UMLS:C0019204 - FACTA Search

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Query: UMLS:C0019204 (hepatocellular carcinoma)
71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The structural parameters necessary for the antineoplastic potency of a new class of anticancer agents, arylsulfonylhydrazones of 2-formylpyridine N-oxide, were examined in mice bearing Sarcoma 180 ascites cells. The findings indicated that (a) replacement of the pyridine ring with benzene, quinoline, or isoquinoline resulted in loss of activity (b) movement of the formylhydrazone side chain from the 2 to the 3 or 4 positions of the pyridine N-oxide produced inactive agents (c) the pyridine N-oxide function was essential for anticancer activity, except for 4-substituted derivatives which were active without the N-oxide group, (d) replacement of the SO2 group by CO resulted in complete loss of activity, and (e) a carbon atom could be inserted between the SO2 and aryl ring with retention of anticancer potency. One of the most active members of this series, 1-oxidopyridine-2-carboxaldehyde p-toluenesulfonylhdrazone, exhibited antineoplastic activity against a broad spectrum of transplanted tumors including Sarcoma 180, Hepatoma 129, Ehrlich carcinoma, leukemia L1210, and a subline of Sarcoma 180 resistant to alpha-(N)-heterocyclic carboxaldehyde thiosemicarbazones. This agent caused inhibition of thymidine-3H and uridine-3H incorporation into DNA and RNA, respectively, of Sarcoma 180 ascites cells; protein biosynthesis was relatively insensitive to the action of this compound.
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PMID:Antineoplastic and biochemical properties of arylsulfonylhydrazones of 2-formylpyridine N-oxide. 18 76

A retrospective cohort study was carried out in 1982-1983 among 28,460 benzene-exposed workers (15,643 males, 12,817 females) from 233 factories and 28,257 control workers (16,621 males, 12,366 females) from 83 factories in 12 large cities in China. All-cause mortality was significantly higher among the exposed (265.46/100,000 person-years) than among the unexposed (139.06/100,000 person-years), as was mortality from all malignant neoplasms (123.21/100,000 versus 54.7/100,000, respectively). For certain cancers, increased mortality was noted among benzene-exposed males in comparison with that among unexposed males; the standardized mortality ratios (SMR) were elevated for leukemia (SMR = 5.74), lung cancer (SMR = 2.31), primary hepatocarcinoma (SMR = 1.12), and stomach cancer (SMR = 1.22). For females only leukemia occurred in excess among the exposed. Risk of leukemia rose as duration to exposure to benzene increased up to 15 years, and then declined with additional years of exposure. Leukemia occurred among some workers with as little as 6 to 10 ppm average exposure and 50 ppm-years (or possibly less) cumulative lifetime exposure (based on all available measurements for the exposed work units). Among the 30 leukemia cases identified in the exposed cohort, the proportion of subjects with acute lymphocytic leukemia was substantially lower and the proportion with acute nonlymphocytic leukemias was higher than in the general population. During 1972 to 1981, the annual incidence of leukemia ranged from 5.83 to 28.33 per 100,000 with higher rates occurring in the interval 1977 to 1981 than in the earlier years of the study period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A retrospective cohort study of leukemia and other cancers in benzene workers. 279 42

