton oil (0.6 +/- 1.1) was also smaller than that in the group which was treated with MAM alone (1.0 +/- 1.8), although the difference was not significant. These results suggest that croton oil may suppress some tumor growth at the proper dose in intestinal carcinogenesis which is initiated by MAM.

Adenoma↗
PubMed1988

Pustular irritant dermatitis due to croton oil. Evaluation of the role played by leukocytes and complement.

To elucidate the pathomechanisms of irritant pustular dermatitis and to evaluate the role of leukocytes in pustulation induced by croton oil, we compared the skin responses in leukopenic-and decomplemented guinea pigs with those in control saline-injected animals, to 1% croton oil application. Both decomplemented and control animals responded similarly to croton oil, showing erythema and pustulation at 24 h after topical application; microscopically numerous mononuclear and polymorphonuclear cells infiltrated the skin. Meanwhile, the clinical and histopathological response of leukopenic animals to croton oil was significantly depressed. Time-course study of inflammatory infiltrate in the dermis of controls revealed that mononuclear cells preceded the infiltration of polymorphonuclears. Although leukocytes constitute an important component in croton oil dermatitis, our results suggest that unclarified chemical mediators, other than complement-derived chemotactic factors, play a crucial role as a primary chemoattractant in the production of pustulation at the croton oil-applied site.

Administration, Cutaneous↗