Biomedical subjects

F Furukawa

Publications and source records attributed to F Furukawa.

At least 217 records · Page 12Linked to original sources

PubMed1990

Binding of antibodies to the extractable nuclear antigens SS-A/Ro and SS-B/La is induced on the surface of human keratinocytes by ultraviolet light (UVL): implications for the pathogenesis of photosensitive cutaneous lupus.

Autoantibodies to the non-histone nucleoprotein antigens SS-A/Ro, SS-B/La, and RNP are highly associated with photosensitive cutaneous lupus erythematosus (LE). In order to better understand the potential mechanisms of ultraviolet (UV) light on photosensitivity in patients with cutaneous LE, we designed immunopathologic in vitro and in vivo experiments to evaluate the effects of UV on the binding of such autoantibodies to the surface of human keratinocytes, one major target of immunologic damage in photosensitive LE. Short-term 2% paraformaldehyde fixation of suspensions of cultured human keratinocytes previously incubated with monospecific antiserum probes enabled the detection of ENA expression on the cell surface by flow-cytometry analysis. UVB light (280-320 nm) induced the binding of monospecific antibody probes for SS-A/Ro and SS-B/La on keratinocytes in a dose-dependent pattern with maximal induction observed at the dose of 200 mJ/cm2 UVB. Binding of SS-A/Ro, SS-B/La, and RNP antibody was augmented strongly, but binding of anti-Sm was very weak. In contrast, UVA (320-400 nm) light had no effect on the induction of binding of these antibody probes. Identical results were seen by standard immunofluorescence techniques. Hydroxyurea-treated keratinocytes showed similar induction of those antigens by UVB irradiation, which suggested that ENA expression on cultured keratinocytes by UVB were cell-cycle independent. Tunicamycin, an inhibitor of glycosylation of proteins, reduced UVB light effect on the SS-A/Ro and SS-B/La antigen's expression. These in vitro FACS analyses revealed that ENA augmentation on the keratinocyte cell surface was dose dependent, UVB dependent, glycosylation dependent, and cell-cycle independent. In vivo ENA augmentation on the keratinocyte surface was examined in suction blister epidermal roofs. Specific antibody probes for SS-A/Ro, SS-B/La, RNP, and Sm bound to human keratinocytes in intact suction blister epidermis following UVL irradiation in vivo. Using three different protocols, we have demonstrated that antibodies to SS-A/Ro, SS-B/La, and U1RNP bind to UVL-irradiated human keratinocytes. We speculate that this antibody binding is an important inducer of antibody dependent keratinocyte damage in photosensitive cutaneous lupus.

Antibodies↗

PubMed1990

Serotonin metabolism in the arthus reaction.

To better characterize the role of serotonin in the Arthus reaction, we examined the concentration of the amine and the activities of serotonin-metabolizing enzymes, monoamine oxidase (MAO) and serotonin-N-acetyltransferase (NAT), in reaction sites induced in guinea pig skin. The specific activity of total MAO in the intact skin was 108.0 +/- 15.9 pmol/min/mg protein, and consisted of about 92% of type A activity and 8% of type B. The activity of total MAO was about 10 times greater than that of NAT. Total MAO activity increased to 130%-150% of control levels at 2 h after initiation of the reaction and approximated the control level at 3 to 6 h. Subsequently, the activity decreased linearly to 50% at 12 h and to 20% at 24 h. Although the time-dependent changes of MAO type A activity were similar to those of total MAO activity, MAO type B activity increased to 42% at 30 min, remained at 30%-40% until 6 h, and then decreased to 20% at 12 h and to 5% at 24 h. NAT activity in the reaction sites decreased with time to 50% of the control at 30 min and to 35% at 4 h and was stationary until 24 h. The serotonin concentration decreased linearly with time to 16% of the control level at 1 h, increased sharply to 240% at 6 h, and remained at more than 200% until 24 h. This biphasic change in serotonin concentration seems to be related to the dynamic changes in the activities of serotonin-degrading enzymes. In addition, the accumulation of platelets in the reaction sites may increase serotonin concentration and MAO activity subsequent to 1 h after the initiation.

Animals↗

PubMed1990

Urothelial damage and tumor initiation by urinary metabolites of sodium o-phenylphenate in the urinary bladder of female rats.

