Ratio Of Alpha Research Articles

Promiscuous subunit interactions: A possible mechanism for the regulation of protein kinase CK2.

Protein kinase CK2 is a ubiquitous eukaryotic ser/thr protein kinase. The active holoenzyme is a heterotetrameric protein composed of catalytic (α and α') and regulatory (β) subunits that phosphorylates many different protein substrates and appears to be involved in the regulation of cell division. Despite important structural studies, the intimate details of the interactions of the α catalytic subunits with the β regulatory subunits are unknown. Recent evidence that indicates that both CK2 subunits can interact promiscuously with other proteins in a manner that excludes the binding of their complementary CK2 partners has opened the possibility that the phosphorylating activity of this enzyme may be regulated in a novel way. These alternative interactions could limit the in vivo availability of CK2 subunits to generate fully active holoenzyme CK2 tetramers. Likewise, variations in the ratio of α- and β-subunits could determine the activity of several phosphorylating and dephosphorylating activities. The promiscuity of the CK2 subunits can be extrapolated to a more widespread phenomenon in which "wild-card" proteins could act as general switches by interacting and regulating several catalytic activities. J. Cell. Biochem. Suppls. 30/31:129-136, 1998. © 1998 Wiley-Liss, Inc.

Alternative splicing of a precursor-mRNA encoded by the Chlorella sorokiniana NADP-specific glutamate dehydrogenase gene yields mRNAs for precursor proteins of isozyme subunits with different ammonium affinities.

Chlorella sorokiniana has seven ammonium-inducible, chloroplastic NADP-specific glutamate dehydrogenase (NADP-GDH) isozymes composed of varying ratios of alpha- and beta-subunits. Southern blot and allele-specific PCR analyses indicate that the C. sorokiniana genome possesses a single 7178 bp nuclear NADP-GDH gene. cDNA cloning and sequencing, 5'-RACE-PCR analysis, and RNase protection analysis identified two NADP-GDH mRNAs that are identical with the exception of a 42 nt sequence located within the 5'-coding region of the longer mRNA. The 42 nt sequence, termed an auxon because it serves as an exon or intron, appears to undergo alternative splicing from the precursor mRNA by a process that is regulated by both nutritional and environmental signals. Depending upon whether the auxon is included or excluded in a mature mRNA, the gene can be considered to consist of 22 or 23 exons, respectively. The 2074 and 2116 nt mRNAs encode precursor proteins of 56,350 and 57,850 Da, respectively. The N-termini of the purified mature alpha- and beta-subunits were sequenced, identifying full-length subunits of 53,501 and 52,342 Da, respectively. The sequences of the subunits are identical except for an 11 amino acid extension at the N-terminus of the alpha-subunit. The alpha-subunit has an additional alpha-helical domain at its N-terminus compared with the beta-subunit. By correlating the abundances of the two mRNAs with the levels (and relative turnover rates) of the alpha- and beta-subunit antigens during induction in Chlorella, the larger mRNA is proposed to encode the larger subunit.

Expression of type XVII collagen alpha 1 chain mRNA in the mouse heart.

The type XVII collagen alpha 1 chain has been identified as a component of the type I hemidesmosome, and is thus thought to play a role in extracellular matrix (ECM) maintenance and signal transduction between the cell and the ECM. We examined the expression of type XVII collagen alpha 1 chain mRNA in the mouse heart by Northern blot analysis and determined the sequential changes of its expression in different developmental stages of the heart using the reverse transcriptase-polymerase chain reaction (RT-PCR) method. Northern blotting: Total RNA was extracted from 10 adult mouse hearts by the guanidine/cesium method. Hybridization was performed with mouse cDNA for alpha 1 (XVII) collagen. RT-PCR: Total RNA was extracted from 7 embryos, 4 neonates and 8 adult mice. Reverse transcription was performed using oligo-dT primer and MMLV. Amplification was carried out in alpha 1 (XVII) collagen and glyceraldehyde 3-phosphate dehydrogenase (GAPDH). GAPDH served as an internal control. Northern blotting revealed a 5.6 kb signal that was identical to that of the alpha 1 (XVII) of skin and transformed keratinocyte reported previously. The sequences of the PCR products were also identical to those reported. The normalized expression ratios of alpha 1 (XVII) were 0.91 +/- 0.20 in the embryonic heart, 0.36 +/- 0.20 in the neonatal heart and 0.96 +/- 0.21 in the adult heart. In conclusion, we identified the expression of type XVII collagen alpha 1 chain mRNA in the mouse heart, suggesting that the type I hemidesmosome is located in the heart. The results of the RT-PCR at different developmental stages of the heart suggest that type XVII collagen contributes not only to cardiogenesis in the embryonic stage but also to maintenance of architecture and function in the adult heart.

