THE SYNTHESIS OF 4,5-DIMETHYL-1,2-BENZANTHRACENE AND 4,5,10-TRIMETHYL-1,2-BENZANTHRACENE.
Explore the source record for details and available documents.
Benz(a)Anthracenes↗
SEARCH · Search PubMed
Results for “BENZANTHRACENES”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
A comparison of the initiating and promoting actions of 9,10-dimethyl-1,2-benzanthracene and 1,2,5,6-di-benzanthracene in skin tumorigenesis.
Explore the source record for details and available documents.
9,10-Dimethyl-1,2-benzanthracene↗
Particulate enhanced membrane uptake of 1,2-benzanthracene observed by fluorescence spectroscopy: a possible role in co-carcinogenesis.
In recognition of the co-carcinogenic effects of particulate matter and chemical carcinogens, we investigated the effect of particulate silica on the rates of membrane uptake of 1,2-benzanthracene. The fluorescence emission spectra and the apparent quantum yields of benzanthracene and dependent upon adsorption to silica and upon the surface density of benzanthracene on the silica. The fluorescence spectral shifts which occur upon transfer of benzanthracene from the silica surface to phospholipid vesicles provided a convenient means to quantitate the membrane uptake of benzanthracene from particulates. The rate of benzanthracene uptake by dipalmitoyl-L-alpha-phosphatidylcholine vesicles was independent of the concentration of lipid, indicating that the rate-limiting step may involve its solubilization in the aqueous phase. These uptake rates were also independent of the surface density of benzanthracene on the silica, indicating that the benzathracene molecules are dispersed uniformly on the silica surface. Rates of membrane uptake of benzanthracene from the crystalline, microcrystalline, and the silica-absorbed states were compared, and are greatly enhanced by a reduction in crystal size. Silica-adsorbed benzanthracene had the most rapid rate of membrane uptake. Silica did not cause disruption of the lipid vesicles. These results indicate that particulates can enhance the cellular availability of the chemical carcinogens.
Benz(a)Anthracenes↗
[Mechanism of increased resistance of thyroidectomized rats to the blastomogenous effect of 9,10-dimethyl-1,2-benzanthracene in cerebellum].
In rat cerebellum development of tumor, induced by 9,10-dimethyl-1,2-benzanthracene, was accompanied by a gradual increase in concentration of corticosterone in peripheral blood and by a decrease in 5-hydroxytryptophane decarboxylase activity. Experimental athyreosis inhibited development of the tumor in cerebellum (the tumor developed in 80.8% of normothyreotic animals treated with the benzanthracene derivatives; in the athyreotic animals this figure did not exceed 55.7%), decreased the corticosterone concentration in blood and caused a subsequent decrease in the 5-hydroxytryptophane decarboxylase activity in cerebellum as compared with the corresponding values determined in rats with intact thyroid gland. These alterations are considered as possible determinants of increased resistance of thyroidectomized rats to the blastomogenous effect of 9,10-dimethyl-1,2-benzanthracene on cerebellum.
5-Hydroxytryptophan↗
Junctional and compound pigmented nevi induced by 9, 10-dimethyl-1,2-benzanthracene in skin of albino guinea pigs.
Seventy albino guinea pigs were used in the experiment to investigate the influence of 9,10-dimethyl-1,2-benzanthracene on amelanotic melanocytes. A field 5 sq cm was marked on the flank of each animal. Hairs from these fields were clipped twice a week and painted for 20 consecutive weeks with 0.3 ml of 1% 9,10-dimethyl-1,2-benzanthracene in acetone. During the 1-year observation period, pigmented sports appeared in 40 animals. Biopsies were taken under local anesthesia, and sections were prepared for light and electron microscopic observations. Melanin formation of unknown mechanism took place in the epidermal melanocytes and in the melanocytes from the outer root sheath. These melanocytes also formed junctional and compound nevi; serial sections revealed various stages of pigmented nevi development. Schwann cells did not participate in the formation of nevi. Evidence is presented that 9,10-dimethyl-1,2-benzanthracene can convert amelanotic melanocytes into melanin-producing cells in the albino guinea pig skin. In addition, this system produces an animal model for the development of junctional and compound nevi.
9,10-Dimethyl-1,2-benzanthracene↗
Effects of sialoadenectomy and epidermal growth factor administration on 9,10-dimethyl-1,2-benzanthracene-induced tumor formation in hamster cheek pouch.