Intravesical instillation of 2-phenyl-1,4-benzoquinone (PBQ), a metabolite of sodium o-phenylphenate (Na-OPP), at a concentration of 0.1% in saline caused acute epithelial injury, prolonged inflammation and epithelial hyperplasia in female F344 rats. Ten such instillations of PBQ within 5 weeks resulted in the development of preneoplastic lesions of the urinary bladder epithelium when followed by 5% sodium saccharin feeding for 31 weeks. Since neither urothelial damage nor tumor-initiating activity was observed with either Na-OPP itself or another metabolite, phenylhydroquinone, PBQ may play an essential role in Na-OPP urinary bladder carcinogenesis.

Administration, Intravesical↗

PubMed1990

Inhibitory effects of antioxidants on N-bis(2-hydroxypropyl)nitrosamine-induced lung carcinogenesis in rats.

Potential second-stage modifying effects of 8 antioxidants on lung tumorigenesis initiated by N-bis(2-hydroxypropyl)nitrosamine (DHPN) were examined in male F344 rats. After an initial 2-week treatment with DHPN (0.1% in drinking water), rats were administered one of the antioxidants supplemented in the diet for 30 weeks. Although the incidences of lung adenomas were not affected, those of carcinomas were lowered by 2% butylated hydroxyanisole (BHA, 2 rats/20 rats), 1% butylated hydroxytoluene (BHT, 1/20), 0.8% ethoxyquin (EQ, 3/20) and 1% a-tocopherol (a-TP, 2/20) treatments as compared to the control level (9/20), while 5% sodium L-ascorbate (SA), 0.8% catechol (CC), 0.8% resorcinol (RN), and 0.8% hydroquinone (HQ) did not exert any significant effect on incidence. Quantitative analysis of adenomas and carcinomas (numbers and areas of lesions per unit area of lung section) revealed obvious inhibitory effects of SA, CC, and RN as well as BHA, BHT, EQ, and a-TP. Among the antioxidants, BHT exerted the strongest inhibitory activity. In contrast, DHPN-induced thyroid tumorigenesis was significantly enhanced by BHT (14/20) and EQ (20/20) treatments (control = 5/20). Thus the antioxidants showed opposite effects on lung and thyroid carcinogenesis in the rat.

Adenoma↗

PubMed1990

[Lectin reactivity in the kidney of newborn rat compared to adult rat].

The distribution of binding sites for 13 lectins with different specificities was studied in adult and new-born rat kidney tissue by staining paraffin sections with the ABC method. Various segments of the uriniferous tubule in both rats showed differential affinity for lectins. None of these lectins showed any reactivity with the immature developmental components of kidney like S-shaped bodies and mesonephric blastema. In the new-born rat kidney, the reactivity of 4 lectins (DBA, PNA, SBA and WGA) on the proximal tubules was very weak compared with the adult rat. Seven lectins (RCA-I, BSL-I, WGA, UEA-I, PHA-E, PSA, LCA), which stained the glomerulus of adult rats, failed to react with glomerular turf in new-born rat kidneys. On the contrary, 4 lectins (RCA-I, WGA, UEA-I and PHA-E) out of these 7 lectins stained the surface of podocyte in the new-born kidney. Colloidal iron stained glomerular turf in adult rats also showed less reactivity in immature glomerulus. These results suggested that changes in lectin binding reactivity are associated with the development and the differentiation of the rat kidney.

Animals↗

PubMed1990

[Effects of crude soybean trypsin inhibitor on pancreatic atrophy induced by BOP treatment in hamsters].

Experiment I: Female Syrian golden hamsters were given 5 weekly sc injections of N-nitrosobis (2-oxopropyl)amine (BOP) while simultaneously being treated with SBTI diet for 5 weeks (BOP+ SBTI). Other two groups were treated with BOP or SBTI alone. Sacrificed at week 30, the numbers of both adenocarcinomas and dysplastic lesions were decreased in the BOP+SBTI group relative to the BOP alone group. Experiment II: Female hamsters were given 3 weekly sc injections of BOP and then fed a SBTI diet for 40 weeks. The numbers of dysplastic lesions was decreased in the BOP and SBTI group relative to the BOP alone group. An inhibitory effect was observed for the pancreas in hamsters fed SBTI after BOP treatment. In experiments I and II, atrophic changes of pancreatic exocrine tissues and fatty tissue infiltration were observed in hamsters treated with BOP. The ratios of exocrine atrophy in pancreas sections were measured with the aid of an image processor. Areas (2.4 mm2) of splenic and gastric lobes were selected randomly, and the included exocrine tissue measured to allow calculation of percentage area of exocrine tissue atrophy. In hamsters simultaneously treated with BOP and SBTI, the percent areas of intact exocrine tissues in both splenic and gastric lobes were significantly higher (87% and 83%) as compared to the BOP group values (61% and 61%), at the level of p < 0.01, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗

