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PubMed2001

Correlation between plasma endotoxin, plasma cytokines, and plasminogen activator inhibitor-1 activities in septic patients.

The objective of this study was to evaluate the relation between the clinical and plasma parameters and the changes in plasma endotoxin activity with 2 hours of endotoxin-adsorbing therapy using polymyxin B (PMX). A total of 88 consecutive patients were admitted for PMX treatment of severe sepsis or septic organ failure. Standard supportive care was continued without alteration during PMX treatment. Endotoxin, tumor necrosis factor-alpha (TNFalpha), interleukin-6 (IL-6), IL-10, and plasminogen activator inhibitor-1 (PAI-1) activities and clinical parameters were measured before, immediately after, and the day after PMX treatment. The mean APACHE II and III scores were 24.2 +/- 1.0 and 85.8 +/- 3.0, respectively. The 2-week survival rate was 51.1%. In survivors, TNFalpha, IL-6, IL-10, and PAI-1 activities were significantly decreased during the 2-hour PMX treatment, the following day, or both times. There was no significant change in the parameters, except for TNFalpha, after PMX in nonsurvivors. In the subgroup whose plasma endotoxin decreased more than 30%, IL-6, TNFalpha, and PAI-1 significantly decreased after 2 hours of PMX or the following day (or both), but all four parameters in nonsurvivors showed no significant change. Hence PMX adsorbed plasma endotoxins and contributed to reductions in plasma proinflammatory cytokine levels and to improved clinical parameters during the 2-hour treatment. Changes in these parameters correlated with changes in plasma endotoxin activity in survivors whose plasma endotoxin levels were adequately reduced.

APACHE↗
PubMed2004

Plasma cathepsin D isoforms and their active metabolites increase after myocardial infarction and contribute to plasma renin activity.

Plasma renin activity (PRA) is often found to increase after myocardial infarction (MI). Elevated PRA may contribute to increased myocardial angiotensin II that is responsible for maladaptive remodeling of the myocardium after MI. We hypothesized that MI would also result in cardiac release of cathepsin D, a ubiquitous lysosomal enzyme with high renin sequence homology. Cathepsin D release from damaged myocardial tissue could contribute to angiotensin formation by acting as an enzymatic alternate to renin. We assessed circulating renin and cathepsin D from both control and MI patient plasma (7-20 hours after MI) using shallow gradient focusing that allowed for independent measurement of both enzymes. Cathepsin D was increased significantly in the plasma after MI (P < 0.001). Furthermore, circulating active cathepsin D metabolites were also significantly elevated after MI (P < 0.04), and contained the majority of cathepsin D activity in plasma. Spiking control plasma with cathepsin D resulted in a variable but significant (P = 0.005) increase in PRA using a clinical assay. We conclude that 7-20 hours after MI, plasma cathepsin D is significantly elevated and most of the active enzymatic activity is circulating as plasma metabolites. Circulating cathepsin D can falsely increase clinical PRA determinations, and may also provide an alternative angiotensin formation pathway after MI.

Angiotensins↗
PubMed1982

The relationship between plasma membrane lipid composition and physical-chemical properties. III. Detailed physical and biochemical analysis of fatty acid-substituted EL4 plasma membranes.

Murine leukemia EL4 cells were modified by supplementation of culture media with fatty acids for 24 h. A plasma membrane-enriched fraction was prepared from substituted and normal cells. Analyses were performed to determine fatty acyl composition, phospholipid headgroup composition and cholesterol content. The two major membrane phospholipids, phosphatidylethanolamine (PE) and phosphatidylcholine (PC) were isolated by thin-layer chromatography and ESR measurements were done on liposomes prepared from these lipids as well as on the intact plasma membrane preparations. Slight perturbations in overall plasma membrane lipid composition were observed when EL4 cells were supplemented with a single exogenous fatty acid. This may be consistent with the idea that the incorporation of exogenous fatty acid induces compensatory changes in membrane lipid composition. On the other hand, we observed no significant difference in two ESR motional parameters between the unsubstituted control and various fatty acid-substituted plasma membranes. ESR measurements carried out on PE and PC liposomes derived from 17:0- and 18:2c-substituted membranes also failed to detect major differences between these liposomes and those made from normal EL4 phospholipids. In the case of liposomes prepared from 18:2t,-substituted membranes, the order parameter was significantly changed from the normal. However, the change was in opposite directions in PE and PC, perhaps accounting for the fact that no change parameter is seen in intact 18:2t-substituted plasma membrane. Measurements of order parameter (S) in mixed lipid vesicles showed that at up to 50 mol% mixture of a synthetic PC with plasma membrane PC, the value of S was only marginally different from that of the plasma membrane PC vesicles. We interpret these data as an indication that the two ESR parameters used are not sufficiently sensitive to detect changes due to modifications of the acyl chain composition of a complex biological membrane.