Clinical significance of integrin alpha 6 mRNA expression in gastric carcinoma

Integrin alpha 6 is believed to be involved in malignant biological development. High tumor/normal (T/N) ratio of integrin alpha 6 was observed in intestinal type tumors in gastric carcinoma. In an immunohistochemical study, an intense and continuous staining was seen at the basement layer in the intestinal type tumors. Concerning the variant, there was a significant correlation between the expression ratio of variant B/variant A and the depth of tumor invasion. In conclusion, i) integrin alpha 6 expression was intimately correlated with histologic differentiation, and ii) the overexpression of variant B may be correlated with tumor invasion of gastric carcinoma.

Searching for hidden information with Gabor Transform in generalized tonic-clonic seizures

The analysis of generalized tonic clonic seizures is usually difficult with scalp EEG due to muscle artifact. We applied Gabor Transform to evaluate 20 seizures from 8 consecutive patients admitted for video-EEG monitoring. We studied the relative intensity ratios of alpha, theta and delta bands over time. In 14 20 events we found a significant decremental activity in the delta band at the onset of the seizure indicating that this is dominated by theta and alpha bands. We conclude that GT is a useful auxiliary tool in the analysis of ictal activity that sheds light on the underlying pathophysiological mechanisms.

Apolipoprotein E ε4 allele decreases functional connectivity in Alzheimer’s disease as measured by EEG coherence

OBJECTIVESThe ε4 allele of apolipoprotein E (APOE) represents a major biological risk factor for late onset Alzheimer’s disease. However, it is still not known whether the APOE genotype affects the...

ANP gene expression in rat hearts during hypoxia.

It is unclear whether the increase in plasma atrial natriuretic peptide (ANP) concentration during hypoxia is due to direct, hypoxia-induced upregulation of ANP secretion in the heart, or to pressure overload of the right ventricle (RV) following hypoxia-induced pulmonary hypertension. To test the hypothesis that hypoxia leads to an early upregulation of the ANP gene, we examined the influence of acute and prolonged inspiratory hypoxia (6 h, 1 or 3 weeks) on the expression of ANP messenger ribonucleic acid (mRNA) in rat heart and compared the results with the expression of the ANP gene after acute pressure overload induced by experimental coarctation of the main pulmonary artery. As a molecular marker for hypertrophy we determined the ratio of alpha- and beta-myosin gene expression. Hypoxia increased systolic RV pressure from 20.0 +/- 1.6 mmHg to 27.8 +/- 1.6 mmHg (P < 0.01) and 41.6 +/- 2.1 mmHg (P < 0. 05) after 1 and 3 weeks hypoxia respectively. The ANP plasma concentration did not change significantly after 6 h or 1 week: 232 +/- 21 pg/ml (control), 246 +/- 25 pg/ml (6 h), 268 +/- 25 pg/ml (1 week), but increased significantly after 3 weeks hypoxia (446.8 +/- 99.56 pg/ml; P < 0.05). ANP mRNA levels in different regions of the heart did not change after 6 h or 1 week hypoxia. After 3 weeks hypoxia ANP mRNA had increased 2.7-fold in the RV (P < 0.05), 4. 2-fold in the left ventricle (LV, P < 0.05), 3.5-fold in the septum (S, P < 0.05) and about 1.4-fold in the right (n.s.) and left atrium (n.s.). Relative ventricular masses increased significantly only for the RV (190%, P < 0.05) during hypoxia. The beta/alpha-myosin mRNA ratio did not change after 6 h hypoxia but, contrary to ANP gene expression, increased after just 1 week (6.1-fold in RV, 7.8-fold in LV, 6-fold in S; P < 0.05) and was more pronounced in the RV after 3 weeks (9.4-fold in RV, 7.6-fold in LV, 9.1-fold in S; P < 0.05). The increase in the beta/alpha-myosin mRNA ratio in the LV contrasts with a lack of increase in relative ventricular mass. Acute pressure overload in the RV after pulmonary arterial banding significantly increased ANP-mRNA and the beta/alpha-myosin mRNA ratio after 1 day in the RV. In the LV ANP mRNA was unchanged. The delayed upregulation of the ANP gene suggests that hypoxia per se is not a significant stimulus for ANP gene expression in the heart and that hypoxia-induced ANP-gene expression in the heart is regulated predominantly by the increase in RV afterload due to hypoxia-induced increased pulmonary pressure. The upregulation of ANP and beta-myosin mRNA in the LV during chronic hypoxia has yet to be elucidated.