The hepatocarcinogen 1'-hydroxysafrole (HOS) exhibited weak initiating activity and strong promoting activity for the induction of enzyme-altered foci and tumors in rat liver. Thus, administration of a single dose of HOS to rats 18 h after a 70% hepatectomy, followed by administration of phenobarbital (PB) in the diet for 6 months, induced a low, but statistically significant, number of foci of enzyme-altered cells. This treatment did not result in gross liver tumors, even when the PB treatment was continued for 16 months. Large numbers of enzyme-altered foci developed when HOS was administered in the diet at levels of 0.05-0.25% to rats previously administered a single dose of N,N-diethylnitrosamine (DEN) 24 h after a 70% hepatectomy. Similarly, rats given a single dose of DEN 24 h after a partial hepatectomy and then fed 0.10 or 0.25% of HOS in the diet for 10 months developed a high incidence of hepatocellular carcinomas. In the absence of pretreatment with DEN, dietary administration for at least 4 months of 0.10 or 0.25% of HOS induced significant numbers of enzyme-altered foci; these data and liver tumor induction by continuous feeding of HOS, in the absence of pretreatment with DEN, provide additional evidence for an initiating, as well as a promoting, activity of HOS in rat liver. Concurrent administration of the hepatic sulfotransferase inhibitor pentachlorophenol with HOS in each of the above assays almost completely inhibited the initiating and promoting activities of HOS for the formation of enzyme-altered foci and tumors; these data strongly suggest that both the initiating and promoting activities are mediated by the sulfuric acid ester, 1'-sulfooxysafrole. HOS also exhibited initiating activity in adult mouse liver. Thus, dietary administration of 0.25% of HOS for only 1 month, followed by administration of the hepatic tumor promoter 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene resulted in a high incidence and multiplicity of hepatomas by 10 months. In the absence of the promoter, administration of HOS for only 1 month induced no hepatomas; 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene alone induced only a low incidence. In mice not given the promoter, continuous administration of HOS for 3-6 months was required for hepatoma development by 16 months.
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PMID:Inhibition by pentachlorophenol of the initiating and promoting activities of 1'-hydroxysafrole for the formation of enzyme-altered foci and tumors in rat liver. 288 29

The early appearance of serum alpha-fetoprotein (AFP) during hepatocarcinogenesis as a function of age of rats and extent of treatment with 3'-methyl-4-dimethylaminoazobenzene is reported. Administration of .06% of the benzene hepatocarcinogen in the diet of 6- to 12-week-old male rats led to the prompt appearance of AFP in the serum within 3-4 weeks. Discontinuation of treatment at Week 5 dropped the AFP in serum to undetectable levels within 2 weeks, and it remained negative over a 30-week period when, at autopsy, no liver cancer was found. Administration of azo dye to 6-week-old rats for 10 weeks also decreased AFP in serum to undetectable levels over the next 2 weeks, except in 2 of 45 rats who developed large hepatomas early and remained positive. In the remainder, AFP reappeared beginning at Week 15, and liver cancer was present at Week 20 except for 13 rats that remained negative, although 7 had hepatoma. The age of the rats played no marked role in the precocious appearance of AFP. The presence of AFP in each group was related to the histological picture of the liver at the time of autopsy. There was no detectable AFP in untreated control rats, nor was there any in rats fed .05% of the hepatotoxic but not carcinogenic alpha-naphthylisothiocyanate which led to extensive jaundice and bile duct proliferation.
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PMID:Early appearance of serum -fetoprotein during hepatocarcinogenesis as a function of age of rats and extent of treatment with 3'-methyl-4-dimethylaminoazobenzene. 411 15

Cytochrome P4502E1 (CYP2E1) activates carcinogenic N-nitrosamines, benzene, urethane and other low molecular weight compounds. This enzyme is also inducible by ethanol, and metabolizes alcohol. A restriction fragment length polymorphism (RFLP) using the Rsa I restriction enzyme has been identified in the CYP2E1 transcription regulatory region; recent studies suggest that this polymorphism may affect gene expression. We investigated the frequency of the Rsa I RFLP in a Japanese population in relation to gastric cancer and liver disease susceptibility. The frequency of this polymorphism was determined in 150 gastric cancer, 16 hepatocellular cancer, 48 liver cirrhosis and 203 benign gastric disease (controls) patients. This preliminary study shows no association of the specific genotype with gastric cancer in all subjects (odds ratio = 1.04, 95% CI = 0.74-3.08 for the heterozygote and 0.57, 95% CI = 0.22-1.50 for the homozygous rare allele, respectively). To further confirm this lack of association, an age and gender matched case-control study should be performed. Separately, there was no association of the Rsa I RFLP with hepatocellular carcinoma (p = 0.911), but there was a suggested difference between the non-viral associated liver cirrhosis patients and control patients. Thus, this polymorphism may be related to ethanol metabolism and consequential liver diseases in a Japanese population.
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PMID:Cytochrome P4502E1 (CYP2E1) genetic polymorphism in a case-control study of gastric cancer and liver disease. 758 84