Animals↗
PubMed1986

Changes of plasma lipids and long-chain n-3 and n-6 fatty acids in plasma, liver, heart and kidney phospholipids of rats fed variable levels of fish oil with or without cholesterol supplementation.

Diets supplemented with 10% by weight of oil, either wholly safflower oil or proportinally (25, 50, 75 or 100%) replaced by fish oil, were given to 60 rats which had previously been deprived of dietary fat for 6 weeks. Half the animals on each dietary regimen were also given 1% of cholesterol. After 4 weeks of feeding, the plasma lipid contents and the phospholipid fatty acid compositions of plasma, liver, heart and kidney were determined. In general, the concentrations of plasma lipids were significantly reduced in animals fed a diet containing 5% or more of fish oil in comparison with those fed only safflower oil. Cholesterol feeding increased the levels of plasma cholesterol, whereas it lowered those of plasma triacylglycerols and phospholipids. The levels of 20:4(n - 6) in all four tissues were sharply reduced, whereas those of 18:2(n - 6) increased when 25% of dietary safflower oil was replaced by fish oil. Both 18:2(n - 6) and 20:4(n - 6) were decreased as the contents of dietary fish oil were further increased. The levels of long-chain n-3 fatty acids, e.g., 20:5(n - 3), 22:5(n - 3) and 22:6(n - 3) were increased as the intake of fish oil increased. The incorporation of 22:6(n - 3) was greater in plasma, liver and heart phospholipids, whereas that of 20:5(n - 3) was greater in kidney phospholipids. Cholesterol feeding also increased the levels of 18:2(n - 6) and 20:5(n - 3), whereas it decreased the levels of 20:4(n - 6) and 22:6(n - 3) in plasma and liver. However, these changes were not observed in heart and kidney.

Animals↗
PubMed1981

Reduction of plasma high-density lipoprotein cholesterol and increase of postheparin plasma hepatic lipase activity during progestin treatment.

Twenty-seven menopausal women were given the synthetic progestin levonorgestrel for two weeks. The mean plasma high-density lipoprotein (HDL) cholesterol concentration decreased from 1.32 mmol/l to 1.01 mmol/l (p less than 0.001) during treatment. This was due to the selective reduction in plasma HDL2 cholesterol from 0.73 mmol/l to 0.44 mmol/l, whereas the plasma HDL3 cholesterol was not changed. The mean hepatic lipase (HL) activity of postheparin plasma increased from 20.6 to 35.3 mumol.h-1.ml-1 (p less than 0.001) while the lipoprotein lipase (LPL) activity was not changed. A significant inverse correlation existed between the HDL2 cholesterol concentration and HL activity both before (r=-0.49, p less than 0.01) and after (r=-0.39, p less than 0.05) treatment, and a significant correlation was observed between the changes in these two variables (r=0.39, p less than 0.05). These results are compatible with the hypothesis that HL participates in the regulation of plasma HDL2 levels and they suggest that progestin treatment reduces plasma HDL2 cholesterol concentration by increasing the hepatic lipase activity. It is not known whether this type of HDL2 reduction is accompanied by increased atherogenesis but as long as the issue is unresolved some caution is needed in the long-term use of levonorgestrel, particularly in women who simultaneously are given some other drug depressing plasma HDL2 concentration.

Cholesterol↗
PubMed1989

Plasma lipoproteins and adrenocortical hormones in men--positive association of low density lipoprotein cholesterol with plasma cortisol concentration.

The associations of plasma lipoprotein lipids with the plasma concentrations of two adrenocortical hormones (sampled at 09.00-11.00 h) have been investigated in a random sample of 70 men aged 52-67 yr (mean, 59 yr). Plasma low density lipoprotein (LDL) cholesterol concentration was found to be positively correlated with plasma cortisol, independently of the concentrations of plasma triglyceride, high density lipoprotein cholesterol and androstenedione. After adjusting for covariates, plasma cortisol explained approximately twelve per cent of the variance in LDL cholesterol. These results suggest that plasma cortisol may significantly influence the metabolism of LDL in healthy humans.

