摘要:

Glutathione peroxidase, a selenium-dependent enzyme, and tocopherol interact and may, indeed, compensate for deficiencies of one or the other. Iron-supplemented, “tocopherol-sufficient,” low-birth-weight premature infants fed (selenium-poor) formulas rich in polyunsaturated fatty acid(> 35% of fat as PUFA) develop severe hemolysis secondary to erythrocyte phosphatidyl ethanolamine loss. By further increasing tocopherol supplementation one can prevent the clinical expression of a relative tocopherol and an absolute selenium-glutathione peroxidase deficiency. Selenium-poor cow's milk preparations containing 12–15% of fat as polyunsaturated fatty acids, trace amounts of iron, and 12–15 mg/liter of tocopherol are sufficient to maintain proper nutrition without risk of increased peroxidation.

ISSN:0192-8562    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

Neutrophils and monocytes are the prime defenders of the body against suppurative bacterial and fungal infections. To accomplish their role in inflammation, they must respond appropriately to chemotactic signals elaborated from complement and bacteria. This response predictably results in the adherence and subsequent directed movement of the phagocytes toward the infected area where they recognize opsonized microbes. Attachment of the microbes to the membrane of the cell leads to their ingestion and subsequent demise, principally by the reduced oxygen by-product H2O2, which is generated by the neutrophils and monoctyes during phagocytosis. Optimal killing requires the translocation of granule myeloperoxidase into the phagocytic vacuole containing the bacteria and a suitable halide ion. Degranulation is controlled, in part, by assembled microtubles whereas ingestion requires assembly of submembrane microfilaments. Deficiency states resulting from vitamin E results in dimished membrane-related chemotaxis and ingestion, whereas depletion of cellular GSH results in defective microtubule assembly preventing the normal increase in adherence, chemotaxis, degranulation, and microbicidal activity of the phagocytic cells. Deficiency states resulting in dysfunction of the microtubule system include neutrophil glutathione synthetase deficiency, rodent glutathione peroxidase deficiency, and the Chediak-Higashi syndrome.

ISSN:0192-8562    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

In both animals and humans, vitamin E deficiency is associated with platelet hyperaggregability. In six E-deficient children, thrombocytosis was associated with marked hyperaggregability of their platelets to ADP, epinephrine, and collagen. Platelet malonyldialdehyde (MDA) formation was used as an indicator of prostaglandin formation, and was found to be increased during the E deficiency state. Following E repletion, both platelet aggregation and platelet MDA formation returned to normal. The addition of vitamin E to plateletsin vitrohas been associated with inhibition of platelet release, aggregation, and MDA formation.Extending thesein vitroobservations further, six normal controls were given 1600 units of vitamin E orally daily for 2 weeks to elevate their plasma E levels and the E content of their plateletsin vivo. Concomitant with the elevation in their plasma E levels, there was an inhibitory effect of 12–20% on platelet MDA formation following E ingestion. These studies suggest that E deficiency increases thein vivosynthesis of platelet endoperoxides and prostaglandins, and that E excess has the opposite effect, i.e., inhibition of the endoperox-ide intermediates of prostaglandin synthesis.Several phenolic antioxidants such as α-tocopherol or vitamin E, butylated hydroxytoluene, and propylgallate inhibit lipid peroxidation. These compounds inhibit the oxidation reactions catalyzed by cyclo-oxygenase(2,1) and lipoxidase(3,4) to varying degrees. In 1966, Nugteren et al.(1)demonstrated that high concentrations of the antioxidants, propylgallate and vitamin E, inhibited prostaglandin biosynthesis in a paniculate fraction of the sheep vesicular gland. These antioxidants inhibit thein vitroperoxidation of arachidonic acid, which is catalyzed by sheep vesicular gland dioxygenase.

ISSN:0192-8562    

出版商:OVID    

年代:1979

数据来源: OVID

ISSN:0192-8562    

出版商:OVID    

年代:1979

数据来源: OVID

摘要:

Focal nodular hyperplasia and adenoma of the liver together represent approximately 2% of all primary hepatic tumors and tumor-like lesions in childhood. This study reports the clinical and pathologic features of focal nodular hyperplasia in three children, all females between 27 months and 15 years of age with asymptomatic hepatomegaly. In contrast, massive hemoperitoneum from a ruptured, hemorrhagic mass was the presentation of the hepatic adenoma in a 14-year-old girl. There was no history of administration of steroids in these four children. Angiography in two cases (one case each of focal nodular hyperplasia and hepatic adenoma) revealed hypervascular lesions with abnormal tortuous vessels suggesting a malignant tumor. Pathologically, the adenoma and focal nodular hyperplasias were readily distinguishable and the necessity for this differentiation was reviewed. All four patients are currently doing well.

ISSN:0192-8562    

出版商:OVID    

年代:1979

数据来源: OVID

ISSN:0192-8562    

出版商:OVID    

年代:1979

数据来源: OVID