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)

Splenic natural killer (NK) cell cytotoxicity was assessed in rats chronically exposed to lead (Pb) as lead acetate in the drinking water or polychlorinated biphenyl (PCB) as Aroclor 1254 in the feed. Rats treated with cyclophosphamide were included as positive immunosuppressed controls. Weanling, male Sprague-Dawley rats exposed to 50 and 500 ppm PCB in the feed for ten weeks exhibited significantly suppressed (P less than 0.01) splenic NK activity. Cyclophosphamide injected i.p. six days prior to termination at a dose of 75 mg/kg also significantly inhibited splenic NK activity. NK cell activity was reduced, though not significantly, in spleen cells isolated from animals exposed to 10 and 1000 ppm Pb as Pb acetate in the drinking water for ten weeks. In vitro exposure of rat spleen cells to PCB at concentrations of 0.4 and 20.0 micrograms/ml similarly resulted in a significant depression of splenic NK cell activity. In addition, in vitro exposure to lead at the same concentrations resulted in suppressed NK cell cytotoxicity of rat splenocytes. These results indicate that two environmental contaminants have the ability to adversely affect NK cell cytotoxicity. The effects seen here with Pb and PCB on NK cells may in part explain the tumor inducing effect these chemicals are suspected of possessing via compromising the immune surveillance system.
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PMID:The effect of lead and polychlorinated biphenyl exposure on rat natural killer cell cytotoxicity. 392 47

The subacute toxic effects of cyclopiazonic acid (CPA; given orally) were characterized in the dog (CPA was purified from cultures of Aspergillus flavus). Four groups of dogs were given CPA in gelatin capsules for 90 days at the following dosage levels: 0.05, 0.25, 0.5, and 1.0 mg/kg of body weight; a 5th group was used as controls. All dogs administered the 0.5 and 1.0 mg of CPA/kg dosages and 1 dog given the 0.25 mg of CPA/kg dosage died or were humanely killed before the scheduled termination of the study. Clinical signs of intoxication appeared 2 to 44 days after dosing was started and consisted of anorexia and, in 1 to 2 days, vomiting, diarrhea, pyrexia, dehydration, weight loss, and CNS depression. Grossly, the entire alimentary tract had diffuse hyperemia with focal areas of hemorrhage and ulceration. Other lesions were renal infarcts, necrotizing epididymitis, and ulcerative dermatitis. Microscopic lesions included ulceration, necrosis, vasculitis, lymphoid necrosis, karyomegaly in several organs, and decreased mitotic activity in intestinal crypt epithelium. Ulcerative and necrotic lesions were usually associated with vascular lesions. Clinical pathologic changes were leukocytosis, neutrophilia, lymphopenia, monocytosis, and increased serum alkaline phosphatase activity.
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PMID:Cyclopiazonic acid mycotoxicosis in the dog. 392 55

Cyclophosphamide (CP) administration to rats in a single i.p. dose (200 mg kg-1), while producing urinary bladder toxicity and 30-40% depression of the hepatic microsomal mixed function oxidase (MFO), failed to produce any depression of MFO activities in extrahepatic tissues such as lung, kidney and intestine. Phenobarbital pretreatment of the rats, which is known to enhance hepatic microsomal activation of CP, protected against CP-induced urinary bladder toxicity and the depression of hepatic MFO activities. This protection appears to be, at least in part, related to phenobarbital induction of hepatic cytochrome P-450 isozyme(s) that metabolizes CP to a new metabolite tentatively identified as didechlorodihydroxycyclophosphamide.
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PMID:Effects of the induction of hepatic microsomal metabolism on the toxicity of cyclophosphamide. 396 72

The actions of three immunosuppressive drugs on normal antibody synthesis in the adult mouse were determined. Inbred mice were given daily intraperitoneal injections of actinomycin D, uracil mustard, or cyclophosphamide for extended periods. The sera of treated and untreated mice were assayed for phage-neutralizing activity to monitor the effect of each drug on the amount of circulating normal antibody. Except for an initial decrease in titer of normal anti-phage MSP2 activity, actinomycin D had no significant effect on normal antibody activity. Uracil mustard caused alternating elevation and depression of normal antibody titers. Cyclophosphamide caused a prolonged depression of normal antibody. The response patterns to the three immunosuppressive agents were the same for both induced and normal antibody.
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PMID:Effect of immunosuppressive agents on normal phage-neutralizing antibody in the mouse. 572 64

Within 1 year 74 children with neuroblastoma were registered, 30 patients with stage I-III (= 41%) and 44 with stage IV-metastatic disease (= 59%). An aggressive chemotherapy regimen employing Adriamycine, Cyclophosphamide, Vincristine, and Dacarbazine yielded 10/24 partial and 9/24 complete remissions after 9 weeks. 5/24 children were treated less than 9 weeks so far. At the end of the chemotherapy protocol (week 33) 6 recurrences were observed; 3 of these children died. 5 patients remained in complete remission, 1 in partial remission. 12/24 of patients were not evaluable because of treatment less than 33 weeks so far. The one year run of the study is too short to evaluate the benefit of Interferon (randomized trial). The toxicity of the regimen is tolerable, including bone marrow depression, vomiting and hyperpyrexia. Breaking off therapy was only necessary in one patient.
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PMID:[Neuroblastoma study NBL79-society of pediatric oncology -- report after 1 year (author's transl)]. 616 57

