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At least 19 recordsLinked to original sources
PubMed2001

Enhancement of salivary secretion and neuropeptide (substance P, alpha-calcitonin gene-related peptide) levels in saliva by chronic anethole trithione treatment.

Anethole trithione, a choleretic, has been reported to be effective in the treatment of dry mouth. We have examined the effects of chronic treatment with anethole trithione on salivary secretion, substance P immunoreactive substance (SP-IS) and alpha-calcitonin gene-related peptide immunoreactive substance (alpha-CGRP-IS) concentrations in human saliva. Anethole trithione caused significant increases of saliva SP-IS concentrations from the day 13 (25.3 +/- 1.6 pg mL(-1)) to day 14 (25.8 +/- 1.7 pg mL(-1)) compared with day 1 (19.9 +/- 1.9 pg mL(-1)). Anethole trithione caused significant increase in saliva alpha-CGRP-IS concentration on day 14 (39.9 +/- 4.7 pg mL(-1)) compared with day 1 (27.7 +/- 4.7 pg mL(-1)). Anethole trithione significantly increased the sialosis volumes from day 11 to day 14 (1.6 +/- 0.1-1.7 +/- 0.2 mL) compared with the day 1 (1.2 +/- 0.2 mL). Simple linear regression of the increase in sialosis volume with saliva SP-IS (r = 0.94) and alpha-CGRP-IS (r = 0.97) concentrations was found. These results demonstrated that chronic treatment with anethole trithione affected saliva SP-IS and alpha-CGRP-IS concentration in human saliva and sialosis volume.

Adult↗
PubMed1992

Effects of chronic anethole trithione and amitriptyline treatment on rat parotid gland signalling.

The present study examines the mechanism(s) of action of anethole trithione (Sulfarlem S25) compared to the sialogogue pilocarpine. The chronic effects (7 days of treatment) of anethole trithione, pilocarpine and/or amitriptyline on autonomic receptor binding (homogenates) were measured together with parallel tests of stimulation-induced rises in delta [Ca2+]i in collagenase-isolated rat parotid acini. The results revealed that chronic treatment with amitriptyline resulted in significantly increased rises in delta [Ca2+]i after stimulation with 20 microM of carbachol or adrenaline, and a significant increase in muscarinic acetylcholine receptor density. In addition, anethole trithione also increased cholinergic and adrenergic responsiveness. The double treatment of amitriptyline and anethole trithione or amitriptyline and pilocarpine did, however, prevent the rise in delta [Ca2+]i observed under conditions when these drugs were administered alone. Furthermore, anethole trithione, but not pilocarpine, was able to prevent the amitriptyline-induced upregulation in muscarinic acetylcholine receptor density. In conclusion, the experimental data presented in this study are compatible with the hypothesis that anethole trithione might stimulate some post-receptor effect in the coupling to the secretory response. In addition, this study supports the beneficial effects of anethole trithione in treating drug-induced xerostomia.

Amitriptyline↗
PubMed1991

Acute effects of a possible sialogogue, anethole trithione, in rat parotid glands.

The present study examines the mechanism(s) of action of anethole trithione compared to the sialogogue pilocarpine. This was done by comparing the acute effects of these drugs on autonomic receptor binding (homogenates) together with parallel tests evaluating the biological activities of the receptor systems in collagenase-isolated rat parotid acini. The responses were measured as receptor-activated changes in cyclic nucleotide formation and acinar oxygen consumption. The results revealed that anethole trithione was unable to bind to muscarinic acetylcholine receptors and unable to stimulate the dynamic processes directly. It did, however, inhibit part (about 50%) of the carbachol-induced cyclic guanosine 3',5'-monophosphate (cyclic GMP) formation and O2 uptake. Furthermore, anethole trithione (greater than 1 microM) displaced [3H]prazosin (but not [3H]dihydroalprenolol ([3H]DHA] binding, without any effect upon the adrenaline-induced cyclic adenosine 3',5'-monophosphate (cyclic AMP) formation and O2 uptake. In conclusion, this study has shown that anethole trithione is not to be considered as a simple cholinergic agonist like pilocarpine, and further elucidation of the mechanism(s) of action of this agent would be useful.

