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At least 163 records · Page 9Linked to original sources
PubMed1989

In vitro effects of cadmium and arsenite on glutathione peroxidase, aspartate and alanine aminotransferases, cholinesterase and glucose-6-phosphate dehydrogenase activities in blood.

The activity of several blood enzymes in the presence and absence of arsenite (As) and cadmium (Cd) was investigated under in vitro conditions. Both human and rat blood glutathione peroxidase (GSH-Px) activities were adversely affected by As at the 0.8 and 1.6 micrograms/ml levels. The latter was completely inactivated whereas the former retained approximately 30% of its original activity. The effect of Cd on this enzyme was much smaller: 650 g Cd/ml were needed to decrease its activity by 30% of the original value. As noted for GSH-Px, the rat's glutamyl oxaloacetate transaminase (GOT) appears to be appreciably more sensitive to the As inhibitory effect than the human enzyme (by a factor of 3). Cd, however, failed to bring about any inhibition of GOT. In the case of glutamyl pyruvate transaminase (GPT) both As and Cd had a marked effect, manifested in 70% and 78% inhibition, respectively. Blood glucose-6-phosphate dehydrogenase (G-G-PD) was inhibited by both Cd and As, however, within the concentration range used, only Cd inhibited it completely. Cholinesterase (ChE) activity was inhibited completely by both Cd and As.

Alanine Transaminase↗
PubMed1984

[Assessment of the exposure of pest control operators to organophosphorus pesticides. Organophosphorus pesticides in blood and alkyl phosphate metabolites in urine].

Pest control operators usually spray pesticides in small areas such as a kitchen in a restaurant and are exposed to various pesticides, especially those of the organophosphorus (OP) type. In order to evaluate their occupational exposure to OP pesticides during the work, OP pesticides in blood and alkyl phosphate metabolites in urine of these operators were analyzed and the relationship between pesticide exposure and analytical results were studied. OP pesticides in blood were analyzed by gas chromatography with flame photometric detector (FPD-GC) after separation of phospholipid in blood with silicagel column chromatography. OP pesticides were not detected in any blood samples (the limit of detection was 1 ng/ml). Dimethylphosphate (DMP) and dimethylthiophosphate (DMTP), being urinary metabolites of OP pesticides, were analyzed by FPD-GC after benzyl derivatization. This method eliminated interfering peaks in gas chromatograms. The ratio of two isomeric derivatives of DMTP was found to be constant. Both DMP and DMTP of the exposed group were significantly higher than those of the non-exposed group, DMP being higher than DMTP. The ratio of DMP to DMTP in the fenitrothion-dichlorvos-exposed group was significantly higher than that in the fenitrothion-exposed group. It was considered that the ratio might reflect a result of pesticide exposure. The urinary metabolites of OP pesticides tended to become lower with the lapse of time since the last exposure. However, small amounts were detected in a few samples even 5 days after the last exposure.

Adult↗
PubMed1975

A clinical evaluation of citrate-phosphate-dextrose-adenine blood.

(1) Blood was stored in polyvinyl-chloride bags containing citrate-phosphate-dextrose (CPD) with adenine in a final concentration of 0.25 mM. (2) Red cell ATP was well maintained (greater than 70% of original) for 4 weeks in whole blood as well as in red cell concentrate (PCV 85 plus or minus 2%). After 5 weeks the ATP level was about 70% in whole blood and about 40% in red cell concentrate. (3) Red cell 2,3-diphosphoglycerate (DPG) was about 60% of the original after 2 weeks and about 30% after 3 weeks of storage when stored both as whole blood and as red cell concentrate. (4) The red cell 24-hour post-transfusion viability was about 80% after 4 weeks of storage both as whole blood and as red cell concentrate. After 5 weeks of storage the 24-hour viability was 78.7 plus or minus 3.5% in whole blood and 76.5 plus or minus 6.7% in red cell concentrate. (5) 820 patients received 3,238 units of CPD-adenine blood, and 761 patients serving as controls received 2,807 units of acid-citrate-dextrose (ACD) blood. The frequency of transfusion reactions was 3.5% for patients receiving CPD-adenine blood and 4.1% for the control group. (6) The maximum storage time was set at 5 weeks for the CPD-adenine blood and 3 weeks for the ACD blood. The longer preservation time decreased out-dating by at least 50%.

ABO Blood-Group System↗
PubMedDate not supplied

Improved red blood cell storage using optional additive systems (OAS) containing adenine, glucose and ascorbate-2-phosphate.

Red blood cells were treated with optional additive system (OAS) solutions to provide component-specific metabolic enhancement for improved storage. Red blood cell viability, as monitored by ATP concentrations, was maintained by use of adenine and extra glucose. Red blood cell oxygen offloading characteristics were improved by maintenance of red blood cell 2,3-DPG concentrations with ascorbate-2-phosphate (AsP). The use of CPD-collected red blood cells with an OAS containing adenine, glucose, and AsP, or CPD-adenine collected red blood cells with an OAS containing AsP demonstrates the potential to store red blood cells at least 42 days and to maintain red blood cell 2,3-DPG.

2,3-Diphosphoglycerate↗
PubMed1975

Clindamycin phosphate: neuromuscular and blood pressure effects in cats.