Advanced malignant testicular tumors can be treated very successfully by chemotherapy. The most effective 3 or 4-drug combinations contain CisPlatin, Vinblastine, Bleomycin, Adriamycin, Cyclophosphamide, Ifosfamide and Vepesid. Complete remissions of 60% can be obtained; depending on histology, frequency of metastases, and former radiation therapy. Resection of residual pulmonary or retroperitoneal metastases render an additional 10-20% of the patients free of tumor. Side effects following chemotherapy should not be neglected: Depression of bone marrow, severe vomiting, alopecia, and azoospermia.
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PMID:[Modern chemotherapy of a malignant testicular tumors (author's transl)]. 617 87

Cyclophosphamide (CY) given before immunization causes greatly increased delayed hypersensitivity skin reactions. Increased cell-mediated immunity is associated with depletion of B-lymphocytes from lymphoid tissue and a depression of those lymphocytes whose precursors turn over more rapidly. In the guinea pig, replacement studies showed that the depleted cells were not T-lymphocytes and had immunoglobulin adherent to their surface, a characteristic of B-lymphocytes. Delayed hypersensitivity reactions increased by CY include chemical contact sensitivity, the tuberculin reaction, delayed hypersensitivity to tularemia vaccine and the Jones-Mote reaction to soluble protein antigens. Pretreatment with CY can also increase the antibody response to some antigens, but depress the response to others. In addition, CY has been found to reverse immunological tolerance where this form of unresponsiveness is due to suppressor cells. CY can also enhance the immune response following depression by antigenic competition or desensitization. Other drugs with a similar, but lesser, effect include melphalan, azathioprine and methotrexate.
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PMID:Effect of cyclophosphamide on immunological control mechanisms. 621 96

Cyclophosphamide (300 mg/kg) given before or up to 2 days after sensitization, induces increased contact skin reactions at 8 days. Reactions were suppressed with cyclophosphamide (CY) given between 3 and 5 days after sensitization; reactivity returned on day 10. CY, given on days 6 to 8, only suppressed reactions when skin tests were made 4 days later. This temporary depression of contact sensitivity corresponds with the maximal reduction of peripheral blood lymphocytes. CY given 1-2 days after DNFB produced decreased T-cell proliferation in local lymph nodes 4 days after sensitization. CY given 3 days after DNFB produced maximal T-cell suppression on 5 day nodes. Massive increase in T-cell proliferation in 5 day nodes occurred when CY was given on the day of sensitization or the day before. Thus CY given around sensitization acts mainly on suppressor cells whereas given later, the action is principally on the effector functions.
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PMID:Kinetics of the relation between suppressor and effector mechanisms in contact sensitivity in the guinea-pig. 621 99

The hypothesis of a serotonergic basis of reward rests partly on data showing that serotonin (5-HT) depletion by para-chlorophenylalanine (p-CPA) causes depression of self-stimulation (SS) rates. These data do not clearly demonstrate a time course relationship between 5-HT depletion and SS suppression. The present study shows that SS behavior has fully recovered from p-CPA induced suppression when 5-HT levels are still maximally depleted. The data reveal that the effects of electrical brain SS on p-CPA induced reductions of 5-HT cannot explain the temporal dissociation between 5-HT depletion and SS suppression. As a whole the data suggest that midbrain 5-HT neurons are not critically involved in SS behavior.
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PMID:Time course analysis of para-chlorophenylalanine induced suppression of self-stimulation behavior. 621 66

The sulphydryl compound WR 2721 has been combined with a range of cytotoxic drugs in the mouse and the effects upon tumours and normal tissues determined. In the acute lethality (LD50/30) assay, mean protection factors produced by WR 2721 (200 or 400 mg kg-1) were generally less than 1.3 for cyclophosphamide (CTX), CCNU and chlorambucil (CHL) but a protection factor of 1.7 was obtained for cisplatinum (cis-P) in combination with 400 mg kg-1 of WR 2721. No protection against the depression of peripheral white cell count seen at 3 days after CTX, CCNU or cis-P was obtained with either 200 or 400 mg kg-1 of WR 2721. Significant protection of the RIF-1 sarcoma by WR 2721 against CTX and cis-P induced growth delay was seen. In the KHT sarcoma, WR 2721 produced small reductions in the growth delay caused by CCNU, melphalan and CHL but these were not statistically significant. These data show less differential normal tissue protection by WR 2721 than do a number of reports in the literature.
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PMID:Modification by WR 2721 of the response to chemotherapy of tumours and normal tissues in the mouse. 629 28


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