Centrosomes isolated from Spisula solidissima oocytes contain rings and an unusual stoichiometric ratio of alpha/beta tubulin.

Centrosome-dependent microtubule nucleation involves the interaction of tubulin subunits with pericentriolar material. To study the biochemical and structural basis of centrosome-dependent microtubule nucleation, centrosomes capable of organizing microtubules into astral arrays were isolated from parthenogenetically activated Spisula solidissima oocytes. Intermediate voltage electron microscopy tomography revealed that each centrosome was composed of a single centriole surrounded by pericentriolar material that was studded with ring-shaped structures approximately 25 nm in diameter and <25 nm in length. A number of proteins copurified with centrosomes including: (a) proteins that contained M-phase-specific phosphoepitopes (MPM-2), (b) alpha-, beta-, and gamma-tubulins, (c) actin, and (d) three low molecular weight proteins of <20 kD. gamma-Tubulin was not an MPM-2 phosphoprotein and was the most abundant form of tubulin in centrosomes. Relatively little alpha- or beta-tubulin copurified with centrosomes, and the ratio of alpha- to beta-tubulin in centrosomes was not 1:1 as expected, but rather 1:4.6, suggesting that centrosomes contain beta-tubulin that is not dimerized with alpha-tubulin.

Transgenic mice overexpressing the beta 1-adrenergic receptor in adipose tissue are resistant to obesity.

The ratio of alpha- to beta-receptors is thought to regulate the lipolytic index of adipose depots. To determine whether increasing the activity of the beta 1-adrenergic receptor (AR) in adipose tissue would affect the lipolytic rate or the development of this tissue, we used the enhancer-promoter region of the adipocyte lipid-binding protein (aP2) gene to direct expression of the human beta 1 AR cDNA to adipose tissue. Expression of the transgene was seen only in brown and white adipose tissue. Adipocytes from transgenic mice were more responsive to beta AR agonists than were adipocytes from nontransgenic mice, both in terms of cAMP production and lipolytic rates. Transgenic animals were partially resistant to diet-induced obesity. They had smaller adipose tissue depots than their nontransgenic littermates, reflecting decreased lipid accumulation in their adipocytes. In addition to increasing the lipolytic rate, overexpression of the beta 1 AR induced the abundant appearance of brown fat cells in subcutaneous white adipose tissue. These results demonstrate that the beta 1 AR is involved in both stimulation of lipolysis and the proliferation of brown fat cells in the context of the whole organism. Moreover, it appears that it is the overall beta AR activity, rather than the particular subtype, that controls these phenomena.

The Non-Ligand Binding β-Isoform of the Human Glucocorticoid Receptor (hGRβ): Tissue Levels, Mechanism of Action, and Potential Physiologic Role

Alternative splicing of the transcripts of the human glucocorticoid receptor gene results in two mutually exclusive products, the classic, ligand-binding glucocorticoid receptor (hGR alpha), and a dominant negative non-ligand-binding isoform, hGR beta. We examined the existence of and quantified both hGR alpha and hGR beta isoforms in a panel of human tissues, as well as in intact and fractionated HeLa cells, using specific quantitative Western blots and/or immunocytochemistry. We studied the potential interactions of hGR beta with heat shock protein (hsp) 90 and/or hGR alpha using cross-immunoadsorption/precipitation procedures followed by Western blots. For the first time, we demonstrated the natural existence of the hGR beta protein, which was widely expressed in human tissues. The ratio of immunoreactive hGR alpha to hGR beta varied from 0.2 to 1.0 among different tissues, and was approximately 0.2 in HeLa cells. In the latter, both isoforms were distributed in the cytoplasm and nucleus in the absence of the hormonal ligand, and translocated into the nucleus after addition of dexamethasone. The cytosolic and nuclear hGR alpha-to-hGR beta ratio remained the same before and after dexamethasone exposure, suggesting that upon activation the two isoforms translocated into the nucleus in equal proportions. hGR alpha- and hGR beta-specific antibodies cross-adsorbed and precipitated cytosolic and nuclear glucocorticoid hGR alpha and hGR beta, respectively, as well as hsp90, suggesting that hGR alpha and hGR beta are in complex with hsp90 and/or each other. The hGR beta protein is widely expressed throughout the human body and present mostly in the cytoplasm of human cells, in complex with hsp90 and other proteins. In the presence of glucocorticoid, hGR beta probably heterodimerizes with ligand-bound hGR alpha and translocates into the nucleus to act as a dominant negative inhibitor of the classic receptor.

