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Membranes damage

As the above mentioned studies with high supplementation dosages exemplarily show, there is no known toxicity for phylloquinone (vitamin Kl), although allergic reactions are possible. This is NOT true for menadione (vitamin K3) that can interfere with glutathione, a natural antioxidant, resulting in oxidative stress and cell membrane damage. Injections of menadione in infants led to jaundice and hemolytic anemia and therefore should not be used for the treatment of vitamin K deficiency. [Pg.1300]

The drying protoplast will be subjected to tension as the result of volume contraction and its adherence to the cell wall. Early observations (Steinbrick, 1900) on desiccation tolerant species showed that the protoplasm does not separate from the wall, but rather that it folds and cavities develop in the wall. Where there are thick-walled cells, localised separation of the plasmalemma from the wall may occur. It seems unlikely, however, that rupture of the plasmalemma normally occurs during desiccation. A more subtle form of membrane damage may arise from dehydration-induced conformational changes. Certainly it is relatively easy to demonstrate that dehydrated membranes exhibit a loss of functional integrity... [Pg.117]

Daniel CS, Agarwal S, Agarwal SS. 1986. Human red blood cell membrane damage by endosulfan. Toxicol Lett 32 113-118. [Pg.281]

In both plant (e.g. [57]) and animal (e.g. [86]) cell systems, cellular respiration has been shown to be a more sensitive indicator of system response to hydro-dynamic stress than membrane integrity, suggesting that intracellular enzymes and/or organelles may be affected at stress levels lower than those required to cause membrane damage. [Pg.150]

In experimental animals, vitamin E deficiency results in resorption of femses and testicular atrophy. Dietary deficiency of vitamin E in humans is unknown, though patients with severe fat malabsorption, cystic fibrosis, and some forms of chronic fiver disease suffer deficiency because they are unable to absorb the vitamin or transport it, exhibiting nerve and muscle membrane damage. Premamre infants are born with inadequate reserves of the vitamin. Their erythrocyte membranes are abnormally fragile as a result of peroxidation, which leads to hemolytic anemia. [Pg.486]

Defen sins j Basic antibiotic peptides of 20-33 amino j acids Apparently kill bacteria by causing membrane damage... [Pg.621]

Kamat, J.P., Boloor, K.K., and Devasagayam, P.A., ChlorophyUin as an effective antioxidant against membrane damage in vitro and ex vivo, Biochim. Biophys. Acta, 1487, 113, 2000. [Pg.48]

Ungemach, F.R. (1985). Plasma membrane damage of hepato-cytes following lipid peroxidation involvement of phospholipase A2. In Free Radicals in Liver Injury (eds. G. Poli, K.H. Cheeseman, M.U. Dianzani and T.F. Slater) pp. 127-134. IRL Press, Oxford. [Pg.96]

Van der Zee, J., Dubbelman, T.M.A.R. and Van Steverinck, J. (1985). Peroxide-induced membrane damage in human erythrocytes. Biochim. Biophys. Acta 818, 38-43. [Pg.182]

Impaired circulation, destruction of RBCs, and vascular stasis are three known problems that are responsible primarily for the clinical manifestations of SCD. These pathologic findings are likely due to HbS polymerization and RBC membrane damage (Fig. 65-3). [Pg.1005]

They can be modified to change their resident circulation time, depending on their surface (cells with little membrane damage can circulate for prolonged periods). [Pg.520]

Bohm et al. (1995) have studied the protective effect of 3-CAR and LYC against cell membrane damage by N02 showing that LYC is more than twice as effective as 3-CAR. These authors observe two species from the reaction, both in the infrared, assigning them to the radical cation and a radical addition product. [Pg.292]

Bohm, F., Tinkler, J.H., and Truscott, T.G. 1995. Carotenoids protect against cell membrane damage by the nitrogen dioxide radical. Nat. Med. 1 98-99. [Pg.304]

Structural changes. At several loci cell membranes of Rn/Rn-d exposed cells appeared to be damaged similar to membrane damages... [Pg.506]

Clinical manifestations of SCD are attributable to impaired circulation, RBC destruction, and stasis of blood flow. These problems are attributable to disturbances in RBC polymerization and to membrane damage. [Pg.384]

Zhang SY, Ito Y, Yamanoshita O et al (2007) Permethrin may disrupt testosterone biosynthesis via mitochondrial membrane damage of Leydig cells in adult male mouse. Endocrinology 148 3941-3949... [Pg.112]


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See also in sourсe #XX -- [ Pg.2 ]

See also in sourсe #XX -- [ Pg.9 ]

See also in sourсe #XX -- [ Pg.403 ]

See also in sourсe #XX -- [ Pg.96 , Pg.345 ]




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