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PubMed2006

Final report on the safety assessment of benzaldehyde.

Benzaldehyde is an aromatic aldehyde used in cosmetics as a denaturant, a flavoring agent, and as a fragrance. Currently used in only seven cosmetic products, its highest reported concentration of use was 0.5% in perfumes. Benzaldehyde is a generally regarded as safe (GRAS) food additive in the United States and is accepted as a flavoring substance in the European Union. Because Benzaldehyde rapidly metabolizes to Benzoic Acid in the skin, the available dermal irritation and sensitization data demonstrating no adverse reactions to Benzoic Acid were considered supportive of the safety of Benzaldehyde. Benzaldehyde is absorbed through skin and by the lungs, distributes to all well-perfused organs, but does not accumulate in any specific tissue type. After being metabolized to benzoic acid, conjugates are formed with glycine or glucuronic acid, and excreted in the urine. Little acute toxicity was seen. The oral LD(50) of Benzaldehyde in rats and mice ranged from 800 to 2850 mg/kg. The intraperitoneal LD(50) in white rats was 3265 mg/kg. In short-term oral studies, the no observed adverse effect level (NOAEL) was 400 mg/kg in rats and mice. In subchronic oral studies, the NOAEL was 400 mg/kg in rats and 600 mg/kg in mice. In a 16-week feeding study, rats given up to 10,000 ppm showed no signs of toxicity. Repeated inhalation of volatilized Benzaldehyde produced ocular and nasal irritation at 500 ppm and death in rabbits at 750 ppm. Undiluted Benzaldehyde was irritating to rabbit eyes, causing edema, erythema, and pain. Benzaldehyde was determined not to be a contact sensitizer, but did produce allergic reactions in a maximization test. Clinical reports of allergy to Benzaldehyde are rare. Benzoic Acid did not produce irritation or sensitization reactions in human clinical studies. Benzoic Acid also failed to produce reactions in phototoxicity and photosensitization tests. Neither Benzaldehyde, Benzoic Acid, nor Sodium Benzoate are reproductive or developmental toxicants at doses that are nontoxic to the mother. In a behavioral study, blood levels of 0.12 ng/ml Benzaldehyde produced a 44% reduction in motor activity in mice. Benzaldehyde did not produce mutations in bacterial assays, but did produce chromosomal abnormalities in Chinese hamster cells and increased mutations in a mouse lymphoma forward mutation assay. Benzaldehyde was evaluated by the National Toxicology Program, which found no evidence of carcinogenicity in rats, and some evidence of carcinogenicity in mice. Several studies have suggested that Benzaldehyde can have carcinostatic or antitumor properties. Overall, at the concentrations used in cosmetics, Benzaldehyde was not considered a carcinogenic risk to humans. Although there are limited irritation and sensitization data available for Benzaldehyde, the available dermal irritation and sensitization data and ultraviolet (UV) absorption and phototoxicity data demonstrating no adverse reactions to Benzoic Acid support the safety of Benzaldehyde as currently used in cosmetic products.

Animals↗
PubMed1976

Activated charcoal-carboxymethylcellulose gel formulation as an antidotal agent for orally ingested aspirin.

The in vivo effect on aspirin absorption of a potentially more palatable form of activated charcoal was compared to that of a simple aqueous slurry of activated charcoal. The experimental formulation consisted of 20.0 g of activated charcoal, 2.25 g of carboxymethylcellulose (CMC) and 42.8 ml of water; it was tested with and without chocolate syrup as a flavoring agent added just prior to administration. Six subjects were treated in crossover fashion following an aspirin dose of 972 mg. Total urinary excretion of salicylate was measured over 48 hours. Although all three treatments appeared to be effective in reducing the rate and extent of aspirin absorption, the slurry was significantly more effective in reducing the total amount absorbed than the charcoal-CMC gel with chocolate syrup. The slight difference in effectiveness between the gel formulation with and without the chocolate syrup was not significant.

Adult↗
PubMed2000

Plaque regrowth effects of a triclosan/pyrophosphate dentifrice in a 4-day non-brushing model.

