Search PubMed⌕ Search

Biomedical subjects

C Tong

Publications and source records attributed to C Tong.

At least 73 records · Page 4Linked to original sources
PubMed1986

Genotoxicity, carcinogenicity, and mode of action of the fried food mutagen 2-amino-3-methylimidazo[4,5-f]quinoline (IQ).

Because mutagens typified by 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) observed in cooked foods are widely consumed, detailed studies of their biochemical and biological properties including carcinogenicity are most important. IQ induces unscheduled DNA synthesis in liver cells, which when taken together with its powerful mutagenicity in the Salmonella typhimurium test system, predicts carcinogenicity. In female Sprague-Dawley rats, IQ did exhibit potent carcinogenicity for the mammary gland, the ear duct, and to a lesser extent, pancreas and bladder. Data from Japanese laboratories indicate carcinogenicity also to the intestinal tract. Thus, one of the mutagens formed during cooking is a versatile carcinogen that because of extensive human intake requires urgent exploration for specific human cancer risk.

Animals↗
PubMed1985

Toxicity of 6-thioguanine and 8-azaguanine to non-dividing liver cell cultures.

8-azaguanine and 6-thioguanine were both toxic to non-dividing liver cells in primary cultures. In addition, these agents were toxic to an established line of liver-derived epithelial cells brought to growth arrest by serum deprivation. These observations demonstrate that the toxicity of 8-azaguanine and 6-thioguanine can occur at least in part through mechanisms that do not involve effects on DNA synthesis or incorporation of the analogs into DNA.

Animals↗
PubMed1985

Genotoxicity of the food mutagen 2-amino-3-methylimidazo-[4,5-f]quinoline (IQ) and analogs.

The food mutagen 2-amino-3-methylimidazo[4,5-f]quinoline (IQ) is an analogue of quinoline, a hepatocarcinogen. 2-Aminofluorene, benzidine and 3,2'-dimethyl-4-aminobiphenyl (DMAB) are potent inducers of unscheduled DNA repair in primary culture rat liver hepatocytes, as was IQ (151 grains/nucleus at 1 X 10(-6) M). Quinoline, on the other hand, is only weakly positive in this assay (15 grains/nucleus at 1 X 10(-3) M). IQ, quinoline and DMAB were applied topically to shaved skin of Sencar mice with promotion by 12-O-tetradecanoylphorbol 13-acetate (TPA) for 20 weeks, when 14 of 20 mice in the quinoline group had 25 tumors, but only one of 30 animals in the IQ group and five of 30 in the DMAB group were tumor-bearing. Analogs of IQ synthesized by substitution at the 2- or 3-position with amino or methyl groups were assayed with the Ames Salmonella typhimurium tester strains TA98 and TA100. Mutagenicity for TA98 is reduced in the absence of the 3-methyl group and is completely abolished with removal of the 2-amino moiety. None of these analogs are strong mutagens for TA100. Exocyclic N-oxidation is a likely obligatory step in the activation of IQ to a mutagen.

Animals↗
PubMed1984

Polybrominated biphenyls are nongenotoxic and produce an epigenetic membrane effect in cultured liver cells.

Polybrominated biphenyls (PBB) were studied for their genotoxic and epigenetic effects in cultured liver cells. PBB did not elicit DNA repair synthesis in rat, mouse, or hamster hepatocytes in primary cultures and did not cause mutations at the hypoxanthine-guanine phosphoribosyl transferase locus in a line of rat liver epithelial cells or in human fibroblasts cocultivated with rat hepatocytes as an activating system. In contrast, PBB inhibited intercellular molecular exchange between rat hepatocytes and liver epithelial cells indicating an epigenetic membrane effect. These data are consistent with the interpretation that PBB act as neoplasm promoters in the production of rodent liver neoplasms.

Animals↗
PubMed1984

Differences in responses of 4 adult rat-liver epithelial cell lines to a spectrum of chemical mutagens.

