Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0153470 (Spleen)
 4,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

RRR-alpha-tocopheryl succinate was demonstrated to be a potent in vitro modulator of retrovirus-induced immune abnormalities. Spleen cells from avian erythroblastosis virus (AEV)-infected chickens exhibit suppressed T cell mitogen-induced proliferative responses and elevated levels of suppressor T cell activity. In vitro addition of RRR-alpha-tocopheryl succinate resulted in amelioration of these abnormalities. Antioxidants including Trolox (a water-soluble analogue of RRR-alpha-tocopherol with antioxidant properties) and a combination of butylated hydroxyanisole and butylated hydroxytoluene were able to restore immune functions to levels similar to those achieved with RRR-alpha-tocopheryl succinate treatment. Aspirin, an irreversible inhibitor of cyclooxygenase activity, was capable of ameliorating some of the AEV-induced immune dysfunctions. These studies suggest a role for the antioxidant functions of RRR-alpha-tocopheryl succinate in modulation of retrovirus-induced immune abnormalities.
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PMID:RRR-alpha-tocopheryl succinate enhances T cell mitogen-induced proliferation and reduces suppressor activity in spleen cells derived from AEV-infected chickens. 182 13

Rats were pretreated with aspirin (5 mg/kg i.p. 5 days) or saline, anaesthetized with pentobarbitone, and blood pressure recorded from the carotid artery. Clonidine (30 micrograms/kg) was injected intravenously via a cannula inserted into the femoral vein. Aspirin pretreatment significantly reduced the hypotensive effect of clonidine. Spleen, heart brain, kidneys and lung were removed from the animals 60 min after clonidine administration. Prostaglandin biosynthesis from endogenous substrate was determined by homogenizing tissues (1:4 w/v) in either Tris buffer (pH 7.4) or in 1 M formic acid: ethanol (1:V/v). Prostaglandins were extracted into ethyl acetate and bioassayed on the rat stomach strip. Clonidine administration significantly increased the prostaglandin formation in heart, brain and kidney. Animals pretreated with aspirin showed a reduction in the clonidine-induced increase in prostaglandin synthesis in heart, brain and spleen. The results suggest that the hypotensive effect of clonidine in anaesthetized rats may in part be secondary to stimulation of central prostaglandin biosynthesis.
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PMID:Effect of aspirin treatment on the hypotensive effect of clonidine in rats. 663 21

Experimental autoimmune orchitis (EAO) developed in (C57Bl/6Cr x A/JCr)F1 mice 3-4 months after neonatal thymectomy (Tx) without any sensitization. The age of Tx was critical for induction of EAO: Tx at day 3 (Tx-3) was effective, but Tx at day 0 or day 7 was not effective. This lesion resulted in atrophy of the testis and was characterized by disappearance of mature sperms, formation of multinuclear giant cells in seminiferous tubules and infiltration of lymphocytes in the stroma. Epididymitis was observed prior to the development of EAO. Presence of circulating autoantibody(s) against sperms (ASA) was demonstrated by indirect immunofluorescence. The acrosomal area of mature sperms, but not of immature spermatids, was strongly. The incidence of EAO and titre of ASA increased when Tx-3 mice were unilaterally vasectomized (Vx). The majority of mice with high titres of circulating ASA were sterile. Epididymitis and orchitis could be prevented in Tx-3 mice by injection of adult spleen cells on day 4. The most effective source was normal male. Spleen cells from normal female donors and day-0 orchidectomized (Orx) donors were less effective, while those of Tx-3 male and female donors failed to prevent epididymis and orchitis. The cell population in normal male spleen effective in preventing epididymitis was shown to be a T cell population (Thy 1+, Ig-) by experiments with respective antisera treatment. These results showed that sensitization with sperm autoantigen occurred in the epididymis after Tx-3, more efficiently after Tx-3 plus unilateral Vx, and that this autosensitization was prevented by a specific suppressor T cell population, which was present in normal males but absent in Tx-3 mice.
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PMID:Experimental autoimmune orchitis after neonatal thymectomy in the mouse. 703 91

The effect of RRR-alpha-tocopheryl succinate (VES) on lectin-induced chicken T cell proliferation was investigated. The T cell mitogens concanavalin A and phytohemagglutinin induce chicken thymic and splenic T cell proliferation. Addition of VES to the in vitro cultures inhibited T cell proliferation in a dose-dependent manner. Addition of VES to spleen cell cultures at different times after mitogen stimulation also suppressed T cell mitogenesis, suggesting that VES is not mediating its antiproliferative effects by interfering with ligand (mitogen)-receptor binding or early ligand-bound receptor-signaling events. Three lines of evidence suggest that the growth-inhibitory properties of VES are unique and may not involve antioxidant properties. 1) Three other forms of vitamin E, dl-alpha-tocopherol, d-alpha-tocopherol, and d-alpha-tocopherol acetate, do not inhibit the proliferation of mitogen-stimulated chicken spleen cells. 2) Spleen cells were treated with an inhibitor of nonspecific esterases to prevent the conversion of VES, which does not exhibit antioxidant properties to d-alpha-tocopherol, a lipid-soluble antioxidant. Treatment of spleen cells with the inhibitor did not affect VES's growth-inhibitory properties. 3) Trolox, a water-soluble vitamin E analogue with potent antioxidant properties and two lipid-soluble antioxidants, butylated hydroxyanisole and butylated hydroxytoluene, did not inhibit mitogen-induced T cell proliferation. Attempts to reverse VES's antiproliferative effects by addition of exogenous interleukin-2 or addition of sodium selenite, an enhancer of interleukin-2 receptors, failed. Acetylsalicylic acid had no effect on VES's inhibition of mitogen-activated T cell proliferation. These studies support the role of VES as a growth inhibitor of lectin-activated normal T cells in chickens.
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PMID:RRR-alpha-tocopheryl succinate inhibition of lectin-induced T cell proliferation. 834 73