Aged↗
PubMed1992

Changes in brain gonadotropin-releasing hormone, pituitary and plasma gonadotropins, and plasma thyroxine during smoltification in chinook salmon (Oncorhynchus tschawytscha).

Concentrations of brain salmon gonadotropin-releasing hormone (sGnRH), plasma gonadotropin I (GTH I), and pituitary GTH I and GTH II were determined in yearling chinook salmon (Oncorhynchus tschawytscha) during the parr-smolt transformation in two successive seasons. There were significant elevations in brain sGnRH content from February to March in 1988, and from February to April in 1989. Increases in brain sGnRH content coincided with elevations in plasma thyroxine levels that occurred from February to March, 1988 and 1989. Plasma GTH levels were relatively constant (1-2 ng/ml) throughout the period of sampling. However, during 1988, plasma concentrations of GTH I decreased significantly between late March and early April. During 1989, plasma GTH I levels appeared to reach a peak (2 ng/ml) in mid-February, but otherwise remained near 1 ng/ml. Previous studies have shown that GTH II was not detectable in plasma at this stage. During 1989, pituitary GTH I concentrations were 50- to 70-fold higher than that of GTH II, and increased, though not significantly, from February through April. Although GTH II was detected in the pituitary by RIA, it is likely that the measurable levels are due to GTH I cross-reaction in the GTH II RIA. Histological examination of the gonads indicated that throughout smoltification the oocytes remained in the perinucleolar stage of oogenesis and the testes were in the spermatogonial stage of spermatogenesis. Although no observable changes in gametogenesis occurred, the changes in brain sGnRH content, plasma GTH I levels, and pituitary GTH content suggest that some changes in the hypothalamic-pituitary axis may occur during smoltification.

Animals↗
PubMed1981

The somatomedin activity in plasma from patients with multiple mechanical injuries: with observations on plasma cortisol.

The somatomedin activity (SMA) was assayed in 247 plasma samples from 30 patients with moderate or severe injuries. The injury severity score (ISS) was assessed for each patient and ranged from 9 to 50. The plasma SMA was reduced or eliminated within 4 days of injury. The activity then increased in the patients who recovered, normal levels being attained within 1 or 2 weeks of the injury. Five patients had at least one further fall in plasma SMA during treatment. Seven patients died and 4 of these had little or no SMA before death. The magnitude and duration of the depression of SMA after injury correlated both with the ISS and with the probability of mortality. The plasma cortisol concentration was elevated in all but 4 patients within 48 hours of injury. There was no relationship between the plasma SMA and the cortisol concentration. When plasma samples from 10 patients taken soon after injury were mixed with normal human serum, samples from only 1 patient were found to contain an inhibitor(s) of SMA. The reduced plasma SMAs in the remaining patients may have resulted from the impaired production of somatomedins (SM), the degradation of SM, the dilution of circulating SM with transfusion fluids or the binding of SM to damaged tissues.

Accidents↗
PubMed1996

Plasma endothelin-1 level in athletes after exercise in a hot environment: exercise-induced dehydration contributes to increases in plasma endothelin-1.

We investigated whether dehydration due to exercise contributes to the increase in plasma endothelin-1 (ET-1) concentration. We measured the plasma concentration of ET-1 before and after exercise in a hot environment (about 30 degrees C). Five male intercollegiate Kendo (Japanese fencing) players entered the present study. Each athlete participated in 15 min of Kendo fighting, followed by 5 min of rest and another 15 min of Kendo fighting (i.e., total exercise 30 min), with or without oral intake of 700 ml of water. Body weight and left atrial diameter, a parameter that reflects changes in circulating plasma volume, were significantly decreased after exercise under both conditions. However, the decreases in both values were significantly greater after exercise without water intake than after exercise with water intake, indicating that dehydration and decreased circulating plasma volume were more marked after exercise without water intake. The extent of the increase in plasma ET-1 concentration appeared to be closely related to the extent of exercise-induced dehydration; the greater the dehydration, the greater the increase in plasma ET-1 concentration. These findings suggest that exercise-induced dehydration may contribute to increases in plasma ET-1 concentrations.