Anethole Trithione↗
PubMed1988

Pharmacological studies on anethole trithione.

Pharmacological studies on trithio-p-methoxy-phenylpropene (anethole trithione, ANTT, Felviten) were performed. ANTT at a dose of 100 mg/kg, p.o. lowered the increased serum transaminases GOT and GPT, and protected the liver from injuries caused by CCl4 in mice. In other studies in vivo, ANTT at a dose of 1000 mg/kg showed no effect on the central nervous system or the autonomic nervous system. In vitro experiments with smooth muscle preparations showed no significant effects of ANTT.

Anethole Trithione↗
PubMed1997

Chemopreventive efficacy of anethole trithione, N-acetyl-L-cysteine, miconazole and phenethylisothiocyanate in the DMBA-induced rat mammary cancer model.

The chemopreventive efficacy of N-acetyl-L-cysteine (NAC), anethole trithione, miconazole and phenethylisothiocyanate (PEITC), each of which would be expected to alter carcinogen metabolism, was examined in the dimethylbenzanthracene (DMBA) mammary carcinogenesis model. In this protocol, animals were exposed to non-toxic doses of the chemopreventives in the diet beginning 7 days prior to DMBA administration and then continuously throughout the duration of the assay (100 days post carcinogen). Miconazole, an antifungal agent with relatively broad inhibitory activity toward a variety of cytochromes P450, increased mammary tumor latency, decreased tumor incidence at the highest dose and decreased tumor multiplicity up to 60%. Anethole trithione, a substituted dithiolthione and an analog of the relatively broad-spectrum chemopreventive oltipraz, was administered in the diet and significantly inhibited mammary cancer multiplicity but not cancer incidence. NAC, an antimucolytic agent, failed to inhibit DMBA-induced mammary tumorigenesis. Surprisingly, treatment with DMBA plus PEITC, a potent inhibitor of cytochrome P450 2E1, actually increased the multiplicity of tumors relative to that observed with DMBA alone.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1989

Enhancement of phosphatidylinositol turnover and cyclic nucleotide accumulation by chronic anethole trithione treatment in rat submaxillary glands.

The effect of chronic treatment with anethole trithione (ANTT) on the phosphatidylinositol (PI) turnover and cyclic (c)AMP and cGMP accumulation in rat submaxillary glands (SMG) has been compared with the effect of chronic treatment with atropine and a cholinesterase inhibitor, diisopropylfluorophosphate (dyflos, DFP). Experiments were performed 24, 48 and 24 h after the last dose of ANTT, atropine and dyflos, respectively. ANTT and atropine enhanced carbachol-stimulated [32P] incorporation into phosphatidic acid in the SMG slices, while dyflos showed no effect. Pilocarpine-stimulated in-vivo incorporation of [3H]myoinositol into inositol phosphates was significantly enhanced by ANTT, but not by atropine or by dyflos. Phospholipase C-dependent hydrolysis of phosphatidylinositol 4,5-bisphosphate was significantly enhanced by ANTT and atropine, but not by dyflos. Pilocarpine-stimulated in-vivo accumulation of cAMP and cGMP was enhanced by ANTT and atropine, but dyflos reduced cAMP accumulation without affecting cGMP accumulation. The enhancement of PI turnover and cyclic nucleotide accumulation seems to contribute to the development of supersensitivity of the salivary gland caused by chronic treatment with ANTT and atropine, while reduction of cAMP accumulation may be responsible for the subsensitivity caused by dyflos.

Anethole Trithione↗
PubMed2006

HPLC determination of anethole trithione and its application to pharmacokinetics in rabbits.

To evaluate the relative bioavailability of anethole trithione (ATT) from self-microemulsifying drug delivery system (SMEDDS) and tablet, a sensitive, accurate and reliable liquid chromatography method was developed and validated to determine ATT in rabbit plasma. Chromatographic separation was performed on a Diamonsil C18 column by using a mixture of methanol-water (90:10, v/v) delivered at a flow rate of 1.0 ml/min. The wavelength was set at 348 nm and mifepristone was used as the internal standard. A linear relationship for ATT was found in the range of 0.5-32 ng/ml. The mean extraction recoveries of ATT determined over three concentrations were 84.7+/-5.8, 92.3+/-3.4 and 89.9+/-5.1%. After administration of SMEDDS and tablets to rabbits, significant differences were found in main pharmacokinetic parameters of Tmax, Cmax and AUC(0-infinity) between these two formulations, and a 2.5-fold enhancement of relative bioavailability of ATT was observed from the SMEDDS compared with tablets.

