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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of the pH, Na+ concentration and osmolality of the culture medium on early passage Syrian hamster embryo (SHE) clonal cell proliferation was examined. The pH of the medium was adjusted from 6.49 to 7.45 by addition of different amounts of NaHCO3 to the medium and incubating the cell cultures in a fixed atmosphere of 10% CO2/90% air. Our results indicate that clonal SHE cell proliferation is optimal at pH 6.65-6.80 while plating efficiency is independent of pH between 6.65 and 7.45. Adjustment of Na+ to that concentration in the medium (3450 p.p.m., 0.15 M) of the greatest NaHCO3 addition caused a moderate depression of cell proliferation over the entire pH series. Adjusting the osmolality of the culture medium to a constant value of 338 mOsm/kg did not alter the pH effect on cell proliferation. The pH of the medium also affected cellular and colony morphology. Below pH 6.90 there was an increase in the number of colonies which exhibited a transformed-like morphology ('altered' colonies). The 'altered' phenotype was characterized by a multilayered, criss-cross pattern of growth throughout the colony. This phenotype was stable upon sub-cloning into pH 6.65 medium but was reversible if sub-cloned into pH 7.36 medium. The induction of 'altered' colonies at low pH could be partially suppressed by Na+ or osmolality adjustment. These results are discussed in terms of optimizing growth conditions for SHE cells in order to enhance their usefulness for cell transformation studies. The induction of 'altered' colonies by low pH is also discussed relative to the involvement of pH regulation in tumor-promoter and growth-factor action on cells in culture.
Carcinogenesis 1986 Sep
PMID:The induction of transformed-like morphology and enhanced growth in Syrian hamster embryo cells grown at acidic pH. 374 17

A reduction in the ratio of tetraploid to diploid liver nuclei has been investigated as an early indicator of hepatocarcinogenesis in the rat using the liver carcinogen 3'-methyl-4-dimethylaminoazobenzene (3'M). In a dose ranging study 3'M was administered by gavage to rats at 5, 12.5 and 25 mg/kg for up to 10 weeks and the following parameters studied: bodyweight gain, dye binding to hepatic protein, nuclear ploidy in liver and histopathology. Significant reduction in bodyweight occurred only with 25 mg/kg; dye binding to protein occurred in a dose-related manner; depression of the percentage of tetraploid nuclei compared with diploids was dose-related and effects were detected even at the lowest dose. These observations were consistent with those from previous studies by other investigators. In a separate experiment 3'M was administered at the maximum tolerated dose (MTD) of 25 mg/kg for 3 weeks, during which time there was a significant reduction in bodyweight gain and a reduction in the ratio of tetraploid:diploid liver nuclei. After cessation of dosing the rate of bodyweight gain returned to normal but there was no corresponding recovery of the ratio of tetraploid:diploid nuclei in the liver. A long-term continuous gavage study at 2.5 mg/kg revealed a time dependent reduction in the ratio of tetraploid:diploid liver hepatocyte nuclei and histopathological changes that included hepatocarcinoma were also observed. There was no correlation between the severity of pathological changes and the change in nuclear ploidy ratio in this experiment and it is concluded that the changes in ploidy ratio are related to the carcinogenic effect of 3'M and are independent of its gross toxicity.
Carcinogenesis 1985 Jan
PMID:Irreversible depression in the ratio of tetraploid:diploid liver nuclei in rats treated with 3'-methyl-4-dimethylaminoazobenzene (3'M). 391 70

Hexachlorobenzene (HCB) was fed to male and female F344 rats as 0.02% of the diet for 15 weeks. Females developed a massive porphyria, due to depression of uroporphyrinogen decarboxylase activity, whereas males did not. Although hepatic non-haem iron levels in control females were 3-5 times greater than males (iron is implicated in the pathogenesis of this condition) preloading the latter with iron did not increase their susceptibility. After 90 weeks of HCB treatment 100% of surviving females had multiple liver tumours which were strongly gamma-glutamyl transpeptidase (GGT) positive and histologically classified as neoplastic nodules or hepatocellular carcinomas. In contrast, only 16% of males developed tumours which were smaller and fewer in number per liver than those in females. Accumulation of porphyrins was still significantly less in males than females although no uroporphyrinogen decarboxylase activity was detected in treated livers of either sex. No differences in porphyrin levels or enzyme activity were found between tumours and surrounding tissue showing that tumours did not revert to a non-porphyric state. The sex difference in tumour response could not be explained by differences in hepatic HCB concentrations. Non-haem iron concentrations of livers fell after HCB treatment for 90 weeks in both sexes and were even lower in tumours. These studies demonstrate that not only are female rats far more sensitive than males to the porphyrinogenic effects of HCB but also to the hepatocarcinogenic actions, suggesting a link between these two manifestations of toxicity that may also apply to other polyhalogenated aromatics.
Carcinogenesis 1985 Apr
PMID:Hepatocarcinogenicity of hexachlorobenzene in rats and the sex difference in hepatic iron status and development of porphyria. 398 65

