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

Changes in T-and B-lymphocytes content in experimental benzene intotication (BI) of CBA-mice were studied. The content of spontaneously rosette-forming cells, B-lymphocytes with C3 -receptors and T-cells in macro-and microtest was determined. It was shown that BI resulted in disorders in the function of thymus, depression of T-cell system and autoimmune shifts. A number of characteristics in kinetics of various fractions of lymphoid cells due perhaps, to different sensitivity of particular types of lymphoid cells to benzene and compensatory response as well. The significance of described phenomena is discussed.
 ...
PMID:[Change in the content of T-and B-lymphocytes in experimental benzene poisoning (author's transl)]. 15 75

Liver enlargement is frequently reported in studies on the short-term toxicity of chemicals. In many such studies no histological evidence of damage is present but biochemically there is often an increased microsomal enzyme activity (MEA) which is interpreted to represent a type of work hypertrophy. In a few instances, the MEA in the enlarged liver is either normal or less than normal. In such instances histochemical evidence of liver damage (depression of G-6-Pase and autophagy) is found. A compound which produced the latter changes is Ponceau MX. When administered for up to 21 months at a dose-level which produces biochemical and histochemical evidence of liver injury, a series of changes were observed consisting of progerssive diminution of MEA, areas of glycogen accumulation and centrilobular fatty change and these were followed first by nodular hyperplasia and then by frank carcinoma. The protective effect of increased MEA in carcinogenesis was shown by the reduction in tumour incidence on the administration of phenobarbitone simultaneously with acetylaminofluorene, 4-dimethyl aminoazo benzene and diethylnitrosamine. But no such protective effect is seen if the phenobarbitone is administered after treatment with these carcinogens. In fact the number of tumours is enhanced presumably due to preferential stimulation of the growth of malignant cells.
 ...
PMID:Liver growth and tumorigenesis in rats. 28 28

Four groups of 4 domestic pigs were exposed to 0, 20, 100, and 500 ppm benzene vapor 6 h/d, 5 d/wk, for 3 wk. Two groups of 10 rats were exposed to 0 and 500 ppm: the exposed rats for 6 h/d, 5 d/wk, for 3 wk, the nonexposed rats for 6 h/d, 5 d. Rats were killed within 72 h after exposure; values for pigs were obtained shortly after exposure and on final examination at 4-16 wk after exposure. Pigs were evaluated for changes in white and red blood cell counts, hemoglobin level, lymphocyte count, proportion of E-rosette-forming lymphocytes, myeloid-erythroid ratio, and presence of multinucleate erythroblasts. With the exception of the E-rosette test, the same parameters were measured in the rat. Statistically significant (p less than 0.05) depression of white cell counts, total lymphocytes, and proportion of E-rosette-forming lymphocytes was observed in pigs exposed to 500 ppm; recovery to values not significantly different from control values was observed on final examination. Fewer postexposure effects were seen at 100 ppm, and there were no significant differences from control values at 20 ppm. Both pigs and rats exposed to 500 ppm showed a significant decrease in the mean myeloid-erythroid ratio within 72 h. These values returned to normal in the pig 4-16 wk after exposure; recovery in the rat was not evaluated. An increased number of bone marrow erythroblasts with more than 2 nuclei was found on final examination of pigs exposed to 500 and 100 ppm, but the difference was significant only at the 100-ppm level because of the variability at the higher level. A significant increase (p less than 0.004) in multinucleate cells was seen in the rats exposed to 500 ppm.
 ...
PMID:Hematologic and myelogenous effects of inhaled benzene in the pig and the rat. 52 38

A pilot study on the immune response in patients with carcinoma of the head and neck has been made. The clinical behaviour of such neoplasia is reasoned as being partly determined by the immunological response. If prognosis is related to competence of the immune system then this parameter should be assessed. DNCB (di-nitro-chloro-benzene) skin sensitization and serial lymphocyte transformation studies were performed on all patients whose progress was studied for at least two years. On analysing the results of survival, patients could be divided into two groups--DNCB positive and DNCB negative. The negative patients could be further subdivided; those with a lymphocyte stimulation index of over fifteen; and those beneath this level--the former had a much better prognosis than the latter. Also, such cancer patients were shown to have both cellular and serum factors causing depression of lymphocyte transformation. In the light of all findings, a future programme of investigation is proposed.
 ...
PMID:On the immunology of head and neck cancer--a prognostic index. Preliminary communication. 118 59