Triclosan is a lipophilic antimicrobial agent which, when present in an aqueous dentifrice vehicle, is complexed by or in close contact with polymers and surface-active molecules, emulsifying agents, flavoring oils and other hydrophobic ingredients. Because of this, dentifrice products containing triclosan may not have triclosan in a bioavailable state and, hence, the products themselves can not be assumed to possess antimicrobial activity. In order to determine the antimicrobial effects on dental plaque of a triclosan/pyrophosphate dentifrice relative to a negative control (without triclosan or pyrophosphate), a crossover 4-day non-brushing study was conducted. Thirty-four subjects were enrolled in this randomized two-period, double-blind crossover investigation with thirty-three subjects completing all aspects. Following a baseline plaque examination and complete plaque removal at the start of the first 4-day treatment period, subjects initiated a twice-daily supervised dosing regimen, during which they rinsed with their first assigned dentifrice in slurry form while refraining from tooth-brushing and all other oral hygiene procedures. Evaluations to quantify test product effects on plaque were conducted on Day 5. After a week-long interim washout period, subjects repeated the twice daily rinsing regimen over Days 1-4 of Treatment Period 2 with their second assigned product, again with examinations on Day 5. Analysis of data demonstrated subjects had significantly (p = 0.0296) less plaque when rinsing with the triclosan/pyrophosphate dentifrice slurry as compared to the negative control dentifrice slurry; the relative treatment difference as determined by the primary examiner was 12.7%. A trainee examiner observed a 16.0% reduction on a subset of subjects (p = 0.0139). This efficacy result compares favorably with results from other studies of triclosan-containing products. The examinations for oral safety demonstrated no meaningful clinical differences between the triclosan/pyrophosphate dentifrice and control dentifrice.

Adult↗
PubMed1998

Evaluation of carcinogenic/co-carcinogenic activity of a common chewing product, pan masala, in mouse skin, stomach and esophagus.

Pan masala, a dry powdered mixture of areca nut, catechu, lime, unspecified spices and flavoring agents, has gained widespread popularity as a chewing substitute in India. In this study, the carcinogenic and tumor-promoting potential of an ethanolic pan masala extract (EPME) was determined using skin of S/RVCri-ba mice and forestomach and esophagus of ICRC mice as the target tissues. Carcinogenic activity of pan masala was tested by painting the mouse skin for 40 weeks with EPME or by gavage feeding for 6 months. Following initiation with 9,10-dimethylbenz(a)anthracene (DMBA), carcinogenesis of mouse skin was promoted with different doses of EPME, while gastric- and esophageal-tumor-promoting activity was determined by administering EPME by gavage to animals initiated with diethylnitrosamine (DEN). The ability of EPME to effect progression of skin papilloma to carcinoma and cutaneous alterations after a single or multiple EPME treatment were also evaluated. EPME at 25 mg per dose promoted skin-papilloma formation between 30 and 40 weeks of treatment and enhanced the rate of conversion of papilloma to carcinoma. Induction of mild epidermal hyperplasia, dermal edema, increase in epidermal mitotic activity and the rate of epidermal and dermal DNA synthesis by EPME correlated well with its skin-tumor-promoting potential. In ICRC mice, EPME was inactive as a complete carcinogen, but effectively promoted the development of forestomach and esophageal papilloma and carcinoma in a concentration-dependent manner. The tumor incidence at 25 mg EPME per dose was comparable with that obtained in the 12-O-tetradecanoylphorbol-13 acetate(TPA)-treated group. The findings indicate that habitual pan-masala use may exert carcinogenic and co-carcinogenic influence.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1979

Studies on some new thiosemicarbazones as potential antitubercular agents.

Twenty-one 4-aryl-3-thiosemicarbazides and their new vanillin-4-aryl-3-thiosemicarbazones have been prepared in good yield. Antitubercular activity of five of the vanillin-4-aryl-3-thiosemicarbazones was evaluated against mycobacterium tuberculosis strain H37 Ra in Löwenstein-Jensen medium. In addition to IR, biological activity and TLC studies for thiosemicarbazones were carried out.