Development of 1,2-dimethylhydrazine (DMH) induced colonic neoplasia were studied using male Wistar rats given 120 mg DMH per kg s.c. weekly for 5 weeks. During the course of colon carcinogenesis, changes in cellular proteins of colonic mucosa were analysed by two-dimensional gel electrophoresis. Rats were sacrificed just before and at 10, 15 and 20 weeks after the initial DMH treatment together with controls. Incidence and number of colorectal tumors gradually increased. At the 20th week, colon carcinoma was found in every rat. Most tumors (92%) were found in the major flexure and the distal colon and rectum, while only 1% and 7% were found in the cecum and proximal colon, respectively. Histologically, most (92%) were classified as well differentiated or moderately differentiated adenocarcinoma. Eighty-five percent of the tumors were semipedunculated or sessile without depression, and the remainder were sessile with depression. All of the latter were carcinomas with invasion to the submucosa or further. Two-dimensional gel electrophoresis revealed 180 spots in cellular proteins before and after the initial treatment. Three new spots appeared and four spots greatly increased during the course of carcinogenesis, while one spot disappeared. The above results suggest that the appearing and increasing spots may be associated with cancer and that the disappearing spot may be associated with the normal colon.
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PMID:[Development of 1,2-dimethylhydrazine-induced colonic neoplasia in rats and changes in cellular proteins of colonic mucosa]. 408 89

The effects of 12-O-tetradecanoylphorbol-13-acetate (TPA), all trans-retinoic acid (RA), 5-azacytidine (5-AC), and phenobarbital (PB) on the activities of seven enzymes and/or isozymes of a diploid rat liver epithelial cell line have been studied. At 0.1 microgram/ml, TPA depressed the specific activities of lactate dehydrogenase and gamma-glutamyl transpeptidase, whereas 2 mM PB depressed gamma-glutamyl transpeptidase and alkaline phosphatase. At 0.01 microgram/ml, RA markedly depressed the activity of NADH-diaphorase and lactate dehydrogenase but enhanced the activity of alkaline phosphatase. Only 2 microM 5-AC caused the most significant shift of lactate dehydrogenase isozyme toward the "muscle"-type isozyme. Histochemical studies revealed that PB and 5-AC induced focal areas of cells with glycogen deposits, but no significant changes in either ultrastructure or alpha-fetoprotein and albumin immunohistochemical staining pattern were observed to suggest hepatocytic differentiation. Although none of the enzymatic changes could be consistently correlated with the effects of these biological modifiers on the cellular growth rate, the effect of RA on NADH-diaphorase, lactate dehydrogenase, and alkaline phosphatase activities was the opposite of the changes observed during carcinogenesis of these rat liver epithelial cells by multiple treatments with N-methyl-N'-nitro-N-nitrosoguanidine. The depression of gamma-glutamyl transpeptidase activity by PB is contradictory to that observed histochemically in hepatocytes in vivo, but such discrepancy may be related to the differences in cell type, growth conditions, or duration of exposure.
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PMID:Biochemical effects of 12-O-tetradecanoylphorbol-13-acetate, retinoic acid, phenobarbital, and 5-azacytidine on a normal rat liver epithelial cell line. 620 84

Incubation of chrysotile and anthophyllite asbestos fibers with normal human peripheral blood monocytes resulted in significant suppression of monocyte metabolic activity as measured by chemiluminescence. Both fiber types were cytotoxic to monocytes and depressed monocyte phagocytosis of latex beads. We conclude that asbestos-induced monocyte cytotoxicity could result in release of lysosomal enzymes and/or degradation products which contribute to fibrosis in asbestosis. The depression of phagocytosis and microbicidal function may contribute to the increased incidence of carcinogenesis observed in asbestosis.
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PMID:Asbestos-induced alteration of human peripheral blood monocyte activity. 629 14