Carcinogenesis is a multistage process consisting of the three distinct stages: initiation, promotion, and progression. The initiation-promotion-progression (IPP) protocol models these stages and establishes a method whereby agents that possess a carcinogenic risk can be classified as acting primarily at any one or combination of these stages. In one hepatocarcinogenesis IPP protocol, rats were initiated with 10 mg of diethylnitrosamine/kg body wt at 5 days of age, started on the promoting agent phenobarbital at weaning, subjected to a 70% partial hepatectomy at 6 months, and, at the peak of proliferation, given a putative progressor agent, ethylnitrosourea ([ENU] 100 mg/kg, ip) or hydroxy-urea ([HU] 3 x 150 mg/kg, ip). Administration of the promoting agent was discontinued after the progressor agent was given, and the rats were sacrificed 6 months later. The number and volume fraction of promoter-independent (growth in the absence of the promoting agent) altered hepatic foci (AHF) were then determined by quantitative stereology. The number of such AHF increased with either ENU or HU treatment compared with animals not given a progressor agent. In addition, hepatocytes isolated from animals subjected to an IPP regimen with ENU as the progressor agent exhibited a greater degree of chromosomal breakage and aneuploidy than animals not given a second initiator. A variation of this model, in which the promoting agent was maintained after administration of the progressor agent, was examined. In this IPP model, the number of heterogeneous AHF (foci-in-foci) increased after application of the progressor agent (ENU or HU). An increased incidence of hepatocellular carcinoma was also observed in animals subjected to the IPP protocol when promotion was maintained until sacrifice. Thus, the characteristics of progression--increased chromosomal damage, aneuploidy, growth of AHF in the absence of continued tumor promotion, the presence of foci-in-foci, and an increased incidence of malignant neoplasia--have been used as end points for the demonstration of progressor activity by ENU. In addition, the potential progressor activity of HU and benzene has been demonstrated with the IPP model of rat hepatocarcinogenesis.
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PMID:The initiation-promotion-progression model of rat hepatocarcinogenesis. 809 13

An extensive body of evidence supports the conclusion that by catalyzing obligatory two-electron reductions of quinones to hydroquinones, NAD(P)H:quinone reductase (QR1) protects cells against the deleterious effects of redox cycling of quinones, their ability to deplete glutathione, and to produce neoplasia. The effects of elevation of QR1 levels by various enzyme inducers, inhibition of the enzyme by dicumarol, and genetic deletion of the enzyme (knockout mouse) are all consistent with the proposed protective functions. Measurement of QR1 activity in murine hepatoma cells grown in 96-well microtiter plates has provided a rapid and quantitative method for detecting inducer activity and determining inducer potency. This constitutes a strategy for the identification of potential chemoprotectors against cancer. Epidemiological studies show that humans who are genetically deficient in QR1 are more susceptible to the hematological toxicity and carcinogenicity of benzene exposure, and may be more susceptible to the development of a number of malignant tumors.
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PMID:Persuasive evidence that quinone reductase type 1 (DT diaphorase) protects cells against the toxicity of electrophiles and reactive forms of oxygen. 1103 51