Anethole Trithione↗
PubMedDate not supplied

Enhancement of salivary secretion by chronic anethole trithione treatment.

Effect on salivary secretion of a single dose and of chronic treatment with trithio-p-methoxyphenylpropene (anethole trithione; ANTT) was investigated in mice, rats and rabbits in relation to changes in function of the autonomic nervous system. Chronic treatment with ANTT enhanced salivary secretion induced by pilocarpine or electrical stimulation of the parasympathetic nerve, but had no effect on salivary secretion induced by isoproterenol or phenylephrine. A single dose of ANTT had no effect on salivary secretion. Chronic treatment with ANTT prevented the inhibition of parotid salivary secretion caused by atropine in rabbits. Choline acetyltransferase and acetylcholinesterase activities in rat submaxillary glands were not affected by chronic treatment with ANTT. These results suggest that chronic treatment with ANTT may enhance salivary secretion by stimulating the postjunctional secretory process involved in the parasympathetic nervous system.

Anethole Trithione↗
PubMed1984

Chronic anethole trithione treatment enhances the salivary secretion and increases the muscarinic acetylcholine receptors in the rat submaxillary gland.

Chronic treatment with trithio-p-methoxyphenylpropene (anethole trithione; ANTT) increased the salivary secretion from the rat submaxillary gland induced by electrical stimulation of the parasympathetic nerve and by injection of pilocarpine. In parallel with the enhancement of the salivary secretion, the number of the muscarinic acetylcholine receptors was significantly increased. The increased number of receptors may be involved in the enhancement of the salivary secretion by ANTT treatment.

Anethole Trithione↗
PubMed1999

Treatment of xerostomia with the bile secretion-stimulating drug anethole trithione: a clinical trial.

BACKGROUND: Saliva protects the oral mucosa, inhibiting microbial overgrowth. Hyposalivation, therefore, induces multiple oral disorders, although treatment of hyposalivation is very difficult. METHODS: A cholagogue, anethole trithione (AT) was administered to patients with symptomatic hyposalivation (xerostomia) caused by senile hypofunction (4 men and 17 women; senile group), medications (6 men and 17 women; drug group), and oral cancer therapy (two men and three women; cancer group). For control groups, an artificial saliva was administered to 45 patients consisting of senile hypofunction (10 men and 16 women), drug-induced xerostomia (3 men and 10 women) and oral cancer therapy-induced xerostomia (four men and two women). RESULTS: Two weeks after administration of AT (6 tablets per day), both nonstimulated salivary flow rate (SFR) and stimulated SFR increased in a statistically significantly manner from 0.76 +/- 0.41 and 5.18 +/- 3.02 to 1.54 +/- 1.33 (P<0.05) and 9.07 +/- 4.10 mL/10 min (P<0.05), respectively. Of the three groups, the drug group showed the largest increases in both SFRs, from 0.90 +/- 0.54 and 6.29 +/- 4.12 to 1.69 +/- 1.65 and 12.09 +/- 5.10 mL/10 min (P<0.05 and P<0.02, respectively). Patients in the control group had almost constant SFRs. After AT administration, the salivary viscosity was, however, mildly decreased and concentrations of secretory-immunoglobulin A, lactoferrin, potassium, and chloride in nonstimulated saliva were almost constant. Corresponding with the increase of salivation, oral discomfort and inflammation were improved or resolved in 41 patients of the AT group within about 4 weeks, whereas improvement was observed in only nine patients of the control group. CONCLUSIONS: These results indicate that AT sufficiently stimulates salivation and improves xerostomia.

Adult↗
PubMed1993

Chemoprevention of colon carcinogenesis by organosulfur compounds.