The effects of removal of the submandibular gland (sialoadenectomy) and administration of human urinary epidermal growth factor on the 9,10-dimethyl-1,2-benzanthracene-induced tumor formation were investigated with the use of a hamster cheek pouch model. Syrian hamsters were treated with 0.5% 9,10-dimethyl-1,2-benzanthracene for 6 weeks. Thereafter hamsters in group 1 underwent a sham operation and those in groups 2 and 3 underwent a sialoadenectomy. Subsequently, hamsters in groups 1 and 2 were given 0.9% sodium chloride and group 3 received the human urinary epidermal growth factor at a dose of 0.25 mg/kg body weight subcutaneously three times a week for 8 weeks. Sixteen weeks after the start of the experiment, the mean number of tumors that were less than 3-mm in diameter in groups 1 and 3 was significantly greater than that in group 2 (p < 0.05). The overall incidence and mean number of all carcinomas irrespective of size showed no differences among the experimental groups. These results indicate that epidermal growth factor synthesized in the submandibular gland may enhance the induction of cheek pouch tumor.
9,10-Dimethyl-1,2-benzanthracene↗
Malignant fibrous histiocytoma induced by intra-articular injection of 9,10-dimethyl-1,2-benzanthracene in the rat. Pathological and enzyme histochemical studies.
Malignant fibrous histiocytoma (MFH) was produced by injection of 9,10-dimethyl-1,2-benzanthracene (DMBA) into the rat knee joint. The tumor was observed in or around the knee in nearly all the animals 13 to 36 weeks after the initial DMBA administration. Histologically, these lesions were of the storiform-pleomorphic type (39/58, 67.2%), myxoid type (9/58, 15.5%), or giant cell type (8/58, 13.8%). Six cell types reported in human MFH were confirmed and phagocytosis of 0.81-micron latex particles by histiocyte-like cells was noted by electron microscopic examination. Acid phosphatase, beta-glucuronidase, and alpha-naphthyl acetate esterase were positive in enzyme histochemical examinations. Acid phosphatase activity was electron microscopically noted primarily in the lysosomes and the Golgi apparatus of the histiocyte-like cells. Cells from the storiform-pleomorphic (M1) and myxoid (M2) type tumors were serially transplanted subcutaneously in the back of the rats, and are now at the thirtieth and fortieth passage, respectively. They also were studied by enzyme histochemical and electron microscopic techniques. Our observations suggested an undifferentiated mesenchymal cell origin of MFH. Transplantable MFH can be produced in rats by intra-articular injection of DMBA, and lesions thus produced are a useful experimental model for the investigation of the histogenesis and the effect of chemotherapy of MFH.
9,10-Dimethyl-1,2-benzanthracene↗
Experimental-induced sarcomas after intra-articular injection of 9-10-dimethyl-1-2-benzanthracene.
The authors describe an experimental study on rabbits whereby the development of sarcomas was induced following injection into the knee joint with 9-10-dimethyl-1-2-benzanthracene. The results of the experiment are in contrast to those of other authors as no "synovialoma" or synovial sarcoma developed but only morphological patterns which might belong to malignant fibrous histiocytoma and occasionally fibrosarcoma. In accord with our results the hypothesis is discussed that all malignant mesenchymal neoplasias result from a not clearly identifiable pluripotent mesenchymal stem cell.
9,10-Dimethyl-1,2-benzanthracene↗
The assessment of cell proliferation during 9,10-dimethyl-1,2-benzanthracene-induced hamster tongue carcinogenesis by means of histone H3 mRNA in situ hybridization.
The aim of this study was to investigate cell kinetics and ultrastructural changes during carcinogenesis using a hamster 9,10-dimethyl-1,2-benzanthracene (DMBA)-induced tongue cancer model. Five squamous cell carcinomas, five dysplastic epithelia, seven hyperplastic epithelia, and four normal epithelia were obtained from 21 hamster tongues by applying 1.0% acetone solution of DMBA on the left lingual mucosa after scratching with a root canal broach. Ultrastructural examination revealed that the number of microvilli increased, whereas that of desmosomes decreased during carcinogenesis. Cell proliferation was analyzed by means of 5-bromodeoxyuridine (BrdU) immunohistochemistry and in situ hybridization (ISH) for histone H3 mRNA. The BrdU and histone H3 mRNA labeling indices (LIs) were lowest for normal epithelium, higher for hyperplastic and dysplastic epithelia, and highest for squamous cell carcinoma. Cytoplasmic histone H3 mRNA and nuclear BrdU were localized in virtually identical areas of serial sections. The correlation coefficient for the relationship between these two LIs was 0.97 ( P << 0.001). These results suggest that the assessment of cell proliferation using H3 mRNA ISH will be a useful technique for investigating biological behavior during carcinogenesis.