Methyleugenol is used as a flavoring agent in jellies, baked goods, nonalcoholic beverages, chewing gum, candy, pudding, relish, and ice cream. It is also used as a fragrance in perfumes, creams, lotions, detergents, and soaps. Methyleugenol has also been used as an insect attractant in eradication programs and as an anesthetic in rodents. Methyleugenol was nominated for testing because of its widespread use and because of its structural resemblance to safrole, a known carcinogen, and isosafrole and estragole. Male and female F344/N rats and B6C3F1 mice received methyleugenol (approximately 99% pure) in 0.5% methylcellulose by gavage for 14 weeks or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium, cultured Chinese hamster ovary cells, and mouse peripheral blood erythrocytes. 14-WEEK STUDY IN RATS: Groups of 9 or 10 male and 10 female F344/N rats were administered 0, 10, 30, 100, 300, or 1,000 mg methyleugenol/kg body weight in 0.5% methylcellulose by gavage 5 days per week for 14 weeks. A water control group of 10 male and 10 female rats received deionized water by gavage. All rats survived until the end of the study. The final mean body weights of 300 and 1,000 mg/kg males and of all dosed groups of females were significantly less than those of the vehicle controls. Erythrocyte microcytosis was demonstrated by decreased mean cell volumes in 300 mg/kg males and 1,000 mg/kg males and females. There was evidence of a thrombocytosis at all time points, demonstrated by increased platelet counts in the 100 mg/kg or greater groups. The serum activities of alanine aminotransferase and sorbitol dehydrogenase were increased in the 100 mg/kg or greater rats at various time points, suggesting hepatocellular injury. Additionally, bile acid concentrations were generally increased in the 300 and 1,000 mg/kg groups at all time points, consistent with cholestasis or altered hepatic function. A hypoproteinemia and hypoalbuminemia, evidenced by decreased total protein and albumin concentrations, occurred in rats in the 300 and 1,000 mg/kg groups at all time points. Liver weights of 100, 300, and 1,000 mg/kg males and 300 and 1,000 mg/kg females and testis weights of 1,000 mg/kg males were significantly increased. Increased incidences of liver lesions occurred in 300 and 1,000 mg/kg males and females and hepatocellular adenoma occurred in one 1,000 mg/kg male. The incidences of atrophy and chronic inflammation of the mucosa of the glandular stomach were significantly increased in rats administered 300 or 1,000 mg/kg. Increased incidences of adrenal gland cortical hypertrophy and/or cytoplasmic alteration in the submandibular gland occurred in the 100 mg/kg or greater groups. 14-WEEK STUDY IN MICE: Groups of 10 male and 10 female B6C3F1 mice received methyleugenol in 0.5% methylcellulose by gavage at doses of 0, 10, 30, 100, 300, or 1,000 mg/kg, 5 days per week for 14 weeks. A water control group of 10 male and 10 female mice received deionized water by gavage. All but one male and all females receiving 1,000 mg/kg died before the end of the study. The mean body weight gains of mice in the 300 mg/kg groups were significantly less than those of the vehicle controls. The only clinical finding was toxicity manifested as generalized morbidity in mice administered 1,000 mg/kg. Liver weights of 30, 100, and 300 mg/kg males and of 300 mg/kg females were significantly increased. Male mice administered 10 or 30 mg/kg had significantly lower cauda epididymis, epididymis, and testis weights; males receiving 100 mg/kg had significantly lower spermatozoal concentrations. Increased incidences of liver lesions occurred in 1,000 mg/kg males and 300 and 1,000 mg/kg females. The incidences of lesions of the glandular stomach were increased in one or more groups administered 30 mg/kg or greater. 2-YEAR STUDY IN RATS: Groups of 50 male and 50 female rats received methyleugenol in 0.5% methylcellulose by gavage at doses of 37, 75, or 150 mg/kg, 5 days per week for 105 weeks; groups of 60 male and 60 female rats received the 0.5% me60 female rats received the 0.5&percnt; methylcellulose vehicle only. Stop-exposure groups of 60 male and 60 female rats received 300 mg/kg in 0.5&percnt; methylcellulose by gavage for 52 weeks followed by just the 0.5&percnt; methylcellulose vehicle for the remaining 53 weeks of the study. Special study groups of 10 male and 10 female rats administered 36, 75, 150, or 300 mg/kg were designated for toxicokinetic studies. Survival and Body Weights: All 150 and 300 mg/kg males died before the end of the study, and survival of 150 mg/kg females was slightly less than that of the vehicle controls. Mean body weights of all dosed groups of rats were less than those of the vehicle controls throughout most of the 2-year study. Pathology Findings: Chemical-related liver neoplasms occurred in all dosed groups of rats and included hepatocellular adenoma, hepatocellular carcinoma, hepatocholangioma, and hepatocholangiocarcinoma; at 2 years, there were positive trends in the incidences of hepatocellular adenoma, carcinoma, and adenoma or carcinoma (combined) in core study rats and in the numbers of rats with multiple liver neoplasms. Nonneoplastic lesions included eosinophilic and mixed cell foci, hepatocellular hypertrophy, oval cell hyperplasia, cystic degeneration, and bile duct hyperplasia (females); the incidences of these lesions in dosed groups of male and female rats were increased at 6 months, 12 months, and/or 2 years. Chemical-related neoplasms and nonneoplastic lesions of the glandular stomach included benign and malignant neuroendocrine tumors in the 150 and 300 mg/kg groups and females in the 75 mg/kg group. In all dosed groups of rats at all time points, the incidences of mucosal atrophy were significantly greater than in the vehicle controls. Neuroendocrine cell hyperplasia was observed in females at 6 months and males and females at 12 months and at 2 years. In core study female rats, there was a positive trend in the incidences of squamous cell papilloma or carcinoma (combined) of the forestomach, and the incidence in the 150 mg/kg group exceeded the historical control range. The incidences