An assay for mutagenesis at the hypoxanthine-guanine phosphoribosyl transferase (HGPRT) locus in adult rat-liver epithelial cell cultures (ARL) has been developed to take advantage of the capacity of this cell type to metabolically activate promutagens/procarcinogens. A survey of the effect of 5 types of activation-dependent mutagens/carcinogens on 4 ARL lines indicates that the ARL/HGPRT mutagenesis assay with the 4 target cell lines is able to detect a spectrum of activation-dependent carcinogens. Individual ARL lines, however, responded quite differently to a given carcinogen. The ARL/HGPRT mutagenesis assay system thus offers distinct possibilities for the study of the control of chemical biotransformation processes. However, in light of the specificity of the various cell lines to respond to a particular class of mutagens under the current assay condition, this particular assay system cannot be readily applied to routine screening of suspected environmental mutagens of unknown requirements for metabolic activation. Nevertheless, for agents with a structure related to those activated by a specific line, this system can be used to study mutagenesis resulting from intact cellular metabolism.

Animals↗
PubMed1984

Evaluation of morpholine, 3-morpholinone, and N-substituted morpholines in the rat hepatocyte primary culture/DNA repair test.

Morpholine and a series of morpholine derivatives were assayed for the potential to induce DNA repair in the rat hepatocyte primary culture/DNA repair assay. Morpholine did not induce DNA repair at dose concentrations which were not toxic (0.0001-0.1 mg/ml). Two animal metabolites of morpholine, N- methylmorpholine oxide and N- hydroxymorpholine , also did not induce DNA repair at the non-toxic concentrations tested (0.0001-10 mg/ml and 0.0001-1 mg/ml, respectively). A putative metabolite of morpholine, 3- morpholinone , was inactive (0.001-10 mg/ml) and a polyurethane foam catalyst, N- butylmorpholine (0.0001-0.1 mg/ml) was also inactive. The chemical intermediate N- hydroxyethylmorpholine induced DNA repair in the dose range 1-5 mg/ml. It was concluded that genotoxicity of substituted morpholines is a function of the substituent moiety rather than morpholine itself.

Animals↗
PubMed1984

Serum dopamine-beta-hydroxylase activity and lateral ventricular size in affective disorders and schizophrenia.

Previous studies have reported a significant negative correlation between cerebrospinal fluid DBH activity and ventricular brain ratio (VBR) in schizophrenic patients. We now report a significant negative correlation between log serum DBH activity and VBR in 28 patients with major depression (r = -0.41, p = 0.04); this correlation was also negative (r = -0.15), but not significant, in 46 schizophrenics. Eight patients (five schizophrenic, three affective disorder) with increased VBR had significantly lower serum DBH activity than the patients with normal VBR. The relationship between low CSF or serum DBH activity and increased VBR may be manifestations of the polygenetic vulnerability common to the major psychoses.

Affective Disorders, Psychotic↗
PubMed1983

Serotonin uptake and imipramine binding in blood platelets and brain of Fawn-hooded and Sprague Dawley rats.

The kinetic parameters of serotonin (5-HT) uptake and imipramine binding of the synaptosomes and blood platelets of male Fawn-hooded rats, which have a 5-HT storage abnormality, and normal Sprague-Dawley rats were compared. The Vmax for 5-HT uptake of synaptosomes from Fawn-hooded rats was significantly greater than that of Sprague-Dawley rats whereas that of the platelets did not differ. The Km values of both the synaptosomes and platelets of the two rat strains were not significantly different. The Bmax values for 3H-imipramine binding in both platelets and brain of Fawn-hooded rats were significantly lower than those of the Sprague-Dawley rats. The Kd of imipramine binding to platelet membranes from Fawn-hooded rats was significantly less than that of the Sprague-Dawley rats but the Kd of the synaptosomes was not significantly different. These results indicate that 5-HT uptake and imipramine binding sites may be independently regulated and that platelets do not always manifest abnormalities present in brain 5-HT neurons and vice versa.

Animals↗
PubMed1983

Enhancement of benzo[a]pyrene mutagenicity by chrysotile asbestos in rat liver epithelial cells.