Adult↗
PubMed1979

Hyperglucagonemia in liver cirrhosis with portal-systemic venous anastomoses: responses of plasma glucagon and gastric inhibitory polypeptide to oral or intravenous glucose in cirrhotics with normal or elevated fasting plasma glucose levels.

Plasma immunoreactive glucagon (IRG) was examined in volunteers with biopsy-proven cirrhosis of the liver after recovery from surgical portal--caval anastomosis. A wide range of increased total plasma IRG concentrations was found after overnight fast in groups of cirrhotic subjects with and without fasting hyperglycemia. Gel filtration chromatography of plasma showed a major component in the 3500-mol wt fraction in all cases so studied. Administration of glucose i.v. caused rapid suppression of total plasma IRG in normoglycemic and non-insulin-dependent hyperglycemic cirrhotic subjects. After administration of oral glucose, total plasma IRG was suppressed rapidly in normoglycemic cirrhotic subjects, while non-insulin-dependent hyperglycemic cirrhotic subjects exhibited delayed but prolonged suppression. Chromatography of selected plasma with glucose-suppressed total IRG showed a major decrease in the 3500-mol wt component in every case. Exaggerated increments of plasma gastric inhibitory polypeptide were demonstrable in both groups of cirrhotic individuals after administration of oral glucose, and it is speculated that this peptide may contribute to stimulation of glucagon secretion in liver disease associated with insulin deficiency.

Administration, Oral↗
PubMed1986

Infusion of synthetic human C-peptide does not affect plasma glucose, serum insulin, or plasma glucagon in healthy subjects.

We studied six healthy male subjects to determine whether a four-hour infusion of synthetic human C-peptide sufficient to achieve mean (+/- SD) peripheral plasma concentrations of 1.3 +/- 0.7 pmol/mL affected plasma glucose, serum insulin, or plasma glucagon. Subjects were studied in a fasting state and following an oral glucose load during four-hour 0.9% NaCl (control) and C-peptide (mean dose: 70 nmol) infusions. No differences were observed between saline and C-peptide infusions for mean values of fasting plasma glucose (94 +/- 6 v 87 +/- 5 mg/dL), serum insulin (3 +/- 1 v 2 +/- 1 microU/mL), or plasma glucagon (124 +/- 65 v 112 +/- 70 pg/dL). Following oral glucose ingestion no differences were detected between saline and C-peptide infusions for mean peak values of plasma glucose (168 +/- 18 v 168 +/- 31) and serum insulin (59 +/- 6 v 57 +/- 21) or mean nadir values of plasma glucagon (80 +/- 73 v 75 +/- 70). There was a slight delay in the insulin rise following oral glucose on the C-peptide infusion day, but differences between mean values for individual sampling times were not statistically significantly different.

Adult↗
PubMed1990

Effect of warfarin on plasma and liver vitamin K levels and vitamin K epoxide reductase activity in relation to plasma clotting factor levels in rats.

Changes in plasma and liver vitamin K1 and vitamin K1 epoxide levels, liver microsomal vitamin K epoxide reductase activity, and plasma clotting factor II and VII levels were determined in rats after a single injection of warfarin (2.5 mg/kg, s.c.). The plasma and liver vitamin K1 levels gradually decreased after warfarin injection, attaining the lowest values at 2-3 hrs and remaining low for 48 hrs. They then returned to the control levels at 72 hrs. The changes in vitamin K1 epoxide levels were opposite, with an increase being seen soon after the warfarin injection, the highest values at 3 hrs and a gradual decrease to the initial levels occurring subsequently. The combined levels of vitamin K1 plus vitamin K1 epoxide, however, remained almost constant in both plasma and liver after the warfarin injection. The liver vitamin K epoxide reductase activity decreased to its lowest level soon after the injection and then gradually increased after 12 hrs, but the activity at 72 hrs was only about 30% of the initial activity. The plasma clotting factor levels gradually decreased after the injection, bottomed at 24 hrs and then began to increase, recovering almost to the initial levels at 72 hrs. A positive correlation was found between plasma and liver levels for both vitamin K1 and vitamin K1 epoxide, and the slope of the vitamin K1 epoxide curve was steeper than that for vitamin K1 in the warfarin-treated rats. A similar positive correlation was found for both vitamin K1 and vitamin K1 epoxide after vitamin K1 injection in normal untreated rats, but the slope of the vitamin K1 epoxide curve was much shallower. These results suggest that warfarin inhibits vitamin K epoxide reductase and decreases blood clotting factor synthesis, thus increasing plasma and liver vitamin K1 epoxide levels. A vitamin K epoxide reductase activity one third of that in normal rats is sufficient to maintain normal reduction of vitamin K1 epoxide and synthesis of blood clotting factors.