of renal tubule proliferative lesions in male rats were suggestive of a neoplastic effect in the kidney. Therefore, additional step sections of the kidneys of male rats were prepared. The incidences of renal tubule hyperplasia and adenoma in the extended evaluation and the combined incidences of standard and step sections in the 75, 150, and 300 mg/kg groups were greater than those in the vehicle controls. The incidences of nephropathy were increased in all dosed groups of females, and the increase was significant in the 300 mg/kg group. In dosed groups of male rats, there was a positive trend in the incidences of malignant mesothelioma, and the incidences were significantly greater in 150 and 300 mg/kg males than in the vehicle controls. The incidences of mammary gland fibroadenoma in 75 and 150 mg/kg males were significantly increased. The incidences of fibroma of the subcutaneous tissue in 37 and 75 mg/kg males and the combined incidences of fibroma or fibrosarcoma in 37, 75, and 150 mg/kg males were significantly increased. 2-YEAR STUDY IN MICE: Groups of 50 male and 50 female mice received methyleugenol in 0.5&percnt; methylcellulose by gavage at doses of 0, 37, 75, or 150 mg/kg for 105 weeks. Special study groups of 10 male and 10 female mice administered 37, 75, or 150 mg/kg were designated for toxicokinetic studies. Survival and Body Weights: Survival of all dosed groups of male mice was similar to that of the vehicle controls. Survival of dosed groups of females was significantly less. Mean body weights of dosed mice were generally less than those of the vehicle controls throughout the studies. Pathology Findings: Chemical-related increases in the incidences of liver neoplasms and nonneoplastic lesions in mice included hepatocellular adenoma and carcinoma, hepatoblastoma, hepatocholangiocarcinoma, eosinophilic foci, oval cell hyperplasia, bile duct hyperplasia, hemosiderin pigmentation, chronic active inflammation, and hematopoietic cell proliferation. In all dosed groups ofmales and females, the incidences of hepatocellular neoplasms and the multiplicity of neoplasms were generally greater than in the vehicle controls. The incidences of hepatoblastoma were significantly increased in all dosed groups of females and slightly increased in 150 mg/kg males. Hepatocholangiocarcinoma was observed in 150 mg/kg females. The incidences of eosinophilic foci, oval cell hyperplasia, portal hypertrophy, hepatocyte necrosis, hematopoietic cell proliferation, bile duct hyperplasia, and hemosiderin pigmentation were significantly increased in two or more dosed groups of male and/or female mice. The incidences of glandular ectasia, mucosal atrophy, chronic active inflammation, epithelial hyperplasia, and neuroendocrine cell hyperplasia of the glandular stomach were increased in one or more dosed groups of male and female mice. In addition, malignant neuroendocrine tumors were observed in the glandular stomach of two 150 mg/kg male mice; one male in this group had a carcinoma. TOXICOKINETIC STUDIES: Methyleugenol is rapidly absorbed following oral administration to rats and mice. The kinetic data are consistent with rapid clearance from the blood, metabolism in the liver, and excretion of the parent and various metabolites in the urine. GENETIC TOXICOLOGY: Methyleugenol was not mutagenic in S. typhimurium strain TA98, TA100, TA1535, or TA1537, with or without exogenous metabolic activation (S9). In cytogenetic tests with cultured Chinese hamster ovary cells, methyleugenol induced sister chromatid exchanges in the presence of S9, but no induction of chromosomal aberrations was noted in cultured Chinese hamster ovary cells following exposure to methyleugenol, with or without S9. In vivo, no increase in the frequency of micronucleated normochromatic erythrocytes was seen in male or female mice administered methyleugenol by gavage for 14 weeks. PHYSIOLOGICALLY BASED PHARMACOKINETIC MODEL: A physiologically based pharmacokinetic (PBPK) model resulting from intravenous and oral exposure was created to characterize tissue concentrations of methyleugenol in rats and mice. Data used to create the model were obtained from the literature or from current studies. The primary conclusions that can be reached from the PBPK model are: 1) absorption of oral doses of methyleugenol in rats and mice is rapid and complete, 2) distribution of methyleugenol to tissues is not hampered by capillary permeability, and 3) metabolism of methyleugenol is saturable and must have some extrahepatic component in the mouse. Model-based plasma methyleugenol concentrations were not found to be good dosimeters for evaluating neoplasm dose-response data. CONCLUSIONS: Under the conditions of these 2-year gavage studies, there was clear evidence of carcinogenic activity of methyleugenol in male and female F344/N rats based on the increased incidences of liver neoplasms and neuroendocrine tumors of the glandular stomach in male and female rats and the increased incidences of kidney neoplasms, malignant mesothelioma, mammary gland fibroadenoma, and subcutaneous fibroma and fibroma or fibrosarcoma (combined) in male rats. A marginal increase in the incidence of squamous cell neoplasms of the forestomach may have been related to methyleugenol administration in female rats. There was clear evidence of carcinogenic activity of methyleugenol in male and female B6C3F1 mice based on the increased incidences of liver neoplasms. Neuroendocrine tumors of the glandular stomach in male mice were also considered related to methyleugenol administration. In male and female rats and mice, methyleugenol administration caused significant increases in nonneoplastic lesions of the liver and glandular stomach. Synonyms: 1-Allyl-1,2-dimethoxybenzene; 4-allylveratrole; 4-allyl-1,2-dimethoxy-benzene; 1,2-dimethoxy-4-allylbenzene; 3,4-dimethoxyallylbenzene; ENT 21040; 1-(3,4-dimethoxyphenyl)-2-propene; eugenol methyl ether; 1,3,4-eugenol methyl ether; veratrole methyl ether.
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PMID:NTP Toxicology and Carcinogenesis Studies of Methyleugenol (CAS NO. 93-15-2) in F344/N Rats and B6C3F1 Mice (Gavage Studies). 1256 49