PubMed1990

[Early histopathological changes in trachea, bronchus and lung, and changes in lipid peroxidation in hamsters, due to inhaled cigarette smoke].

The main objective of this work was to determine the influence of cigarette smoke exposure on the mechanisms which promote respiratory tumors. And another aim was the accumulation of basic data regarding the effect of cigarette smoke exposure in hamsters in the Hamburg II smoking machine. Male Syrian golden hamsters were caused to inhale cigarette smoke in the Hamburg II smoking machine. The hamsters inhaled cigarette smoke twice a day, for 9 minutes, 5 times a week. The administration period were 1,2,4,8 and 12 weeks. For each inhalation, the rotating disk was fitted with 30 cigarettes. Each puff, 35 ml in volume, was diluted seven times with room air. At the completion of administration, subjects were examined histopathologically, and lung and serum lipid peroxidation levels were also measured. Histopathological examination of the respiratory tract and alveolar epithelium disclosed no cigarette smoke-related hyperplastic lesion in any animal. And in the hamsters which inhaled cigarette smoke, "smoke cells" accumulation were observed in the alveolar space after 8 and 12 weeks exposure. Significant increase in the number of BrdU positive cells were not observed following cigarette smoke exposure, but a tendency for lung malondialdehyde (MDA) levels to increase was evident. On the other hand, serum lipid peroxide (LPO) levels showed a marked decrease in the animals exposed to cigarette smoke for 2,4 and 8 weeks in comparison with the identically handled control animals. But serum LPO levels showed a tendency to increase with cigarette smoking during all experimental periods. The above results suggested that cigarette smoking may cause a change in lipid peroxidation levels such as lung MDA and serum LPO levels.

Animals↗

PubMed1990

[Ultrastructural localization of myelin bodies and acid phosphatase activities in the liver and kidney induced by quinacrine in rats].

Electron microscopic studies were conducted to reveal the ultrastructural aspects of the myelin body and acid phosphatase activity in rats induced by quinacrine, an antimalarial drug. Each of 22 rats in three groups were examined. The first group of control rats was initially given a single i.p. dose (200 mg/kg) of diethylnitrosamine (DEN) only and then fed a CRF-1 basal diet for 8 weeks. The second and third group were treated with DEN or saline, and starting 2 weeks later, were fed a CRF-1 basal diet supplemented with 500 ppm quinacrine for 6 weeks. All animals were subjected to a partial hepatectomy at week 3, and then sacrificed at week 8. Liver and kidney tissues specimens from 2 rats per group were collected for routine electron microscopic study. Furthermore, the activity of acid phosphatase, a key enzyme for lysosomal activity, was also investigated. In this study, tissues were fixed with a solution of 2.5% glutaraldehyde in 0.1 M sodium cacodylate buffer. After fixation, tissues were frozen and their 8 microns sections were treated with Gomori's lead nitrate buffer solution, and post-fixed with a 1% osmium solution. After being embedded in Epon 812, ultrathin sections were made. Intracellular myelin bodies were observed in the hepatocytes, interlobular bile duct cells, renal glomerular podocytes and renal tubular cells in the quinacrine treated groups, but not were observed in rats treated with DEN alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid Phosphatase↗

PubMed1990

[Twenty-eight day repeated dose toxicity test of dicyclopentadiene in F344 rat].