It has been reported that several naturally occurring and related synthetic organosulfur compounds exert chemopreventive effects in several target organs in rodent models. The chemopreventive actions of 40 and 80% maximum tolerated doses (MTD) of organosulfur compounds, namely anethole trithione, diallyl disulfide, N-acetylcysteine, and taurine, administered in AIN-76A diet, on azoxymethane (AOM)-induced neoplasia were investigated in male F344 rats. Also, the effects of these agents on the activities of phase II enzymes, namely glutathione S-transferase (GST), NAD(P)H-dependent quinone reductase, and UDP-glucuronosyl transferase, in the liver and colonic mucosa and tumors were assessed. The MTD levels of anethole trithione, diallyl disulfide, N-acetylcysteine, and taurine were determined in male F344 rats and found to be 250, 250, 1500, and 1500 ppm, respectively. At 5 weeks of age, animals were fed the control diet (AIN-76A) or experimental diets containing 40 or 80% MTD levels of each test agent. All animals in each group, except those allotted for vehicle (saline) treatment, were administered AOM s.c. at a dose rate of 15 mg/kg body weight once weekly for 2 weeks. All animals were necropsied during week 52 after the second AOM injection. Colonic mucosal and tumor and liver enzyme activities were measured in animals fed 80% MTD levels of each test agent. Colon tumors were subjected to histopathological evaluation and classified as invasive or noninvasive adenocarcinomas. Colon tumor incidence (percentage of animals with tumors) and tumor multiplicity (tumors/animal) were compared among various dietary groups. The results indicated that administration of 200 ppm (80% MTD) anethole trithione significantly inhibited the incidence and multiplicity of both invasive and noninvasive adenocarcinomas, whereas feeding of 100 ppm (40% MTD) anethole trithione or 100 (40% MTD) or 200 ppm (80% MTD) diallyl disulfide suppressed only invasive adenocarcinomas of the colon. Although diets containing N-acetylcysteine and taurine inhibited colon tumor multiplicity, the effect was somewhat marginal. GST, NAD-(P)H-dependent quinone reductase, and UDP-glucuronosyl transferase activities in colonic mucosa and tumor and liver were significantly elevated in animals fed anethole trithione or diallyl disulfide, compared to those fed the control diet. N-Acetylcysteine and taurine slightly but significantly increased only the GST activity in the liver. Although other mechanisms are not excluded, inhibition of AOM-induced colon carcinogenesis by anethole trithione and diallyl disulfide may be associated, in part, with increased activities of phase II enzymes such as GST, NAD(P)H-dependent quinone reductase, and UDP-glucuronosyl transferase in the liver and colon.

Acetylcysteine↗
PubMed1986

[Protective effect of malotilate (diisopropyl 1,3-dithiol-2-ylidenemalonate) on chemical-induced hepatotoxicity].

Protective effect of malotilate on the liver injuries induced by several hepatotoxins was studied in mice and rats. Malotilate suppressed the elevation of plasma glutamate pyruvate transaminase (p-GPT) activity induced by chloroform (CHCl3) in rats when the animals were treated with 25 mg/kg or more dose of malotilate at 6 hours prior to the treatment with CHCl3. The effect was observed even in the rats treated with malotilate 24 or 48 hours prior to the treatment with CHCl3. Malotilate, when orally administered 6 hours prior to treatment with hepatotoxins such as CHCl3, allyl alcohol, bromobenzene, dimethylnitrosamine or thioacetamide, suppressed the elevation of p-GPT activity, liver triglyceride content and/or the decrease of bromosulphalein clearance induced by these hepatotoxins in mice. Anethole trithione, which was used as a possible protective agent against chemical-induced hepatotoxicity, tended to normalize changes in the parameters induced by the most of these hepatotoxins, but enhanced the elevation of p-GPT activity induced by CHCl3. In a case of CHCl3-induced liver injury, the protective effect of malotilate was histopathologically confirmed. Malotilate and anethole trithione reduced p-nitroanisole 0-demethylation activity in rat liver 6 hours after the administration but increased or tended to increase the activity 48 hours after the administration. Malotilate showed a protective effect on the liver injury induced by CHCl3 even when the activity of drug metabolizing enzymes in the liver was increased, although anethole trithione enhanced the CHCl3-induced liver injury regardless of the activity of drug metabolizing enzymes.