Antitubercular Agents↗
PubMed2004

Antimutagenic activity of spearmint.

The antimutagenic activity of spearmint (Mentha spicata), a popular food flavoring agent, was studied in the Salmonella assay. Spearmint leaves were brewed in hot water for 5 min at concentrations up to 5% (w/v), and the water extracts were tested against the direct-acting mutagens 4-nitro-1,2-phenylenediamine (NPD) and 2-hydroxyamino-3-methyl-3H-imidazo[4,5-f]quinoline (N-OH-IQ) using Salmonella typhimurium strain TA98. Nontoxic concentrations of spearmint extract inhibited the mutagenic activity of N-OH-IQ in a concentration-dependent fashion, but had no effect against NPD. These experiments by design focused on the water extract consumed commonly as an herbal tea, but chloroform and methanol extracts of spearmint also possessed antimutagenic activity against N-OH-IQ. Water extract of spearmint inhibited the mutagenic activity of the parent compound, 2-amino-3-methyl-3H-imidazo[4,5-f]quinoline (IQ), in the presence of rat liver S9; however, the concentration for 50% inhibition (IC50) against IQ was approximately 10-fold higher than in assays with N-OH-IQ minus S9. At concentrations similar to those used in the Salmonella assays, spearmint extract inhibited two of the major enzymes that play a role in the metabolic activation of IQ, namely, cytochromes P4501A1 and 1A2, based on ethoxyresorufin O-deethylase and methoxyresorufin O-demethylase assays in vitro. In vivo, rats were given spearmint water extract (2%; w/v) as the sole source of drinking fluid before, during, and after 2-week treatment with IQ; colonic aberrant crypt foci were inhibited significantly at 8 weeks (P < 0.05, compared with rats given IQ alone). Collectively, these findings suggest that spearmint tea protects against IQ and possibly other heterocyclic amines through inhibition of carcinogen activation and via direct effects on the activated metabolite(s).

Animals↗
PubMed1983

Spectrophotometric promethazine hydrochloride determination using bromcresol green.

A spectrophotometric method was developed for determining promethazine hydrochloride (I) complexed with bromcresol green and then extracted with chloroform. The complex in chloroform showed maximum absorption at 415 nm and obeyed Beer's law over 1.2-8.5 micrograms/ml. The complex molar absorptivity was 1.93 X 10(4) M. Complex formation and extraction were complete and quantitative over pH 2.7-2.8. The promethazine hydrochloride-bromcresol green molar ratio was 1:1. Excipients, coloring matter, flavoring agents, and other substances likely to be present in promethazine preparations did not interfere in the determination. Direct determination in tablet, syrup, and injection preparations were carried out satisfactorily.

Bromcresol Green↗
PubMed1998

Isobutyraldehyde administered by inhalation (whole body exposure) for up to thirteen weeks or two years was a respiratory tract toxicant but was not carcinogenic in F344/N rats and B6C3F1 mice.