A twenty-eight day repeated dose toxicity test of dicyclopentadiene (DCPD) was carried out in male and female F344 rats at the dose levels of 200, 40, 8 or 0 mg/kg/day. Thirty six animals of both sexes were divided into 6 groups of equal number. All groups were treated i.g. administration for 28 days daily, and two groups of them, at the dose levels of 200 and 0 mg/kg, were used for investigation of recovery. Inhibition of body weight gain was observed in the 200 mg/kg groups in both sexes and the 40 mg/kg group in male, but in female this inhibition was recovered at day 17 of the treatment. Increases in liver and adrenal gland weights, and decrease in thymus weight were noted in the 200 mg/kg groups in both sexes, and increase in kidney weight was also observed in the 200 and 40 mg/kg groups in male. On histopathological examination, hypertrophy of the adrenal cortex, and foamy cytoplasm in hepatocytes were observed in the 200 mg/kg groups of both sexes. Repair of histopathological lesions occurred within 14 days resting period. Based on these findings, it was concluded that the No Observed Effect Level of DCPD would be 8 mg/kg/day.

Administration, Oral↗

PubMed1990

[Lipid peroxidation as a biological marker of mucosal changes in the stomach].

Dose-related increase of malondialdehyde (MDA) was found in both gastric mucosa and urine after 5-week administration of 4.0, 2.0, 1.0, 0.5, 0.25 or 0% NaCl supplemented diet to rats. NaCl, a gastric tumor promoter, is associated with enhanced lipid peroxidation in the gastric mucosa. The urinary MDA level was found to be a good indicator of lipid peroxidation state in the gastric mucosa, higher levels of MDA in the urine clearly correlating with data for stomach glandular tissue. In man, elevation of MDA was also observed in the urine of patients with gastric lesions such as chronic gastritis, precancerous and cancer, as well as in individuals suffering from liver and kidney disease.

Animals↗

PubMed1989

Determination of thiols and disulfides in normal rat tissues and hamster pancreas treated with N-nitrosobis(2-oxopropyl)amine using 4-(aminosulfonyl)-7-fluoro-2,1,3-benzoxadiazole and ammonium 7-fluoro-2,1,3-benzoxadiazole-4-sulfonate.

Biological thiols and disulfides in rat and hamster tissues were simultaneously determined by HPLC-fluorescence detection using 4-(aminosulfonyl)-7-fluoro-2,1,3-benzoxadiazole (ABD-F) and ammonium 7-fluoro-2,1,3-benzoxadiazole-4-sulfonate (SBD-F). The coefficients of variation (CV) of the method for reduced glutathione (GSH) and oxidized glutathione (GSSG) in liver and for cysteine (CySH) and cystine (CySSCy) in kidney were less than 3.1%. In 11 tissues of Wistar rats (liver, spleen, heart, lung, stomach, bladder, ovary, uterus, adrenal, kidney and pancreas), only CySH, CySSCy, GSH and/or GSSG were detected. Other thiols and disulfides were at extremely low levels in all samples. Both concentrations of CySH and CySSCy in the livers of old rats (111 weeks old, F344) were significantly higher than those of young rats (8 weeks old) (CySH, 0.246 +/- 0.099 vs 0.130 +/- 0.020 mumol/g; CySSCy, 0.051 +/- 0.027 vs 0.013 +/- 0.002 mumol/g). Administration of N-nitrosobis(2-oxopropyl)amine (BOP), a selective carcinogen of hamster pancreatic cancer, to Syrian golden hamsters (38 weeks old) resulted in the increase in the pancreas of GSH to a level 19 times as high and of GSSG to a level 14 times as high as those in untreated hamsters (GSH, 1.173 +/- 0.272 vs 0.062 +/- 0.017 mumol/g; GSSG, 0.155 +/- 0.063 vs 0.011 +/- 0.001 mumol/g).

Animals↗

PubMed1989

Evaluation of ATPase-positive Langerhans' cells in skin lesions of lupus erythematosus and experimentally induced inflammations.