Alanine Transaminase↗
PubMed1987

Systemic therapy of salivary gland hypofunction.

Salivary gland hypofunction occurs most often as a consequence of numerous drug therapies, anti-neoplastic treatments, or systemic disease. There are no universally accepted means of treating gland dysfunction and the resultant subjective xerostomia. A few studies have suggested that treatment of underlying inflammatory connective tissue disease will improve salivary performance in Sjögren's syndrome. Most of these reports, however, have either been limited to a small number of patients or have failed to include objective measures of salivary gland output. A larger body of literature deals with attempts using many different sialogogues to stimulate salivary function in a variety of conditions. Again, many studies have failed to document salivary improvement objectively. Recently, interest has focused on three drugs: bromhexine, anethole-trithione, and pilocarpine hydrochloride. Studies with these agents are reviewed, and current clinical investigations with pilocarpine are presented in detail.

Anethole Trithione↗
PubMedDate not supplied

Chemoprevention of colon cancer by minor dietary constituents and their synthetic analogues.

Large bowel cancer is one of the leading causes of cancer deaths in the United States and other Western countries. Based on epidemiologic and mechanistic studies, preclinical studies were designed to evaluate the chemopreventive efficacy of several nonsteroidal antiinflammatory drugs (NSAIDs) and phytochemicals and their synthetic analogues in colon carcinogenesis. These studies demonstrated that NSAIDs such as piroxicam, ibuprofen, aspirin and sulindac, D,L-alpha-difluoromethylornithine, oltipraz, anethole trithione, and diallyl disulfide inhibited colon adenocarcinomas. These results provide compelling rationale to pursue clinical trials in humans.

Adenocarcinoma↗
PubMedDate not supplied

Chemoprotective effects of two dithiolthiones and of butylhydroxyanisole against carbon tetrachloride and acetaminophen toxicity.

Administration of tert-butyl-4-hydroxyanisole or of two dithiolthiones to female CD-1 mice protected against the acute toxic effects of two hepatotoxic agents, acetaminophen and carbon tetrachloride. Reduced mortality of mice was observed following pretreatment with tert-butyl-4-hydroxyanisole or dithiolthiones. Pretreatment reduced or prevented hepatic glutathione depletion produced by these two hepatotoxic agents. Liver damage, i.e., as determined by serum transaminase and sorbitol dehydrogenase activities, was less after pretreatment with tert-butyl-4-hydroxyanisole or dithiolthiones. Administration of dithiolthiones resulted in increased (from four- to over six-fold) activities of liver glutathione-S-transferases.

Acetaminophen↗
PubMed2001

Lens epithelial cell protection by aminothiol WR-1065 and anetholedithiolethione from ionizing radiation.

Lens epithelium disorganization, glutathione (GSH) depletion, and epithelial cell death have been incriminated in the cytopathogenic mechanisms that lead to cataract formation following UVB and x-ray exposures. The objective of this study was to determine the in vitro capacity of the aminothiol WR-1065, the active metabolite of amifostine, and anetholedithiolethione (ADT or Sulfarlem) to protect bovine lens epithelial cells against x-ray irradiation. WR-1065 and ADT were used at a concentration of 20 microM. A single dose of 10 Gy was delivered at a rate of 2 Gy/min. Fluorimetric assays were then performed using a neutral red probe to evaluate cell viability, a Hoechst 33342 probe (HO) to evaluate nuclear condensation and apoptosis, and a monobromobimane probe to estimate the intracellular GSH pool. Twenty-four hours after x-ray exposure, cells pretreated with WR-1065 showed increased GSH levels, improved cell viability, and decreased HO fluorescence in addition to a lesser proportion of cells with apoptotic nuclear modifications. Between 72 and 120 hr postirradiation, ADT-pretreated cells also showed increased intracellular GSH levels and cell viability and decreased HO fluorescence and apoptotic cell morphology. This in vitro study demonstrates that WR-1065 and ADT protects lens epithelial cells from x-ray injury; thus, ADT and amifostine are appropriate candidates for clinical trials in humans. They are currently used in preventing radiation-induced xerostomia and should be further tested in the prevention of late radiation-induced ocular complications such as sicca syndrome and cataract.

Amifostine↗