Isobutyraldehyde (a chemical structurally related to formaldehyde and used as a flavoring agent) was studied for toxicity and carcinogenicity by exposing male and female F344/N rats and B6C3F1 mice. Animals were exposed to isobutyraldehyde vapors 6 h per day, 5 days per week for up to 13 weeks or 2 years. In the 13-week studies, groups of 10 male and 10 female F344/N rats and B6C3F1 mice were exposed to concentrations of 0, 500, 1000, 2000, 4000, or 8000 ppm. Chemical-related body weight depression and deaths occurred in rats and mice exposed to 4000 and 8000 ppm. Necrosis of the epithelium accompanied with acute inflammatory reaction was observed in the nasal turbinate, larynx, and trachea of rats exposed to 8000 ppm. Exposure of rats to 4000 ppm resulted in metaplasia of the nasal respiratory epithelium, inflammation, degeneration of the olfactory epithelium, and osteodystrophy of the nasal turbinate bone. In the 13-week mouse study, exposure to 8000 ppm or 4000 ppm resulted in necrosis of the epithelium lining of the nasal turbinates. Osteodystrophy of the nasal turbinate bone and squamous metaplasia of the nasal respiratory epithelium were noted in mice exposed 4000 ppm. Degeneration of the olfactory epithelium was noted in males exposed 2000 ppm and in females exposed to 4000 ppm. In the 2-year studies, groups of 50 male and 50 male F344/N rats and B6C3F1 were exposed to concentrations isobutyraldehyde vapors of 0, 500, 1000, or 2000 ppm 6 h per day, 5 days per week. There were no differences in survival rates or mean body weights between exposed groups and control rats. Survival of male mice exposed to 2000 ppm and mean body weights of female mice exposed to 1000 or 2000 ppm were lower than those of the of the controls. No increase in neoplasm incidence was observed in rats and mice in the 2-year studies that could be attributed to isobutyraldehyde exposure. Chemical-related nonneoplastic lesions were limited to the nose of rats and mice. They included squamous metaplasia of the respiratory epithelium (rats), suppurative inflammation (rats), and olfactory epithelial degeneration (rats and mice) at 1000 and 2000 ppm.

Aldehydes↗
PubMed1990

Fluid replacement drinks during high intensity exercise: effects on minimizing exercise-induced disturbances in homeostasis.

The purpose of these experiments was to examine the influence of various fluid replacement drinks on exercise-induced disturbances in homeostasis during heavy exercise. Nine trained cyclists performed constant load exercise on a cycle ergometer to fatigue on three occasions with 1-week separating experiments. The work rate was set initially at approximately 85% of VO2max (range 82-88%) with fatigue being defined as a 10% decline in power output below the initial value. During each experiment subjects consumed one of the following three beverages prior to and every 15 min during exercise: (1) non-electrolyte placebo (NEP; 31 mosmol.kg-1); (2) glucose polymer drink containing electrolytes (GP; 7% CHO, 231 mosmol.kg-1), and (3) electrolyte placebo drink without carbohydrate (EP; 48 mosmol.kg-1). Both the GP and EP beverage contained sodium citrate/citric acid (C) as a flavoring agent while C was not contained in the NEP drink. Although seven of nine subjects worked longer during the GP and EP treatment when compared with the NEP trial, the difference was not significant (P greater than 0.05). No differences (P greater than 0.05) existed between the GP and EP treatments in performance time. Exercise changes in rectal temperature, heart rate, delta % plasma volume and plasma concentrations of total protein, free fatty acids, glucose, lactate, potassium, chloride, calcium, and sodium did not differ (P greater than 0.05) between trials.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2002

Highly sweet compounds of plant origin.

The demand for new alternative "low calorie" sweeteners for dietetic and diabetic purposes has increased worldwide. Although the currently developed and commercially used highly sweet sucrose substitutes are mostly synthetic compounds, the search for such compounds from natural sources is continuing. As of mid-2002, over 100 plant-derived sweet compounds of 20 major structural types had been reported, and were isolated from more than 25 different families of green plants. Several of these highly sweet natural products are marketed as sweeteners or flavoring agents in some countries as pure compounds, compound mixtures, or refined extracts. These highly sweet natural substances are reviewed herein.

Animals↗
PubMed2004

Suppression of protein kinase C and nuclear oncogene expression as possible action mechanisms of cancer chemoprevention by Curcumin.