Benzene is a well-established hematotoxin that affects developing leukocytes and erythrocytes as well as bone marrow stromal cells. In the present studies we analyzed the effects of benzene on the morphology and functional activity of bone marrow phagocytes. Male Balb/c mice were treated with benzene (660 mg/kg) once per day for 3 days. Bone marrow cells were then isolated and fractionated by density gradient centrifugation. Using highly sensitive techniques in flow cytometry/cell sorting, we found that we could separate three distinct populations of bone marrow cells that differed with respect to size and density. Monoclonal antibody binding and cell sorting revealed a large, dense population that consisted predominantly of granulocytes, a smaller, less dense population of lymphocytes, and a population of intermediate size and density consisting of mononuclear phagocytes and precursor cells. Differential staining of sorted mononuclear phagocytes revealed that benzene treatment of mice caused a marked increase in the number of mature, morphologically activated macrophages in the bone marrow. Benzene treatment of mice also resulted in enhanced chemotaxis and production of hydrogen peroxide by bone marrow granulocytes and mononuclear phagocytes. In contrast, treatment of mice with the combination of hydroquinone and phenol (50 mg/kg each, 1 x/day, 3 days), two metabolites of benzene, resulted in a significant (p < or = 0.02) depression of granulocyte chemotaxis and had no effect on hydrogen peroxide production by bone marrow phagocytes compared to cells from control animals. Taken together these results demonstrate that benzene causes increased differentiation and/or activation of phagocytes in the bone marrow.
 ...
PMID:Alterations in the morphology and functional activity of bone marrow phagocytes following benzene treatment of mice. 147 Nov 47

1. The rate of oxygen consumption has been monitored continuously in M. edulis during acute exposure to high sublethal concentrations of formaldehyde, phenol and benzene and subsequent recovery periods of 96 hr. 2. The results are discussed in relation to changes in the electrochemical potential difference of sodium, the content of ATP and the tissue concentration of strombine. 3. After exposure to benzene and phenol, an increase in the rate of oxygen consumption that could not be explained by oxygen debt from the exposure period was observed. 4. Depression of the rate of oxygen consumption after exposure to formaldehyde may be explained by a reduced ability to extract oxygen from the water. 5. The pattern of oxygen consumption and behavioural responses, as well as the combined changes in the biochemical markers, were distinctly different in the three cases.
 ...
PMID:Measurements of oxygen consumption in Mytilus edulis during exposure to, and recovery from, high sublethal concentrations of formaldehyde, benzene and phenol. 167 79

After exposure of C57BL6 x DBA/2 mice to benzene in air their number of bone marrow fibroblastoid precursor cells, CFU-F, was determined. The CFU-F exhibited an increasing plating efficiency, giving rise to a larger number of colonies and to colonies of greater size. This effect was dose dependent. When the mice were exposed for 16 weeks and were then allowed to rest, their CFU-F plating efficiency returned to normal within 6 weeks, but then increased again. Hematopoietic stem cells, such as CFU-S and CFU-C exhibited a dose-dependent depression. The in vitro exposure of bone marrow cells to benzene metabolites resulted in a dose-dependent depression of CFU-F numbers.
 ...
PMID:Effect of benzene on fibroblastoid colony-forming units in mice. 180 83