Differential co-expression of nicotinic acetylcholine receptor alpha 4 and beta 2 subunit genes in various regions of rat brain.

The predominant nicotinic acetylcholine receptor (nAChR) subtype in brain binds nicotine with high affinity and has an alpha 4:beta 2 subunit stoichiometry of 2:3. In this study, the mRNA levels of nAChR alpha 4 and beta 2 subunits were simultaneously quantitated by ribonuclease protection assay and compared with the number of alpha 4 beta 2 receptor subtype, measured by (-)-[3H]nicotine binding in the cerebellum, brain stem, hippocampus, cortex, thalamus and striatum of rat brain. The rank order of abundance of alpha 4 and beta 2 mRNA was different from that of alpha 4 beta 2 receptor subtype levels in the six brain regions studied. The ratio of alpha 4:beta 2 transcripts varied from 2:2.6 to 2:33 in these brain regions. These results reveal a differential co-expression of alpha 4 and beta 2 subunit genes in various regions of rat brain.

Characterization of F-actin bundling activity of Tetrahymena elongation factor 1 alpha investigated with rabbit skeletal muscle actin.

Elongation factor 1 alpha (EF-1 alpha) is an essential factor for protein synthesis in eukaryotes. Here, we demonstrated that Tetrahymena EF-1 alpha induced bundles of rabbit skeletal muscle F-actin as well as Tetrahymena F-actin in vitro, although Tetrahymena and skeletal muscle actins are different in some parts of their primary structures and in the binding abilities to some actin-binding proteins. Co-sedimentation experiments showed that the binding ratio of Tetrahymena EF-1 alpha to skeletal muscle F-actin in the bundles was 1 : 1. Electron microscopic observation showed that alkaline pH or high ionic strength reduced the bundling activity of Tetrahymena EF-1 alpha to some extent, although the EF-1 alpha seemed to be able to induce bundling of the F-actin within the range of physiological condition.

Clinical Features and Studies of Erythropoiesis in Israeli Bedouins With Congenital Dyserythropoietic Anemia Type I

Congenital dyserythropoietic anemia (CDA) type I is a rare macrocytic anemia of unknown etiology. In the present study, we redefined the clinical and laboratory picture of CDA type I, some of its pathogenic aspects, and the association with thalassemia-like features in 20 patients, all of whom belong to one Bedouin tribal group and are probably descended from a common ancestor. In each case ultrastructural studies of bone marrow (BM) erythroblasts showed the classic morphological findings of CDA type I. Serological tests for CDA type II were negative. The clinical picture was variable, but mostly benign. Some patients displayed elevated hemoglobin A2 levels or high ratio of alpha- to non-alpha- globin. However, neither family studies nor complete sequence analysis of the beta-globin was compatible with beta-thalassemia. Increased erythropoiesis was manifested by a high number of BM erythroid burst-forming units. Serum erythropoietin was also elevated. BM flow cytometry studies demonstrated arrest of erythroid precursors in the S phase of the cell cycle. The ultrastructural morphological features of the erythroid precursors, showing peripheral chromatin condensation, suggest apoptosis. Additional studies are indicated to define the molecular basis of this disease.

Clinical features and studies of erythropoiesis in Israeli Bedouins with congenital dyserythropoietic anemia type I

Congenital dyserythropoietic anemia (CDA) type I is a rare macrocytic anemia of unknown etiology. In the present study, we redefined the clinical and laboratory picture of CDA type I, some of its pathogenic aspects, and the association with thalassemia-like features in 20 patients, all of whom belong to one Bedouin tribal group and are probably descended from a common ancestor. In each case ultrastructural studies of bone marrow (BM) erythroblasts showed the classic morphological findings of CDA type I. Serological tests for CDA type II were negative. The clinical picture was variable, but mostly benign. Some patients displayed elevated hemoglobin A2 levels or high ratio of alpha- to non-alpha- globin. However, neither family studies nor complete sequence analysis of the beta-globin was compatible with beta- thalassemia. Increased erythropoiesis was manifested by a high number of BM erythroid burst-forming units. Serum erythropoietin was also elevated. BM flow cytometry studies demonstrated arrest of erythroid precursors in the S phase of the cell cycle. The ultrastructural morphological features of the erythroid precursors, showing peripheral chromatin condensation, suggest apoptosis. Additional studies are indicated to define the molecular basis of this disease.