Curcumin (diferuloylmethane) is a major naturally-occurring polyphenol of Curcuma species, which is commonly used as a yellow coloring and flavoring agent in foods. Curcumin has shown anti-carcinogenic activity in animal models. Curcumin possesses anti-inflammatory activity and is a potent inhibitor of reactive oxygen-generating enzymes such as lipoxygenase/cyclooxygenase, xanthine dehydrogenase/oxidase and inducible nitric oxide synthase; and an effective inducer of heme oxygenase-1. Curcumin is also a potent inhibitor of protein kinase C (PKC), EGF(Epidermal growth factor)-receptor tyrosine kinase and IkappaB kinase. Subsequently, curcumin inhibits the activation of NF(nucleor factor)kappaB and the expressions of oncogenes including c-jun, c-fos, c-myc, NIK, MAPKs, ERK, ELK, PI3K, Akt, CDKs and iNOS. It is proposed that curcumin may suppress tumor promotion through blocking signal transduction pathways in the target cells. The oxidant tumor promoter TPA activates PKC by reacting with zinc thiolates present within the regulatory domain, while the oxidized form of cancer chemopreventive agent such as curcumin can inactivate PKC by oxidizing the vicinal thiols present within the catalytic domain. Recent studies indicated that proteasome-mediated degradation of cell proteins play a pivotal role in the regulation of several basic cellular processes including differentiation, proliferation, cell cycling, and apoptosis. It has been demonstrated that curcumin-induced apoptosis is mediated through the impairment of ubiquitin-proteasome pathway. Curcumin was first biotransformed to dihydrocurcumin and tetrahydrocurcumin and that these compounds subsequently were converted to monoglucuronide conjugates. These results suggest that curcumin-glucuronide, dihydrocurcumin-glucuronide, tetrahydrocurcumin-glucuronide and tetrahydrocurcumin are the major metabolites of curcumin in mice, rats and humans.

Animals↗
PubMed2001

Chiral discrimination of limonene by use of beta-cyclodextrin-coated quartz-crystal-microbalances (QCMs) and data evaluation by artificial neuronal networks.

The enantiomeric composition of the chiral flavoring agent limonene was analyzed by means of a quartz-crystal microbalance (QCM) sensor. As chiral selectors three different modified beta-cyclodextrins were investigated. The selector molecules were applied as mixtures in different polysiloxane matrices. The chiral separation factors alpha for limonene obtained at 30 degrees C by gas chromatography and by use of the QCM sensor were comparable. Evaluation of sensor data was performed by use of an artificial neuronal network (ANN); this enabled prediction of the enantiomeric composition of the gas mixtures.

Cyclodextrins↗
PubMed1983

Taste and nicotine as determinants of voluntary tobacco use by hamsters.

Syrian hamsters consumed a commercial chewing tobacco in daily amounts equivalent to 2.6% of their body weights, even though food and water were always available. Daily intake increased gradually to this level over a period of 4 months. Commercial tobaccos contain a variety of flavoring agents, including sugars. Moistened, unflavored tobacco was consumed in much smaller amounts than the commercial tobacco. Addition of sucrose to the unflavored tobacco produced a concentration-dependent increase in daily consumption. Addition of nicotine to the drinking water did not affect daily fluid intake or food consumption, but produced a selective, dose-related decrease in consumption of the commercial tobacco. These results indicate interactive roles for taste and nicotine in controlling the daily, voluntary, high-level use of tobacco by hamsters.

Animals↗
PubMed1992

Suppressing effect of vanillin on chromosome aberrations that occur spontaneously or are induced by mitomycin C in the germ cell line of Drosophila melanogaster.

In order to investigate the anticlastogenic effect of vanillin on ring-X loss, D. melanogaster females exposed to different vanillin concentrations were crossed with non-treated, MMC- or MMS-treated males. The results obtained with this in vivo investigation showed a significant inhibition of vanillin in the frequencies of spontaneous ring-X loss--59, 56, 38 and 36%--at the different concentrations used. In addition, vanillin treatment caused a significant suppression of MMC-induced ring-X loss. This decrease was observed only in the first 3 days after the interruption of vanillin treatment and at the concentrations of 0.5 and 1% of this flavoring agent. In contrast, vanillin did not show any effect on chromosome loss provoked by MMS. Therefore, the ring-X loss-decreasing effect of vanillin seemed to depend on the quality of DNA lesions and consequently on a specific enzymatic repair process present in the oocytes of D. melanogaster.

Animals↗
PubMed1994

Cinnamaldehyde-induced micronuclei in rodent liver.

