Prostaglandin F2α levels in peripheral sera of man

Cernosek, R.M. Gutierrez; Morrill, Linda M.; Levine, Lawrence

doi:10.1016/0090-6980(72)90066-4

Cited by 54 publications

(10 citation statements)

References 6 publications

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“…Calcium levels in serum were determined immediately (see below), and the remaining serum was frozen at --70°C for 1-7 days before extraction for assay of prostaglandins. Sera from individual mice were combined into pools of 3.5-5.0 ml, extracted with methylal-ethanol, and concentrated as previously described for human sera (12).…”

Section: Radioimmunoassay Of Prostaglandlns--prostaglandinsmentioning

confidence: 99%

Evidence That the Bone Resorption-Stimulating Factor Produced by Mouse Fibrosarcoma Cells Is Prostaglandin E2

Tashjian

Voelkel

Levine

et al. 1972

The Journal of Experimental Medicine

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354

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Goldhaber has described a transplantable mouse fibrosarcoma which enhances the resorption of bone in tissue culture (2, 3). When fragments of the tumor (HSDM1) were placed in the same culture vessel with mouse calvaria, marked resorption of the bone was observed. Fragments of HSDM1 tumor could be cultured alone, and the medium from such explants also s t i m u l a t e d bone resorption when it was added to calvaria in organ culture. These findings suggested that the tumor was synthesizing and secreting a bone resorption-stimulating factor. Results of our previous experiments revealed that the factor could be extracted from the tumor tissue and recovered from the medium of HSDM1 cells grown in monolayer culture (1). Of particular interest was the finding that the HSDM1 factor could be extracted into organic solvents, and that it had several chemical and biological properties of a prostaglandin.We have recently reported that HSDM1 cells in culture synthesize and secrete large amounts of prostaglandin E2 (4). In the present report, we wish to present evidence that leads us to conclude that the bone resorption-stimulating factor produced b y the HSDM1 tumor is prostaglandin Ee. Materials and MethodsThe HSDM1 Tumor.--A fibrosarcoma was induced in a Swiss albino mouse by subcutaneous implantation of a Millipore filter (5, 6). The tumor has been passed serially in mice of the same strain for more than a decade. Excised tumor from a donor mouse is minced into

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Section: Radioimmunoassay Of Prostaglandlns--prostaglandinsmentioning

confidence: 99%

Evidence That the Bone Resorption-Stimulating Factor Produced by Mouse Fibrosarcoma Cells Is Prostaglandin E2

Tashjian

Voelkel

Levine

et al. 1972

The Journal of Experimental Medicine

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354

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“…The homologous PgE 2 Pl~ and anti-P~ anribodm in the same serum, bind. ,me of oar mtisera apmst PgA 2 and PIll [10,12] m s P~ and PIgB better than the anti-P~ antibodies raN/Shill [5] amtimra dhould provide a a~nnp4e do. might contribute to tim ~fkity of the PI~ amy.…”

Section: Discussionmentioning

confidence: 93%

“…The antisera exhibited specificity for both the cyclopentane ring structure and the degree of unsaturation of the side chains. However, while the specificity of antisera against prostaglandins of the F series was considerable [2,3,[6][7][8][9] and PgFla and PgF2~ could be differentiated by radioimmunoassay [ 10], antisera against prostaglandins of the A and E series often showed strong cross-reactions with prostaglandins A, B and E [1--4, 11]. In fact, several investigators [2,3] have suggested that it would be impossible to obtain sufficiently specific antibodies against PgE and PgA.…”

Section: Introductionmentioning

confidence: 99%

On the specificity of antisera against prostaglandins A₂ and E₂

Jobke

Peskar

Peskar³

1973

FEBS Letters

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“…Increased cyclooxygenase activity and thromboxane production in males as compared to females 15 also suggest the significant effect of aspirin in the former group.…”