In vivo induction of gamma interferon (IFN-gamma) by sensitization of mice with Mycobacterium bovis strain BCG and subsequent challenge with tuberculin depressed the ability of liver homogenates from treated animals to metabolically activate promutagens. The Ames Salmonella typhimurium revertant assay was used for analyses of metabolic conversion of promutagens by liver homogenates. Relative to the mutant frequencies determined with control liver homogenates, induction of IFN-gamma depressed the abilities of homogenates from treated animals to activate N-acetylaminofluorene (AAF), aflatoxin B1 (AFB1), and benzo[a]pyrene (BP) by 55%, 44% and 95%, respectively. Within 18-24 h of Aroclor 1254 treatment, liver P-450 content had increased 43%, and the relative mutant yields per unit protein for all three promutagens had approximately doubled. In vivo induction of IFN-gamma suppressed the Aroclor 1254-dependent increases in mutagenesis by AAF (63%), AFB1 (90%), and BP (reduced to a level 23% below non-Aroclor 1254 treatment). In all cases, the levels of depression of promutagen activation qualitatively correlated with cytochrome P-450 content and the induction of IFN-gamma.
Carcinogenesis 1984 Jan
PMID:Gamma interferon induction depresses murine hepatic promutagen/procarcinogen activation. 641 4

The effect of inhaled ammonium sulfate on benzo[a]pyrene carcinogenesis in the lungs of Syrian golden hamsters was studied. Exposure to ammonium sulfate at an airborne concentration 20 times average United States ambient levels resulted in a significant depression (p less than 0.05) of benzo[a]pyrene carcinogenesis in the first 6 mo of the study. However, at 2 yr, the termination of the study, there were no differences in cancer incidence between groups receiving benzo[a]pyrene and benzo[a]pyrene plus ammonium sulfate. In addition, at the concentration studied, inhaled ammonium sulfate did not significantly increase the incidence or severity of pneumonitis or pulmonary fibrosis in the hamster. However, this inhalation did increase the incidence of emphysema but not the severity. The decreased incidence of cancer during the first 6 mo of this study in animals receiving both benzo[a]pyrene and ammonium sulfate suggests that interaction between sulfate and benzo[a]pyrene does occur, but is insufficient to afford long-term protection against the development of cancer. No enhancement of carcinogenesis by benzo[a]pyrene occurs in the presence of inhaled sulfate.
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PMID:Effects of inhaled ammonium sulfate on benzo[a]pyrene carcinogenesis. 650 34

The effect of chronic applications of HN2 on acute responses of DNA synthesis to UVB radiation was studied in Uscd strain hairless mouse skin in vivo. 0.1 mg of HN2 in 95% ethyl alcohol and the diluent were applied weekly to the backs of the mice for 69 wk. The mice were then exposed to 1.98 X 10(2) J/m2 of UVB energy and were sacrified 4 hours and 48 h post-irradiation. The effects on DNA synthesis were evaluated using TdRH3 as the radioactive tracer. The results of the study revealed that the chronic HN2 applications increased the number of basal cells in the DNA synthesis phase of the mitotic cycle. This was associated with acanthosis and cellular hypertrophy. 4 h post-irradiation there was the expected depression in DNA synthesis in both the HN2- and diluent-treated mice. In addition, 48 h post-irradiation the number of basal cells synthesizing DNA was accelerated in both the HN2- and diluent-treated mice. However, it was much more noticeable in the HN2-treated animals. Whether this increased activity is related to the additive carcinogenesis generated between UVB and HN2 remains to be determined.
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PMID:A study of the effect of chronic applications of nitrogen mustard (HN2) on acute responses of mammalian skin to UVB irradiation in vivo. 653 1

Epidemiological data indicate that life style, including dietary "imbalances", play a major role in etiology of human cancers. Although two thirds of the world population suffer from varying grades of protein-caloric malnutrition (PCM) today, no consistent pattern is found to be associated wih PCM both in man and laboratory animals. At the tissue level, depression of cellular proliferation by prolongation of DNA-synthetic phase is a characteristic lesion of PCM. Due to changes in liver mixed function oxidases, metabolism of drugs is affected. The cell-mediated immunity is depressed and there is a defective mobilisation of macrophages. These alterations would modulate carcinogenesis; some tend to enhance, while others inhibit tumorigenesis. The balance of evidence suggest that PCM is unlikely to have dominant modulating influence on carcinogenesis.
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PMID:Implications of malnutrition in chemical carcinogenesis. 678 74


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