High phosphatidylcholine hydroperoxide level in plasma of guinea pigs with low and excess supplementation of ascorbic acid.

Graded amounts (0, 50, 500 and 5,000 mg/liter) of ascorbic acid (AsA) were given in drinking water to guinea pigs for 21 days to prepare AsA-deficient, low-AsA, moderate-AsA and excess-AsA animals, and the plasma phospholipid hydroperoxide level and lipid concentration were quantitatively determined to investigate the antioxidant effect of AsA in vivo. Phosphatidylcholine hydroperoxide (PCOOH) was a predominant phospholipid hydroperoxide present in the plasma, and the PCOOH concentration was significantly higher in AsA-deficient, low-AsA and excess-AsA animals (80.4 nM, 54.8 nM and 42.2 nM, respectively) as compared with that in moderate-AsA animals (27.2 nM). Hyperlipidemic plasma characterized as high cholesterol and high triacylglycerol concentrations was confirmed in AsA-deficient animals. Molar ratios of plasma AsA and alpha--tocopherol against 10(4) moles of phospholipids were significantly lower in AsA-deficient and low-AsA animals (0.6-2.1 and 5.5-8.5, respectively) than in moderate-AsA and excess-AsA animals (14.2-18.0 and 11.2-11.9, respectively). In plasma, a high correlation coefficient (r = 0.979) was observed between PCOOH and AsA for which there was optimum AsA level to keep the low PCOOH and such correlation was stronger than that (r = 0.558) observed with alpha-tocopherol. The results indicated that AsA has an important function to control the phospholipid hydroperoxide level in plasma and that moderate supplementation of AsA is required to reveal its optimal antioxidant effect in vivo. The present study also showed that AsA-deficiency especially invites an increase in plasma PCOOH together with a hyperlipidemic state which are risk factors in developing atherogenesis.

The expression of lymphocyte function associated antigen-1, intercellular adhesion molecule-1 on peripheral blood lymphocytes in patients with systemic lupus erythematosus.

The ratios of CD11a, CD18, HLA-DP on T cells and CD54 on B cells of 54 patients with active systemic lupus erythematosus (SLE) were examined. The ratios of LFA-1 alpha, beta, ICAM-1, HLA-DP among SLE patients were significantly higher when compared with normal healthy controls, and the significant correlation between the ratio of LFA-1+ T cells and HLA-DP+ T cells, and LFA-1+ T cells and ICAM-1+ B cells was recognized. These results may suggest that LFA-1, ICAM-1 is related to the mutual action between activated T cells and B cells.

Distribution of α- and β-Subunits of Glycoprotein Hormones in Thyrogonadotroph in the Anterior Pituitary Cells of the Musk Shrew (&lt;i&gt;Suncus murinus&lt;/i&gt;)

In order to examine the distribution pattern of alpha- and beta-subunits of glycoprotein hormones in small and large granules in the thyrogonadotrophs of the musk shrew, we used an antiserum against a synthesized peptide consisting of the sequence 37-53 of the rat alpha-subunit, which is highly conservative among several mammalian species, and also antisera to LH beta, FSH beta and TSH beta. Both alpha- and LH beta-subunits were colocalized in what appeared at the light-microscopic level to be the same cells, and the population ratio of alpha- and LH beta-subunit immuno-reactive cells was almost equal within each group of animals. In addition, we also demonstrated thyrogonadotrophs in the infant musk shrew as well as in the adult. Concerning small and large granules in thyrogonadotrophs of the musk shrew, we could observed small granules immunoreactive for only the alpha-subunit, for the LH beta-subunit and for both the alpha- and LH beta-subunits; while only the LH beta-subunit was observed in the large granules and the alpha-subunit was absent. Consequently, we propose that the large granules observed in the thyrogonadotrophs of the musk shrew may be storage sites for beta-subunits and are not secretory-type granules.