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confidence: 93%

“…13 Augmentation of this effect by aspirin would decrease the platelet assembly even further, leading to more bleeding in males. Moreover, prostaglandin F2 alpha is a platelet aggregator inhibitor that produces its effect even in aspirin treated cells 14 is present in greater amount in males 15 , hence producing more significant bleeding as compared to the opposite gender.…”

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confidence: 99%

Sex hormones alter the effect of aspirin on bleeding

Aftab

Shakeel

Tariq

et al. 2013

Int J Basic Clin Pharmacol

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INTRODUCTIONHormones and drugs interact with each other as demonstrated by different responses of drugs in variety of individuals. These can either be direct, when drugs and hormones have common locus of action or indirect that is, by modifying some other factors, for example pharmacokinetics of a drug. These phenomena might be the reason behind the gender related dissimilarities in drug responses.Aspirin which is acetyl-salicylic acid, is the most commonly used antiplatelet drug in the prevention of cardiovascular diseases.1 The use is attributed to its effect as irreversible inhibitor of enzymes cyclo-oxygenases, COX-1 and COX-2. Owing to its irreversible inhibition of COX-1 in platelets and decreasing a potent vasoconstrictor and platelet aggregator thromboxane (TX-A2) 2 , aspirin increases bleeding time. Thus bleeding time is considered as the measure of response to aspirin.Testosterone is the major hormone in a male, while estrogen and progesterone are highly important in a female body. Since, these hormones effect bleeding tendency, they can be the reason of gender related discrepancies in responses to aspirin. Such a relationship is investigated in our study. ABSTRACTBackground: Interaction of aspirin and sex hormones was investigated through bleeding time. Methods: Bleeding time in 32 males and 105 unmarried females with previous 6 normal menstrual cycles and all aged between 18 to 21 years was found by Duke's method before and after 2 hours of aspirin administration. Phase of menstrual cycle of each female was determined by present menstrual history. Results: Bleeding time in 32 male was 69.33± 4.94 seconds and in 105 female was 73.03±1.89 seconds which were not statistically different (P>0.05).This time was increased to 107.66±4.76 seconds in males and 113.65±3.73 seconds in females after aspirin administration which were statistically different (P<0.05). The response in males was relatively greater (P<0.0005) as compared to females (P<0.0025). Among females, 44 were in follicular phase while 29 were in luteal phase as per their menstrual histories. Bleeding time in females in Follicular phase was increased from 70.22±2.90 seconds to 109.65±3.82 seconds and in females in luteal phase from 81.13±4.26 seconds to 117.95±7.49 after aspirin administration. The statistics of bleeding time in follicular and luteal Phases shows a statistically significant (P<0.05) difference before aspirin but non-significant (P>0.05) difference after aspirin administration with a greater effect in Follicular phase probably due to estradiol. Conclusion: Males respond to aspirin more as compared to females which is likely the effect of the drug and testosterone interaction. Similarly females in the follicular phase respond to aspirin more as compared to females in the luteal phase which may be a result of interaction of estrogen and aspirin.

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Prostaglandin F2α levels in peripheral sera of man

Cited by 54 publications

References 6 publications

Evidence That the Bone Resorption-Stimulating Factor Produced by Mouse Fibrosarcoma Cells Is Prostaglandin E2

Evidence That the Bone Resorption-Stimulating Factor Produced by Mouse Fibrosarcoma Cells Is Prostaglandin E2

On the specificity of antisera against prostaglandins A₂ and E₂

Sex hormones alter the effect of aspirin on bleeding

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Prostaglandin F2α levels in peripheral sera of man

Cited by 54 publications

References 6 publications

Evidence That the Bone Resorption-Stimulating Factor Produced by Mouse Fibrosarcoma Cells Is Prostaglandin E2

Evidence That the Bone Resorption-Stimulating Factor Produced by Mouse Fibrosarcoma Cells Is Prostaglandin E2

On the specificity of antisera against prostaglandins A2 and E2

Sex hormones alter the effect of aspirin on bleeding

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On the specificity of antisera against prostaglandins A₂ and E₂