Animals↗
PubMed1992

Increase in plasma thrombomodulin and decrease in plasma von Willebrand factor after regular radiotherapy of patients with cancer.

In this study, we investigated plasma levels of thrombomodulin (TM) and von Willebrand factor (vWF) in 51 patients suffering from cancer or tumor undergoing 60 cobalt radiotherapy. Plasma TM and vWF antigen were measured by immunoradiometric assay and ELISA, respectively. During radiotherapy, an increase in plasma TM in patients was observed, which was radiation-dose dependent and there was a positive correlation between plasma TM level and radiation doses. However, the level of plasma vWF in the patients was decreased during radiotherapy and there was an inverse correlation between the amount of plasma vWF and radiation doses. Our data indicate that plasma TM is an useful molecular marker for early detection of radiation injury to endothelial cells in patients undergoing radiotherapy.

Adolescent↗
PubMed1992

Purification of tissue factor pathway inhibitor (TFPI) from rabbit plasma and characterization of its differences from TFPI isolated from human plasma.

Tissue factor pathway inhibitor (TFPI) is a Kunitz-type protease inhibitor that is thought to function as a natural anticoagulant to regulate tissue factor-induced coagulation (Proc. Natl. Acad. Sci. U.S.A. 88, 708, 1991). TFPI's mechanism of action has been well characterized as a two step reaction in which TFPI combines with factor Xa and subsequently TFPI/factor Xa combines with and effectively neutralizes factor VIIa/tissue factor. In human plasma, TFPI occurs in two major molecular weight forms of 34 and approximately 40 kDa. The 40 kDa form is a heterodimer of TFPI in covalent disulfide linkage to human apolipoprotein AII. TFPI circulates in human plasma primarily in association with the plasma lipoproteins. We have now isolated and partially characterized TFPI from rabbit plasma and find that, although functionally and immunologically related to TFPI isolated from human plasma, it differs from human TFPI in some of its physical properties. Rabbit TFPI is larger (approximately 45 kDa) and more extensively glycosylated than human TFPI, does not form mixed disulfides with other proteins in plasma, and unlike its human counterpart, does not circulate in plasma associated with lipoproteins.

Amino Acid Sequence↗
PubMed1994

Purification and characterization of a novel substrate for plasma kallikrein (PK-120) in human plasma.

A 120 kDa plasma protein, which is susceptible to plasma kallikrein, was purified from human plasma by polyethylene glycol fractionation followed by ion exchange chromatography using Q-Sepharose, S-Sepharose, and hydroxyapatite and gel filtration on Sephacryl S-200. The 120 kDa protein, termed PK-120 in this paper, was a single polypeptide chain containing about 20% sugar by weight and its concentration in plasma was estimated to be 80 micrograms/ml by ELISA. At least three fragments, 100, 70, and 35 kDa, were produced from PK-120 by plasma kallikrein. The N-terminal sequence and Western blot demonstrated that PK-120 was first cleaved to yield the 100 and 35 kDa fragments, then the 100 kDa fragment was cleaved into the 70 kDa fragment. N-Terminal sequence analyses of PK-120 and its fragments demonstrated that it is a novel plasma protein, distinct from high molecular weight kininogen, a natural substrate for plasma kallikrein.

Amino Acid Sequence↗
PubMed1993

Consumption of carotenoids in photosensitized oxidation of human plasma and plasma low-density lipoprotein.