We examined the time-dependent dynamics of epidermal Langerhans' cells (LC) in human systemic lupus erythematosus (SLE), in MRL/Mp-lpr/lpr(MRL/lpr) mice, and in various experimental cutaneous inflammations, such as the Arthus reaction, dinitrochlorobenzene allergic dermatitis, and croton oil primary irritant dermatitis, in order to clarify the pathomechanisms of lupus skin lesions. The numbers of LC in untreated SLE patients with newly developed skin lesions decreased in the central lesional sites and increased significantly in the peripheral lesional sites. In MRL/lpr mice, the number of LC increased significantly in the central lesional sites during the initial stage and increased in the peripheral lesional sites and decreased in the central lesional sites 2-4 weeks after the onset of skin lesions. In contrast, with experimental cutaneous inflammations of guinea pigs, the increase in numbers of LC in the peripheral lesional sites was not significant during the time course of the reaction. These results suggest that the increased numbers of LC during the active and early stages of skin lesions in human SLE and MRL/lpr mice are closely related to the specific spontaneous development of skin lesions, unlike the dynamics of LC in experimental cutaneous inflammations.

Adenosine Triphosphatases↗

PubMed1989

Elevated activity of pancreatic type amylase in the urine as an early indicator of pancreatic tumors in hamsters.

Levels of amylase isozymes in the urine and serum of Syrian hamsters during pancreatic carcinogenesis, induced by N-nitrosobis(2-oxopropyl)amine (BOP), were investigated. BOP was injected subcutaneously (sc) into female Syrian golden hamsters at a dose of 10mg/kg once weekly for 6 wk and amylase activities in urine and serum samples were measured every other week from the first treatment of BOP. Although total amylase in the urine showed no remarkable changes, the pancreatic type isozyme demonstrated only very low levels for the first 6 wk and then from wk 8, became elevated showing continuously high levels in all animals thereafter. Animals were sacrificed at wk 10, 14, and 18. Dysplastic lesions of the pancreas developed in all the hamsters investigated. Furthermore, pancreatic adenocarcinomas were also observed in all animals sacrificed at wk 18. Thus, the results suggest that measurement of pancreatic isoamylase in the urine might allow early indication of pancreatic tumor development in hamsters.

Adenocarcinoma↗

PubMed1989

Susceptible cytotoxicity to ultraviolet B light in fibroblasts and keratinocytes cultured from autoimmune-prone MRL/Mp-lpr/lpr mice.

The MRL/Mp-lpr/lpr (MRL/l) mouse is an autoimmune model of spontaneous lupus erythematosus (LE), in addition to lupus nephritis. In order to better understand the mechanisms of photosensitivity in LE, in vitro photocytotoxicity was examined by using fibroblasts and keratinocytes cultured from MRL/l mice, control MRL/Mp- +/+ (MRL/n) mice, and normal BALB/c mice. A colorimetric 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay and the acridine orange/ethidium bromide assay were used for determination of cytotoxicity. Fibroblasts cultured from newborn MRL/l mice showed higher susceptibility to single ultraviolet light B (UVB) light irradiation at a dose of 100-500 mJ than those from MRL/n, F1 hybrid of (MRL/l x MRL/n mice), and BALB/c mice. However, the susceptibility to UVB was not observed in young (1-month-old) and adult (4-month-old) MRL/l mice. UVA light irradiation was not cytotoxic. Keratinocytes cultured from MRL mice showed lower cytotoxicity to UVB irradiation than fibroblasts cultured. However, keratinocytes from newborn MRL/l mice showed higher cytotoxicity to 50 mJ UVB irradiation than cells from MRL/n mice. Syngeneic or allogeneic sera augmented UVB-induced cytotoxicity of fibroblasts cultured. UVB irradiation of spleen cells induced no significant difference of cytotoxicity between MRL/l and MRL/n mice. Based on the results of F1 hybrid of (MRL/l x MRL/n) mice, the susceptibility seemed to be associated with autoimmune traits and to be regulated by genetical background.

Animals↗

PubMed1989

Effects of glyoxal and methylglyoxal administration on gastric carcinogenesis in Wistar rats after initiation with N-methyl-N'-nitro-N-nitrosoguanidine.

Glyoxal and methylglyoxal were tested for tumor-promoting potential in a two-stage stomach carcinogenesis model. Male outbred Wistar rats were initially given N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in the drinking water (100 mg/l) along with a 10% sodium chloride dietary supplement for 8 weeks. Thereafter, they were returned to basal diet and maintained on drinking water containing no addition or either 0.5% glyoxal or 0.25% methylglyoxal for 32 weeks and then killed for necropsy and histological examination at week 40. Glyoxal treatment significantly increased the incidence of adenocarcinomas in the pylorus of the glandular stomach of rats pretreated with MNNG and sodium chloride. Furthermore, although methylglyoxal did not enhance the development of adenocarcinomas, the incidence of hyperplasias in the pylorus was significantly increased. The results indicate that glyoxal exerts tumor promoting activity on rat glandular stomach carcinogenesis and that methylglyoxal might also have promoting potential.