The co-mutagenicity of chrysotile asbestos and benzo[a]pyrene (B(a)P) was studied in adult rat liver (ARL-18) epithelial cells. Exposure to chrysotile alone did not increase the mutant incidence whereas B(a)P was mutagenic. Simultaneous exposure of the cells to chrysotile and B(a)P resulted in an enhanced mutant recovery compared to exposure to either of these substances alone. However, chrysotile did not enhance the mutagenicity of the carcinogen, N-methyl-N'-nitro-N-nitrosoguanidine.

Animals↗
PubMed1982

Epigenetic membrane effects of a possible tumor promoting type on cultured liver cells by the non-genotoxic organochlorine pesticides chlordane and heptachlor.

The organochlorine pesticides chlordane and heptachlor were evaluated for their genotoxicity and epigenetic membrane effects. Both compounds were non-genotoxic in the ARLHGPRT mutagenesis assay in which the genotoxic carcinogens 7, 12-dimethylbenz[a]anthracene and benzo[a]pyrene induced significant increases in mutant incidence. The pesticides both markedly inhibited intercellular communication between cultured liver cells, a property demonstrated by many tumor promoting agents, whereas benzo[a]pyrene did not produce this epigenetic effect.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1982

Plasma dopamine-beta-hydroxylase in depressed patients.

Plasma dopamine-beta-hydroxylase (DBH) activity was determined for 28 patients with a major affective disorder (Research Diagnostic Criteria) and 34 controls with no current, past, or family history of a psychiatric disorder. Plasma DBH activity was higher among patients (24.6 IU +/- 25.4 IU) than controls (14.5 IU +/- 8.9 IU), and subjects with plasma DBH activity greater than 25 IU were more common among patients. Unemployment and never marrying were associated with plasma DBH activity greater than 25 IU. Finally, referred patients (n = 9) had higher DBH activity (41.8 IU +/- 37.2 IU) than those responding to newspaper advertisements (n = 19, 16.5 IU +/- 11.5 IU) although these groups differed on no other variable including past history of treatment. We conclude that high plasma DBH activity may represent a vulnerability factor for depression.

Adult↗
PubMed1981

The use of adult rat liver cultures in the detection of the genotoxicity of various polycyclic aromatic hydrocarbons.

The hepatocyte primary culture (HPC)--DNA repair test and the adult rat liver epithelial cell (ARL)--hypoxanthine-guanine phosphoribosyl transferase (HGPRT) mutagenesis assay are two in vitro short-term tests that possess intrinsic capability for xenobiotic biotransformation. Both assays detected the genotoxicity of a variety of carcinogenic polycyclic aromatic hydrocarbons. Thus, these two tests, which embody intact cellular metabolism, are useful for the evaluation of this class of carcinogens and provide results that strengthen those obtained in tests dependent upon subcellular metabolism.

Animals↗
PubMed1981

Sister-chromatid exchange induction by polycyclic aromatic hydrocarbons in an intact cell system of adult rat-liver epithelial cells.

Adult rat-liver epithelial cell lines possess intrinsic metabolic capability for the biotransformation of xenobiotics and thus, are sensitive to a broad spectrum of mutagens/carcinogens in a mutagenesis assay at the hypoxanthine-guanine phosphoribosyl transferase locus. To provide another end-point of biological significance in these lines, we have investigated the application of adult rat-liver epithelial cell line 18 in a sister-chromatid exchange assay. Significant dose-dependent increases in the sister-chromatid exchange frequency occurred when liver cells were exposed to benzo[a]pyrene and 7,12-dimethylbenz[a]anthracene. A weak but positive response was elicited by benz[a]anthracene. The present observations thus confirm the capacity of these cells to generate genotoxic metabolites from activation-dependent mutagens/carcinogens and indicate a relationship between the production of mutations and sister-chromatid exchanges by polycyclic aromatic hydrocarbons.

Animals↗
PubMed1981

Inhibition of intercellular communication between liver cells by the liver tumor promoter 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane.

A dose dependent inhibition of intercellular communication (metabolic cooperation) between primary cultures of rat liver hepatocytes and an established adult rat liver epithelial cell 6-thioguanine resistant strain by the liver tumor promoter 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) is demonstrated. This in vitro assay is proposed to evaluate the tumor promoting activity of oncogenic agents shown to be non-genotoxic in the liver culture systems.

Animals↗