Chronic exposure of humans to benzene (BZ), a myelotoxin, causes aplastic anemia and acute leukemia. The stromal macrophage that produces interleukin-1 (IL-1), a cytokine essential for hematopoiesis, is a target of BZ's toxicity. Monocyte dysfunction and decreased IL-1 production have been shown to be involved in aplastic anemia in humans. Hydroquinone (HQ), a toxic bone marrow (BM) metabolite of BZ, causes time- and concentration-dependent inhibition of processing of the 34-Kd pre-interleukin-1 alpha (IL-1 alpha) to the 17-Kd mature cytokine in murine P388D1 macrophages and BM stromal macrophages, as measured by Western immunoblots of cell lysate proteins using a polyclonal rabbit antimurine IL-1 alpha antibody. HQ over a 10-fold concentration range had no effect on the lipopolysaccharide (LPS)-induced production of pre-IL-1 alpha precursor or on cell viability or DNA and protein synthesis. Stromal macrophages obtained from the femoral BM of C57Bl/6 mice exposed to BZ (600 or 800 mg/kg body weight) for 2 days were incapable of processing the 34-Kd pre-IL-1 alpha to the mature 17-Kd cytokine when stimulated in culture with LPS. Stromal macrophages from mice coadministered BZ and indomethacin, a prostaglandin H synthase (PHS) inhibitor that has been shown to prevent BZ-induced myelotoxic and genotoxic effects in mice when coadministered with benzene were able to convert the pre-IL-1 alpha to mature cytokine. Administration of recombinant murine IL-1 alpha (rMuIL-1 alpha) to mice before a dose of BZ that causes severe depression of BM cellularity completely prevents BM depression, most probably by bypassing the inability of the stromal macrophage in BZ-treated animals to process pre-IL-1 alpha to the mature cytokine.
 ...
PMID:Role for interleukin-1 (IL-1) in benzene-induced hematotoxicity: inhibition of conversion of pre-IL-1 alpha to mature cytokine in murine macrophages by hydroquinone and prevention of benzene-induced hematotoxicity in mice by IL-1 alpha. 186 53

The alteration of the hemopoiesis is the result of a lot of particular cases. The inhibition of the microtubuli assembly suppresses the cell division because of the missing of the spindle formation. This is associated with an inhibition of the supporting stroma of the bone marrow and of the different lymphocytes complicated with a depression of colony stimulating factors. There is also an alkylation of the nuclear and mitochondrial RNA, DNA and proteins together with an inactivation of the DNA polymerase. Immunosuppressive effects are associated with autoimmune events. Benzene is classified as a weak carcinogenic initiator.
 ...
PMID:[Current status of knowledge of the effect of benzene. Impairment of blood and hemopoiesis]. 218 78

The effects of treatment with phenobarbital, 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene (TCPOBOP), pregnenolone-16 alpha-carbonitrile (PCN), 3-methylcholanthrene (3-MC) and isosafrole on the hepatic microsomal formation of nine monohydroxy metabolites of testosterone and the O-dealkylation of the ethyl and pentyl ethers of resourfin were evaluated in adult male C57BL/6J and DBA/2NCR mice. In both strains, phenobarbital, TCPOBOP and PCN induced testosterone 2 beta-, 6 beta-, 15 beta- and 16 beta-hydroxylases up to 5-fold, while phenobarbital and TCPOBOP increased the rate of dealkylation of pentoxyresorufin by approximately 30-fold. However, phenobarbital and TCPOBOP did not exhibit identical patterns of induction for the testosterone oxidation reactions. Hepatic microsomes from C57BL/6J mice treated with TCPOBOP displayed a depression in 6 alpha-testosterone hydroxylase activity, which was also observed in PCN-treated animals, whereas phenobarbital-treated mice exhibited an elevation in this monooxygenase activity. A dose of TCPOBOP (0.5 mumol/kg) previously demonstrated to represent an ED50 for mouse aminopyrine N-demethylase activity was also found to approximate the ED50 for pentoxyresorufin O-dealkylase activity in the C57BL/6J mouse. Isosafrole or 3-MC treatment had little effect on testosterone metabolism or pentoxyresorufin O-dealkylase activity in either strain, while 3-MC induced ethoxyresorufin O-deethylase activity in C57BL/6J but not DBA/2NCR mice. This study confirms that TCPOBOP is a potent cytochrome P-450 inducer which most closely resembles phenobarbital in its mode of action. However, TCPOBOP and phenobarbital do not evoke identical modulations of cytochrome P-450-dependent monooxygenases in mice.
 ...
PMID:Effects of cytochrome P-450 monooxygenase inducers on mouse hepatic microsomal metabolism of testosterone and alkoxyresorufins. 235 39


1 2 3 4 5 6 7 8 9 Next >>