9,10-Dimethyl-1,2-benzanthracene↗
Phospholipase A2 activity in 9,10-dimethyl-1,2-benzanthracene-induced mammary tumors of rats.
The activities of phospholipase A2 were compared in mammary glands from virgin and mid-pregnant rats and in 9,10-dimethyl-1,2-benzanthracene-induced rat mammary tumors. Enzyme activities were not different in the 150 000 x g pellet fractions of mammary gland homogenates from virgin and mid-pregnant rats, but enzyme activity in the 150 000 x g supernatant fraction was about twice as high in the homogenates from the mid-pregnant rat glands. Phospholipase A2 activities in the 150 000 x g pellet and supernatant fractions of homogenerates of growing tumor tissues were more than an order of magnitude higher than in the normal tissues. The elevated activity of phospholipase A2 in the tumor tissues may be related to their rapid rate of proliferation.
9,10-Dimethyl-1,2-benzanthracene↗
Involvement of protease in L-glutamine control of nucleic acid and polyphosphate metabolism in cells transformed by 9,10-dimethyl-1,2-benzanthracene, SV40 and H-ras oncogene.
Mammalian cells transformed with either 9,10-dimethyl-1,2-benzanthracene, SV40 or H-ras oncogene dramatically changed their ability to synthesize DNA and RNA and metabolize polyphosphate when L-glutamine was withdrawn from the growth medium or when heat shocked (growth at 42 degrees C). Untransformed, DNA and RNA synthesis decreased by 50-80% when glutamine was withdrawn, but polyphosphate accumulated whether or not glutamine was supplied. Heat shock did not alter this response. Transformed isogenic cells responded differently; at 37 degrees C, they decreased their synthesis of DNA and RNA if starved for glutamine, whereas at 42 degrees C, synthesis was optimal without glutamine. Transformed cells accumulated polyphosphate at 37 degrees C when starved for glutamine, but at 42 degrees C, no polyphosphate accumulated. This apparent non-dependence on glutamine by transformed cells when heat shocked was found to be due to the production of glutamine from serum proteins through induction of a protease(s).
9,10-Dimethyl-1,2-benzanthracene↗
Effect of continuous light on the incidence of 9,10-dimethyl-1,2-benzanthracene induced mammary tumors in female Holtzman rats.
The pineal has been recently implicated in mammary tumorigenesis. Effect of physiological pinealectomy brought about by subjecting female Holtzman rats to permanent lighting (24 h/day) from birth was studied on the incidence of 9,10-dimethyl-1,2-benzanthracene (DMBA) induced mammary tumors. The incidence of adenocarcinoma was 95% in animals maintained in continuous photoperiod in contrast to that (60%) observed in control animals maintained on a light/dark (10/14 h) schedule. Further, the latency period of tumor appearance (61.5 +/- 9 days) in the former group was found to be significantly shorter than that seen in the latter group (93.7 +/- 8.3 days). Explanations are offered for this difference in the observed incidence.
9,10-Dimethyl-1,2-benzanthracene↗
Pineal ablation in varying photoperiods and the incidence of 9,10-dimethyl-1,2-benzanthracene induced mammary cancer in rats.
Our earlier observation of increased incidence of 9,10-dimethyl-1,2-benzanthracene (DMBA) induced mammary carcinoma in young, virgin 'functionally' pinealectomized Holtzman rats poses the question whether or not a comparable incidence would occur in surgically pinealectomized rats reared in varying photoperiods (e.g. light/dark (LD) 24/0 or LD 10/14 schedules). Results show that functionally or surgically pinealectomized rats in LD 24/0 schedule have comparable mammary tumor incidence (95% and 83%, respectively) and latency period of tumor appearance (60 +/- 3.1 and 69.2 +/- 6.6 days, respectively). However, when surgically pinealectomized rats were kept in short photoperiods (LD 10/14), a significant difference was observed in both tumor incidence (60.9%) and latency period (91.8 +/- 11.0 days). Our data suggest that the susceptibility of the mammary gland to carcinogenic insult may be modulated by the concentration of the pineal hormone, melatonin, in the CNS.