Cinnamaldehyde, a widely used flavoring agent, has so far been subjected to a limited range of genotoxicity tests, mainly carried out in vitro, which produced contradictory results. Therefore we have examined cinnamaldehyde using additional in vivo genotoxicity end-points. In Sprague-Dawley rats, a single oral dose equal to 1/2 LD50 did not induce DNA fragmentation in liver and gastric mucosa as evaluated by the alkaline elution technique, increased the frequency of micronucleated hepatocytes but not of bone marrow micronucleated polychromatic erythrocytes, and gave rise to a significantly higher incidence of total nuclear anomalies but not of micronucleated cells in forestomach mucosa. In Swiss mice, the equitoxic dose of cinnamaldehyde caused the same clastogenic effect in the liver, whilst a negative response was observed in both bone marrow and forestomach mucosa. Finally, in rats initiated with N-nitrosodiethylamine the administration of 500 mg/kg/day cinnamaldehyde for 14 successive days produced a modest but statistically significant increase of the average diameter and area of gamma-glutamyltranspeptidase-positive foci that, together with changes observed in other parameters, might be considered indicative of a potential promoting activity. Taken as a whole, these findings confirm that high doses of cinnamaldehyde may induce genetic alterations at the chromosomal level, and suggest that the liver is the preferential target of its undesirable effects.

Acrolein↗
PubMed1985

Benzyl acetate carcinogenicity, metabolism, and disposition in Fischer 344 rats and B6C3F1 mice.

Carcinogenesis studies of benzyl acetate (a fragrance and flavoring agent) were conducted in F344 rats and B6C3F1 mice. The chemical was given in corn oil by gavage once daily, 5 days/week for 103 weeks, to groups of 50 animals of each sex and species. For rats the doses were 0, 250, and 500 mg/kg body weight and for mice the doses were 0, 500, and 1000 mg/kg. Mean body weights of control and dosed rats and mice were not affected adversely by benzyl acetate. The survival of control and low dose female mice was lower than that of the high dose group. A genital tract infection may have contributed to the reduced survival. No other significant difference in survival was observed for dosed rats or mice. Benzyl acetate was absorbed from the gastrointestinal tract of rats and mice, with approximately 90% of the administered dose recovered as various metabolites in the urine within 24 h. The primary metabolite was hippuric acid, with minor amounts of a mercapturic acid, and one or more unidentified metabolites. This capacity for absorption, metabolism, and disposition was unaffected by the amount or number of doses administered. Under the conditions of these studies, benzyl acetate administration was associated with an increased incidence of acinar cell adenoma of the exocrine pancreas in male F344/N rats. No evidence of carcinogenicity was found for female F344/N rats. For male and female B6C3F1 mice there was evidence of carcinogenicity, in that benzyl acetate caused an increased incidence of hepatocellular neoplasms (particularly adenomas) and squamous cell neoplasms of the forestomach.

Absorption↗
PubMed2005

Vanillin suppresses in vitro invasion and in vivo metastasis of mouse breast cancer cells.

Vanillin, a food flavoring agent, has been reported to show anti-mutagenic activity and to inhibit chemical carcinogenesis. In this study, we examined the effect of vanillin on the growth and metastasis of 4T1 mammary adenocarcinoma cells in BALB/c mice. Mice orally administered with vanillin showed significantly reduced numbers of lung metastasized colonies compared to controls. In vitro studies revealed that vanillin, at concentrations that were not cytotoxic, inhibited invasion and migration of cancer cells and inhibited enzymatic activity of MMP-9 secreted by the cancer cells. Vanillin also showed growth inhibitory effect towards cancer cells in vitro. However, vanillic acid, a major metabolic product of vanillin in human and rat, was not active in these in vitro activity assays. Our findings suggest that vanillin has anti-metastatic potential by decreasing invasiveness of cancer cells. Since vanillin is generally regarded as safe, it may be of value in the development of anti-metastatic drugs for cancer treatment.

Animals↗