Human plasma and plasma low-density lipoprotein (LDL) were exposed to photoirradiation in the presence of methylene blue (water-soluble photosensitizer) or 12-(1-pyrene)dodecanoic acid (P-12, lipid-soluble photosensitizer). In methylene-blue-sensitized photooxidation of human plasma and LDL, endogenous carotenoids and tocopherols were consumed with the accumulation of cholesteryl ester hydroperoxides (CE-OOH). Xanthophylls (zeaxanthin and lutein) decreased faster than lycopene and carotenes in the case of human plasma. In P-12-sensitized photooxidation of human plasma and LDL, the decrease rate of xanthophylls was slower than that of lycopene and carotenes. A lower level of beta-carotene exerted the effective inhibition of lipid peroxidation and retarded the oxidative loss of alpha-tocopherol, when the phosphatidylcholine liposomes containing these two lipid-soluble antioxidants were subjected to methylene blue- or P-12-sensitized photooxidation. These results suggest that antioxidant activity of carotenoids in photosensitized oxidation (Type II) of human plasma LDL depends on the site of singlet oxygen (1O2) to be generated and that carotenoids can protect tocopherols from the oxidative loss by 1O2 in the plasma.

Carotenoids↗
PubMed2004

Influence of the photocycle and thermocycle on rhythms of plasma thyroxine and plasma and ocular melatonin in late metamorphic stages of the bullfrog tadpole, Rana catesbeiana.

The diel fluctuations in plasma thyroxine (T(4)) and plasma and ocular melatonin entrain to the light/dark (LD) cycle in the bullfrog tadpole, although the phase of the rhythms changes during development. Previous studies on the rhythmicity of these hormones were conducted under various LD cycles, but with a constant temperature, raising the question of the role of the natural thermocycle in determining the phase of the rhythms, and the changes that occur in the hormone levels and rhythms during late metamorphosis. To study this question, tadpoles were acclimated to simulated natural conditions of 14.5L:9.5D with a corresponding thermocycle in which the thermophase was 28 degrees C and the cryophase was 18 degrees C, or to the same thermocycle under constant light (24L). On both photoregimens, the diel fluctuations changed between prometamorphosis and metamorphic climax. However, more statistically significant rhythms, as indicated by the cosinor, occurred on 14.5L:9.5D than on 24L. At climax on the LD cycle, all hormones peaked around the same time in the late scotocryophase, whereas on 24L, plasma T(4) peaked in the thermophase and plasma and ocular melatonin peaks occurred some distance from each other early in the cryophase. The earlier peaks of plasma and ocular melatonin on 24L were due to a transient rise in these hormones at the onset of the cryophase, which was not sustained in the absence of an LD cycle. On 14.5L:9.5D with a corresponding thermocycle, the hormone rhythms had nearly the same phases as was found in previous work on 12L:12D at a constant temperature of 22 degrees C, allowing for minor phase shifting due to the photocycle differences, indicating that in this species laboratory studies on constant temperature give valid results even in the absence of a thermocycle. The findings show that the phases of the hormone rhythms are determined by the LD cycle although the onset of the cryophase, in the absence of a photocycle, may exert some influence on the nighttime rise in melatonin. The developmental rise in plasma T(4), and drop in plasma melatonin, occurred on both 14.5L:9.5D and 24L, indicating, taken together with previous work, that these climactic changes were independent of temperature and light cycling.

Animals↗
PubMed2005

Determination of phosphoric acid triesters in human plasma using solid-phase microextraction and gas chromatography coupled to inductively coupled plasma mass spectrometry.

A simple and sensitive method for determination of phosphoric acid triesters at trace levels in human plasma sample is described. In this work, solid-phase microextraction (SPME) is employed as a sample preparation procedure for extraction and pre-concentration of alkyl and aryl phosphates followed by gas chromatography coupled to inductively coupled plasma mass spectrometry (GC-ICP-MS) for phosphorus-specific and very sensitive determination of these compounds in human plasma. The detection limits from blood plasma were 50 ngL(-1) (tripropyl phosphate), 17 ngL(-1) (tributyl phosphate), 240 ngL(-1) (tris(2-chloroethyl) phosphate) and 24 ngL(-1) (triphenyl phosphate). Sample preparation involves plasma deproteinization followed by direct immersion SPME with 65 microm poly(dimethylsiloxane/divinylbenzene) fiber. Extraction was performed at 40 degrees C for 30 min and at pH 7.0 in 10 mM sodium carbonate buffer. The reported method, to our knowledge, describes the first application of SPME with element-specific detection for analysis of phosphoric acid esters. Application of the method to the plasma samples, previously stored in poly(vinyl chloride) plasma bags revealed the presence of triphenyl phosphate, which was further confirmed by SPME GC time-of-flight high-resolution mass spectrometry.

Chemical Fractionation↗