Three doses (10, 20, and 40 mg/kg) of clindamycin phosphate were tested in each of three feline neuromuscular preparations in a Latin-square sequence, and the muscular responses and blood pressures were compared. No statistically significant dose-related neuromuscular or blood pressure effects were observed.

Animals↗
PubMed1981

Pyridoxal 5'-phosphate in whole blood, plasma and blood cells of postpartum nonlactating and lactating rats and their pups.

Pregnant rats were fed either a diet containing 20.2 mg pyridoxine/kg (control) or a diet containing 1,430 mg/kg (high vitamin B-6). At the time of delivery, pups were removed from half of the dams fed each diet. This resulted in four treatment groups: lactating and nonlactating dams fed the control diet and lactating and nonlactating dams fed the high vitamin B-6 diet. At delivery and at weeks 1, 2, and 3 postpartum, groups of dams and pups were killed and the content of pyridoxal 5'-phosphate (PLP) in whole blood, plasma and blood cells was measured. The PLP content in the whole blood of dams and pups was increased significantly by the high vitamin B-6 diet. Lactation had no effect on the PLP in whole blood of dams. Diet increased the PLP content in the plasma of dams and pups only slightly, whereas lactation greatly depressed PLP in the dams' plasma. In the blood cells, the PLP content was increased by diet and decreased by lactation.

Animals↗
PubMedDate not supplied

Pyridoxal 5'-phosphate and pyridoxamine 5'-phosphate concentrations in blood and tissues of mice fed ethanol-containing liquid diets.

The effects of chronic ethanol administration on vitamin B-6 metabolism were studied in female Long-Sleep (LS) and Short-Sleep (SS) mice. Animals were fed an ethanol containing liquid diet (AIN-76) for four weeks. Concentration of ethanol in the diet increased from 10 to 25% ethanol-derived calories (EDC) during weeks 1-3 and was maintained at 30% EDC for 1 additional week. We measured concentrations of pyridoxal 5'-phosphate (PLP) in plasma, erythrocytes and whole blood, and liver and brain PLP and pyridoxamine 5'-phosphate (PMP) in ethanol-fed and pair-fed control mice. Chronic ethanol administration significantly increased PMP and total (PLP + PMP) levels in the liver of SS mice. In LS mice ethanol feeding significantly decreased PMP and total (PLP + PMP) levels in the brain, but these values were still within normal limits. These results suggest that both control and ethanol-containing liquid diets are nutritionally adequate with respect to vitamin B-6, and that chronic ethanol administration does not adversely affect vitamin B-6 metabolism in adult mice.

Animals↗
PubMed1978

Quantitation and immunochemical characterization of carcinoembryonic antigen and glucose phosphate isomerase in blood and washings of patients with gastric and colonic diseases.

Circulating levels of carcinoembryonic antigen (CEA) and glucose phosphate isomerase (GPI) have been measured and compared in 51 subjects with gastric and colonic diseases. Levels were higher in gastric and colonic cancer patients than in normals or patients with other diseases. Elevations of both these markers were most frequent in patients with metastases. Concentrations of CEA and GPI in gastrointestinal washings were also measured. No correlation was found between total protein content and concentrations of CEA or GPI in the washings. Further characterization of the perchloric acid-soluble material from colon washings by gel filtration indicated that the CEA-like substance from colon cancer patients was higher in molecular weight than standard radiolabeled CEA and CEA from normal colon washings. When tested against anti-CEA antiserum and pure CEA from a colonic cancer metastasis, all CEA preparations showed immunological identity in gel-diffusion plates; on immunoelectrophoresis similar mobility was indicative of a similar charge.

Carcinoembryonic Antigen↗
PubMed1998

Sphingosine 1-phosphate is a blood constituent released from activated platelets, possibly playing a variety of physiological and pathophysiological roles.

We have found that sphingosine 1-phosphate (Sph-1-P) acts as an autocrine stimulator of platelets, being abundantly stored in platelets and released extracellularly, and that its exogenous addition induces platelet activation (Yatomi et al., Blood 1995, 86, 193-202) through a specific receptor on the platelet surface (Yatomi et al., J. Biol. Chem. 1997, 272, 5291-5297). Very recently, we identified Sph-1-P as a normal constituent of human plasma and serum. Sph-1-P levels in plasma and serum were 191+/-79 and 484+/-82 pmol/ml (mean +/- S.D., n = 8), respectively. Platelets are most likely the source of Sph-1-P discharged during blood clotting, since they abundantly store Sph-1-P as compared with other blood cells, and release considerable amounts of stored Sph-1-P extracellularly upon stimulation. The Sph-1-P released from activated platelets may be involved in a variety of physiological processes, including thrombosis, atherosclerosis, and wound healing. Moreover, we often observed that Sph-1-P injection into mice (iv., 10 mg/kg) caused immediate rigor and death. This may be related to the recent observations from an other laboratory that nanomolar concentrations of Sph-1-P affected atrial myocyte K+ channel. These observations taken together strongly suggest pathophysiological roles of the released Sph-1-P in the blood. As one example, we found that Sph-1-P content in the plasma of platelet concentrates correlated with poor platelet increments after transfusion and with the occurrence of transfusion reactions in patients.

Animals↗