Differential expression of alpha- and beta-enolase genes during rat heart development and hypertrophy

We have analyzed the transition between isoforms of the glycolytic enzyme enolase (2-phospho-D-glycerate hydrolyase; EC 4.2.1.11) in rat heart during normal and pathological growth. A striking fall in embryonic alpha-enolase gene expression occurs during cardiac development, mostly controlled at pretranslational steps. In fetal and neonatal hearts, muscle-specific beta-enolase gene expression is a minor contributor to total enolase. Control mechanisms of beta-enolase gene expression must include posttranscriptional steps. Aortic stenosis induces a rapid and drastic decrease in beta-enolase transcript level in cardiomyocytes, followed by the fall in beta-subunit level. In contrast, alpha-enolase transcript level is not significantly altered, although the corresponding subunit level increases in nonmuscle cells. We conclude that, like fetal heart, hypertrophic heart is characterized by a high ratio of alpha- to beta-enolase subunit concentrations. This study indicates that the decrease in beta-enolase gene expression may be linked to beneficial energetic changes in contractile properties occurring during cardiac hypertrophy.

Glycosidic specificity of fucosyltransferases present in rat epididymal spermatozoa.

We have recently demonstrated multiple fucosyltransferase (FT) activity in rat spermatogenic cells. To complement these findings, here we identify and partially characterize the glycosidic linkage specificity of FTs present in spermatozoa from caput and cauda epididymides. Analysis of the acceptor substrate specificity of the FTs by thin-layer chromatography indicated that both caput and cauda sperm expressed alpha(1-2)-, alpha(1-3)-, alpha(1-4)-FTs as demonstrated by fucose incorporation into phenyl-beta-D-galactoside, 2'-fucosyllactose, and lacto-N-fucopentaose-I, respectively. Spermatozoa from the cauda epididymidis exhibited significant decreases in the levels of alpha(1-2)-, alpha(1-3)-, alpha(1-4)-FTs, and of total soluble FTs in comparison to spermatozoa from the caput epididymidis. The relative ratio of alpha(1-3)-FT to total FT activity appeared to be significantly higher than those of alpha(1-2)- or alpha(1-4)-FTs, in spermatozoa both from caput and cauda epididymides. Using different types of low molecular weight acceptors and the selective inhibition of the FT by N- ethylmaleimide, we have demonstrated that at least alpha(1-2)-FT is different from alpha(1-3)- or alpha(1-4)-FTs. Kinetic studies also showed that alpha(1-2)-FT is different from alpha(1-3)- or alpha(1-4)-FTs as demonstrated by apparent Km and Vmax values. Moreover, alpha(1-3)- and alpha(1-4)-FT activities in cauda sperm were found to be highly sensitive to Mn2+ but showed differential responses to divalent cations. In contrast, both alpha(1-3)- and alpha(1-4)-FTs seemed to be relatively less sensitive to Mg2+. Thus, these results not only demonstrate the presence of multiple FTs in rat epididymal sperm but also differentiate individual FTs with regard to their kinetic properties and sensitivity to both inhibitor and divalent cations.

Placental prostanoid release in severe intrauterine growth retardation

Our objective was to evaluate prostanoid release from the placentae of pregnancies complicated by severe intrauterine growth retardation (IUGR) and without hypertension, compared with placentae from normal, uncomplicated term pregnancies. A perifusion system was utilized to study the release of prostanoids 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), thromboxane B2(TxB2), prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha) from human placentae from pregnancies complicated by normotensive severe IUGR (n = 9, five at term and four preterm) and normal control pregnancies (n = 6). For each placenta, triplicate chambers of tissue were perifused at a rate of 6 ml/h, and samples were collected from hours 5-10. Prostanoids were measured using specific and sensitive radioimmunoassays. In the IUGR group, the basal placental production of the vasoconstrictor thromboxane was not increased, nor was the ratio of cumulative TxB2 to 6-keto-PGF1 alpha elevated compared with normal term controls. In three term IUGR placentae, the ratio was significantly decreased compared with controls. The basal placental production of the vasoconstrictor PGF2 alpha was likewise not increased compared with controls, nor was the ratio of PGF2 alpha to PGE2 elevated. Two of the placentae in the term IUGR group demonstrated significant elevations of PGE2 and 6-keto-PGF1 alpha. Overall, the IUGR placentae released normal or low normal levels of the prostanoids studied. The pattern of placental prostanoid release over time was similar to that of the normal term placentae. The term and preterm placentae of pregnancies complicated by severe IUGR did not exhibit an excess production of vasoconstrictor prostanoids. Therefore, strategies designed to reduce thromboxane production in severe IUGR without hypertension may be unjustified.