A dichloromethane extract from the leaves of Lithraea molleoides (Anacardiaceae), an argentine medicinal plant, showed cytotoxicity on human hepatocellular carcinoma cell line. Bioassay guided fractionation of this extract led to the isolation of a new active 5-alkyl resorcinol: 1,3-dihydroxy-5-(tridec-4',7'-dienyl)benzene. Chemical structure was established based on spectroscopic data (UV, IR, MS, 1H-NMR, 13C-NMR, COSY). This compound presented cytotoxic activity on 3 human tumoral cell lines: hepatocellular carcinoma cell line-Hep G2 (IC50 +/- SD of 68 +/- 2 microM), mucoepidermoid pulmonary carcinoma cell line-H292 (IC50 +/- SD of 63 +/- 5 microM) and mammary gland adenocarcinoma cell line -MCF7 (IC50 +/- SD of 147 +/- 5).
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PMID:1,3-dihydroxy-5-(tridec-4',7'-dienyl)benzene: a new cytotoxic compound from Lithraea molleoides. 1569 16

This paper presents a comparison of the dipole moment derivatives with respect to internal coordinates in the liquid and gas phases for benzene-h(6), benzene-d(6) and benzene-d(1). The literature values of the integrated intensities of the infrared active fundamentals of the three gaseous isotopomers are used to determine the dipole moment derivatives with respect to internal coordinates, using the methods described in the previous paper for the liquid phase. As was found for the liquid phase in the previous paper, there is uncertainty surrounding the intensities of the individual CH stretching fundamentals of benzene-d(1) due to intensity sharing with active combinations. The magnitudes of the dipole moment derivatives with respect to internal coordinates in the gas phase are partial differentialmicro/ partial differentials=0.50+/-0.03DA(-1), partial differentialmicro/ partial differentialt=0.28+/-0.03, partial differentialmicro/ partial differentialbeta=0.24+/-0.01, and partial differentialmicro/ partial differentialgamma=0.65+/-0.02DA(-1), where s, t, beta and gamma are the CH stretching, and CC stretching, the HCC bending and the HCCC torsion displacements, respectively. The experimental intensities are different for the three isotopomers in the liquid and gas phases, and the calculations show that these differences are mainly due to a difference between the CH stretch dipole moment derivatives in the two phases. This difference was related qualitatively to the intermolecular interaction of the H with the pi-cloud of the nearest neighbour creating a pseudo-hydrogen bond.
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PMID:Dipole moment derivatives with respect to the internal coordinates of benzene in the liquid and gas phases. 1651 Mar 6

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