Aldehydes↗

PubMed1989

In situ freezing of the urinary bladder: a trigger of rapid development of sodium o-phenylphenate-induced urinary bladder tumors in the rat.

The effect of in situ freezing of the urinary bladder on sodium o-phenylphenate (OPP-Na)-induced urinary bladder tumor development was investigated in male F344 rats. Freezing was performed at the start of the experiment by touching the serosal surface of the bladder with a frozen steel rod. As a result, three out of 27 rats (11%) developed bladder tumors within 78 weeks when 0.5% OPP-Na feeding was started 2 weeks after freezing and one out of 27 rats (4%) when the feeding was started 12 weeks after freezing. 0.5% OPP-Na alone did not induce any bladder lesions. In a second experiment, 19 out of 25 rats (76%) developed bladder tumors (carcinomas in 12 rats and papillomas in seven rats) when 2% OPP-Na was administered from 6 weeks after freezing, whereas only one rat (5%) demonstrated a bladder carcinoma in the group given 2% OPP-Na without prior freezing. In neither experiment were tumors induced by freezing alone. Enzyme histochemistry revealed no remarkable changes in enzyme activities of regenerative hyperplasia induced by freezing. The results indicate that in situ freezing of the urinary bladder acts as a trigger of rapid development of OPP-Na-induced rat urinary bladder tumors.

Animals↗

PubMed1989

Sequential analysis of quinoline-induced hepatic hemangioendothelioma development in rats.

The effect of duration of quinoline treatment on the induction of hepatic hemangioendotheliomas was examined. Groups of male Wistar rats were given 0.25% quinoline in the diet for 4, 8, 12, 16 or 20 weeks and sequentially killed at these time points. Hemangioendotheliomas were only induced in the livers of rats given quinoline for more than 12 weeks and the incidences of small foci of dysplastic endothelial cells and tumors at week 20 did not differ between the 12-, 16- and 20-week-treated groups. Quantitative analysis of the liver sections at week 20 revealed increased relative area occupied by sinusoidal space even after only 4-week exposures. Parenchymal hyperplastic nodules were observed only in one rat each of the 16- and 20-week-treated groups. The present study indicates that dysplastic endothelial foci may develop into hemangioendotheliomas irrespective of whether the carcinogenic stimulus is continued.

Animals↗

PubMed1989

Sodium o-phenylphenate (OPP-Na) promotes skin carcinogenesis in CD-1 female mice initiated with 7,12-dimethylbenz[a]anthracene.

Sodium o-phenylphenate (OPP-Na) was applied at a dose level of 5.0 mg/animal dermally to the fur-clipped dorsal area of female CD-1 mice twice weekly for 47 weeks after applications of 10 micrograms of 7,12-dimethylbenz[a]anthracene (DMBA) as an initiator twice weekly for 5 weeks. A total of 25 skin tumors (21 papillomas and four carcinomas) developed in 15 out of 20 mice (75%). The incidence and yield of skin tumors in this DMBA/OPP-Na group were significantly higher than in the DMBA/acetone-treated group where only six tumors (five papillomas and one carcinoma) were observed in five out of 20 mice (25%). Only one papilloma developed in OPP-Na/12-o-tetradecanoylphorbol 13-acetate (TPA) treated animals (initiation testing group), and no tumors were observed in mice receiving OPP-Na/acetone. OPP-Na elevated 5-bromodeoxyuridine(BrdU) incorporation in basal cells of mouse epidermis dose-relatedly and the thickness of the skin in the treated group was also increased to approximately 2- or 3-fold that of controls. In addition, high dose application (20 mg/mouse) caused ulceration. O-Phenylphenol (OPP) administration was associated with extensive corrosive effects. The data suggest that OPP-Na is an ulcerogenic agent which induces epidermal proliferation and which can act as a promoter, but not as an initiator or a complete carcinogen, in two-stage mouse skin carcinogenesis.

9,10-Dimethyl-1,2-benzanthracene↗