Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Deoxycytidine antagonizes the analgesic action of morphine in the rat, morphine-induced respiratory depression in the rabbit and mitigates withdrawal in the dependent mouse. Administration of deoxycytidine does not precipitate the abstinence syndrome in dependent mice, a property shared by certain other endogenous morphine antagonsits. Cytidine and thymidine closely related in structure to deoxycytidine, are interchangeable with saline as controls, indicating a high degree of specificity in the receptor involved in the "action-effects" sequence. The requirement for deoxycytidine in countering the effects of morphine parallels the requirement for certain other DNA pyrimidines in the antagonism of barbiturate and alcohol. The rapidity of antogonist action suggests that such a DNA species would presumably be localized in the synaptosome, at outer membrane or the synaptic junction.
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PMID:Deoxycytidine: a morphine antagonist. 2

Pulmonary explants from adult mice were cultured for periods up to six days in medium with and without one of the following agents: prednisolone, thyroxine, puromycin, actinomycin. Both DNA synthesis and tritiated palmitic acid uptake were greatly reduced by puromycin and actinomycin, which killed the cultures in six days. Prednisolone accelerated uptake of lipid precursor and decelerated DNA synthesis; thyroxine treated explants were not different from controls. Lamellar bodies were observed only in the epithelial cells of cultured explants exposed to prednisolone. Similarly, cultures of fetal lung exhibited maturation with appearance of lamellar bodies only when prednisolone was administered. The depression of cellular division and the stimulation of palmitic acid uptake with coicident appearance of lamellar bodies in cultures exposed to prednisolone supports the hypothesis that control of the differentiation of alveolar epithelium with synthesis of phospholipid surfactant, is a function of the adrenal cortex.
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PMID:Reaction of cultured adult and fetal lung to prednisolone and thyroxine. 4 50

The administration of 5-azacytidine to rats resulted in enhancement of thymidine incorporation into liver DNA. Repeated doses of the drug caused a greater than 10-fold increase of thymidine incorporation. In 5-azacytidine-treated intact rats no changes in the activity of thymidine and thymidylate kinases were observed, whereas a marked depression of thymidine phosphorylase activity occurred. In intact animals the mitotic activity in the drug-treated livers changed slightly; however, 5-azacytidine administration before partial hepatectomy resulted in a dramatic increase of mitotic activity in 24-hr regenerating livers. In this case the observed increase in incorporation of thymidine was paralleled both by increased activity of thymidine and thymidylate kinases and by a decline in thymidine phosphorylase activity. The higher incorporation of radioactivity into liver DNA in intact rats pretreated with the drug can be accounted for, at least partially, by the lower cellular degradation of the injected radioactive thymidine used for labeling. In addition, alterations in the labeling and in the mitotic activity of hepatocytes and nonparenchymal cells caused by 5-azacytidine should be taken into consideration.
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PMID:Enhanced incorporation of thymidine into DNA in the liver of intact and partially hepatectomized rats pretreated with 5-azacytidine. 5 4

Mice were immunized with picryl chloride and the regional nodes taken at various times afterwards. These cells spontanesouly synthesized DNA in vitro as measured by thymidine incorporation over an 18-hour period and the peak incorporation occurred when the cells were takin on day 3. When the mice were injected with cells taken 5 days after immunization with picryl chloride and then immunized, there was a depression of the spontaneous DNA synthesis in vitro. This was absent on day 2, most marked on day 3 and still present on day 4. Cells from donors immunized with 4-ethoxymethylene-2-phenyloxazolone had a smaller but definite effect. Attempts to reproduce the phenomenon by in vitro mixtures of cells taken at various times after immunization in vivo were unsuccessful.
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PMID:DNA synthesis in vitro by cells from mice immunized with picryl chloride: effect of injection of immune cells. 5 28

Phytohemagglutin (PHA)-induced lymphocyte transformation (PILT) was determined in 217 women taking oral contraceptives and 203 control women by means of the uptake of 3H-thymidine into DNA of lymphocytes cultured in heterologous serum. Depressed PILT responses were observed in oral contraceptive users as compared with age-matched controls, and the magnitude of depression correlated with the duration of oral contraception and was inversely related to the clinical progestagenic potency of the component steroids. An additional group of 21 women, tested within 1 year (mean 3 months) of cessation of oral contraception, showed persistent depression of PILT responses. Suppression of lymphocyte transformation in autologous as compared with homologous, normal serum suggests that serum inhibitory factors amy be important. We found no evidence for a direct suppressive in vitro effect of synthetic estrogens and gestagens. The prevalence of autoantibodies in oral contraceptive users was similar to that in control subjects.
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PMID:Phytohemagglutin-induced lymphocyte transformation in oral contraceptive users. 6 29