9,10-Dimethyl-1,2-benzanthracene↗
Inhibitory effect of prostaglandin oligomeric derivatives on 9,10-dimethyl-1,2-benzanthracene-induced hamster lingual carcinomas.
The inhibitory effects of prostaglandin oligomeric derivatives OC-3186 and OC-5186 were examined in hamster lingual carcinoma induced by 9,10-dimethyl-1,2-benzanthracene (DMBA). These compounds caused a regression of 40-90% in the size of lingual carcinomas in the hamster within several days after systemic or local administration.
9,10-Dimethyl-1,2-benzanthracene↗
Effect of local administration of epidermal growth factor on 9,10-dimethyl-1,2-benzanthracene-induced tumour formation in hamster cheek pouch.
The effect of local administration of epidermal growth factor (EGF) on 9,10-dimethyl-1,2-benzanthracene (DMBA)-induced tumour formation was investigated in a hamster cheek pouch carcinogenesis model. DMBA-treated hamsters underwent either sialoadenectomy (groups 1 and 2) or a sham operation (groups 3 and 4). Thereafter, EGF (groups 1 and 3) or vehicle (groups 2 and 4) was applied to the cheek pouches for 6 weeks. Fourteen weeks after the beginning of the experiment, the number of cheek pouch tumours was significantly greater in EGF-treated hamsters than in vehicle-treated hamsters, irrespective of whether the submandibular glands had been removed. The number of forestomach tumours, induced by DMBA application to the cheek pouches, was also increased by EGF. These results suggest that EGF applied from the luminal side of the mucosa stimulates tumour formation in the hamster cheek pouch and forestomach.
9,10-Dimethyl-1,2-benzanthracene↗
Transannular dioxygenation of 9,10-dimethyl-1,2-benzanthracene by cytochrome P-450 oxygenase of rat liver.
9,10-Dimethyl-1,2-benzanthracene is oxygenated by rat liver microsomal cytochrome P-450 oxygenase to its 9,10-epidioxide. This transannular 1,4-peroxide is converted further into the diol by the microsomal preparation and NADPH. These two products constitute the majority of the metabolites found under the conditions described.
9,10-Dimethyl-1,2-benzanthracene↗
Lymph node metastases in hamster tongue cancer induced with 9,10-dimethyl-1,2-benzanthracene: association between histological findings and the incidence of neck metastases, and the clinical implications for patients with tongue cancer.
An experimental study was carried out in hamster tongue cancer induced with 9,10-dimethyl-1,2-benzanthracene (DMBA) to examine the association between the histological features and the incidence of lymph node metastases. Squamous cell carcinoma was induced in 64 of 71 hamsters exposed to DMBA 3 times weekly for a period of 10-24 weeks, and lymph node metastases were found in 8 necks. Various histological variables in the primary lesion were examined, and the mode of invasion, degree of keratinization, and stage of invasion were found to be closely related to the development of neck metastases. We then did a prospective study in 37 human patients with T1-2 tongue cancer, which also showed a close association between the incidence of neck metastases and the histological variables of mode of invasion and degree of keratinization. These experimental and clinical studies suggest that the mode of invasion and degree of keratinization may be risk factors for neck metastases that are independent of T stage, and that the indications for elective neck dissection should be re-evaluated in that light.
9,10-Dimethyl-1,2-benzanthracene↗
A possible modulatory influence of melatonin on representative phase I and II drug metabolizing enzymes in 9,10-dimethyl-1,2-benzanthracene induced rat mammary tumorigenesis.
The oncosuppressive effect of melatonin on 9,10-dimethyl-1,2-benzanthracene (DMBA) induced rat mammary tumorigenesis led us to assess its possible modulatory influence on representative hepatic and mammary drug metabolizing enzymes in DMBA treated female Holtzman rats, reared in short and long photoperiods. Melatonin treated rats in either photoperiod showed a significant induction in hepatic and mammary levels of glutathione (GSH) and cytosolic activities of glutathione S-transferase (GST) when compared with the corresponding controls, along with a significant drop in hepatic microsomal contents of cytochromes b5 and P450. This induction of GSH and GST, and depletion of cytochromes b5 and P450 by melatonin may possibly be related to its anticarcinogenic potential in this tumor model.
9,10-Dimethyl-1,2-benzanthracene↗