Distribution of a label was studied in nuclear fraction and in tissues of rats with transplanted sarcoma 45 within a day after an administration of immune and nonimmune 131I-gamma-globulins. When gamma-globulins, containing antibodies to one-stranded DNA, were administered the more intensive accumulation of the label was observed in nuclei of malignant tissue as compared with other tissues (liver, heart, thymus and muscles). The diffuse distribution of the label was found if nonimmune gamma-globulins were used. The phenomenon was apparently related to the active penetration of labelled antibodies to the replicating matrix and binding of them with one-stranded DNA sites. The suggestion is discussed that the effect of accumulation of immune gamma-globulin in proliferating tissue might be used for depression of the proliferative process.
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PMID:[Distribution of antibodies to DNA in the tissues of rats with sarcoma-45]. 6 22

Treatment of formalin-fixed mammalian tissues with concentrated or 50% phosphoric acid at 5 degrees C for 20 and 50 min. respectively reveals complete extraction of RNA as judged by methyl green followed by staining with pyronin. This procedure also causes depolymerisation of DNA as indicated by the red staining of the nuclei. Sections treated with concentrated phosphoric acid at 5 degrees C for 30 min. causes disruption of the double helical structure of DNA what results in the depression of the pyronin staining. Similarly treated sections show Feulgen positive nuclei. Treatment of sections in 25 % phosphoric acid at 60 degrees C for 15 min. followed by staining with methyl green and pyronin show red nuclei, nucleoli and the cytoplasm. This indicates that extraction of RNA is only possible in cold and not at elevated temperature.
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PMID:A new rapid method for selective extraction of RNA from fixed mammalian tissues. 7 98

Three different doses of bleomycin (BLM) (2,1, and 0.01 mg/animal) were injected ip into groups of hairless mice. Cell kinetic alterations in the basal layer of the epidermis were studied up to 10 days after BLM administration. The two highest doses of BLM affected the epidermal cell kinetics in a similar way but with different time courses. Only a moderate depression of the labeling index was observed during the first 24 hours. The results indicate that cells affected by BLM in the middle of the G1 phase are arrested in their subsequent S phase, and that thereafter an increase in the rate of DNA synthesis may occur in the arrested cells without increasing the number of cells in S phase. The percentage of cell accumulated in S and G2 phases as determined by flow cytofluorometry never exceeded 130% of control values with any of the doses. Phase durations were determined from percentage of labeled mitoses curves after the highest dose of BLM and were not significantly different from normal values, indicating that the accumulated cels are probably out of cycle and unable to proliferate again. Calculations based on cell counts and mitotic rate showed that the cells had a prolonged lifespan. No block and subsequent release of cells specifically caused by BLM were observed. BLM has a complex effect on the epidermis, and therefore does not seem to be a promising agent for cell synchronization as a basis for combination chemotherapy in vivo.
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PMID:Epidermla cell kinetics in hairless mice after bleomycin. I. Perturbations after different single doses. 7 87

Weanling male Sprague-Dawley rats were fed either a nutritionally complete synthetic diet (Diet 1) or a diet marginally deficient in choline and methionine, and lacking folacin (lipotrope deficient, Diet 2) to determine the role of hepatic mixed-function oxidase metabolism of aflatoxin B1 (AFB1) in the Diet 2-induced enhancement of AFB1 hepatocarcinogenesis previously reported. Hepatic microsomal mixed-function oxidase activities, as assayed by ethylmorphine N-demethylation, ethoxycoumarin O-dealkylation, cytochrome c reduction, AFB1 metabolism, and cytochrome P-450 content, were all depressed by Diet 2. Furthermore, the proportion of an i.p. dose of AFB (1 mg/kg) that became covalently bonded to DNA and RNA was similarly reduced when measured 6 hr after administration. The formation of AFB1-protein adducts was not influenced by dietary treatment. The depression of DNA and RNA adduct formation in the Diet 2 animals was probably related to the lower mixed-function oxidase activities and not to an alteration of glutathione levels, which remained unchanged by dietary treatment. These results suggest that the marginally lipotrope-deficient diet does not enhance tumor formation through an increased microsomal activation of AFB1. Alternative hypotheses without data are suggested.
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PMID:Dietary lipotropes, hepatic microsomal mixed-function oxidase activities, and in vivo covalent binding of aflatoxin B1 in rats. 8 78

Administration in complete Freund's adjuvant of encephalitogenic protein (EP), derived from central nervous tissue to guinea pigs, regularly results in the development of experimental allergic encephalitis (EAE) which leads to the death of the animals. Administration of EP in incomplete Freund's adjuvant at an appropriate time will completely suppress the clinical development of disease. Results reported herein show that animals receiving suppressive injections of EP for 7 days show depression of lymphocyte DNA synthesis and macrophage migration inhibition, but not of skin reactivity, in response to EP immediately following the injections, and subsequently show recovery of lymphocyte reactivity but do not develop clinical manifestations of EAE. Humoral or other factors may prevent the development of disease in these animals. Guinea pigs receiving injections of EP for 14 days show profound and prolonged depression of lymphocyte reactivity to EP and macrophage migration inhibition. Possible mechanisms for these results include a diminished number or function of reactive cells or activity of a population of cells with the capacity to suppress cellular immune responses. Nonspecific suppression of reactivity to an unrelated antigen during the suppressive injections was not observed.
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PMID:Experimental allergic encephalitis: study of cellular immunity during disease suppression. 8 9


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