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Physiological concentrations

This reaction is strongly exergonic and AG° at 37°C is —42.8 kj/mol. Physiological concentrations of phosphocreatine, creatine, and inorganic phosphate are normally between 1 mMand 10 mM. Assuming 1 mMconcentrations and using Equation (3.12), the AG for the hydrolysis of phosphocreatine is... [Pg.65]

The regulation of smooth muscle and nonmuscle myosin-II is substantially different from the mechanism described above for two important reasons. First, there is no troponin in smooth muscle and nonmuscle cells. Second, although the rate of hydrolysis of ATP by these myosins is low in the presence of physiological concentrations of Mg % the addition of actin does not necessarily result in the stimulation of ATP hydrolysis by smooth muscle or nonmuscle myosin-II. These observations suggest the presence of a unique mechanism for Ca " regulation in smooth and nonmuscle cells, and that these myosins require an activation process before actin can stimulate ATP hydrolysis. [Pg.67]

Traut TW (1994) Physiological concentrations of purines and pyrimidines. Mol Cell Biochem 140 1-22... [Pg.52]

The spherocytes are much more susceptible to osmotic lysis than are normal red blood cells. This is assessed in the osmotic fragility test, in which red blood cells are exposed in vitro to decreasing concentrations of NaCl. The physiologic concentration of NaCl is... [Pg.617]

TASINATO A D, BOISCOBOINIK D, BARTOLI G M, MARONi p and Azzi A (1995) d-a-tocopherol inhibition of vascular smooth muscle cell proliferation occurs at physiological concentrations, correlates with protein kinase C inhibition, and is independent of its ntioydd ait xo eriie% Proceedings National Academy Sciences USA 92, 12190-4. [Pg.17]

Lee et al., 2001 Murine osteoblastic MC3T3 cells Genistein at physiological concentrations stimulates cell proliferation and prevents oxidative damage. [Pg.99]

LEE Y-s, CHEN X and ANDERSON J B (2001) Physiological concentrations of genistein stimulate the proliferation and protect against free radical-induced oxidative damage of MC3T3-E1 osteobast-like Nutr Res 21, 1287-98. [Pg.104]

As mentioned earlier, physiological concentrations of carotenoids in vivo are in the micromolar range, mainly because of limited bioavailabiUty. Also, the antioxidant efficiencies of carotenoids after absorption are probably limited. Concentrations before absorption are much higher and can justify possible antioxidant actions in vivo. To test this hypothesis, Vulcain et al. developed an in vitro system of lipid peroxidation in which the oxidative stress is of dietary origin (metmyoglobin from meat) and different types of antioxidants (carotenoids, phenols) are tested. [Pg.179]

Pastori, M. et al., Lycopene in association with alpha-tocopherol inhibits at physiological concentrations proliferation of prostate carcinoma cells, Biochem. Biophys. Res. Com., 250, 582, 1998. [Pg.192]

In summary, unoxidized lycopene can act as a lipid and a DNA antioxidant at physiological concentrations but oxidized lycopene or high concentrations of lycopene, and depending upon the oxidizing conditions, may increase lipid peroxidation and oxidative DNA damage. Furthermore, the pro-oxidant effects may result in an increased apoptosis and a decreased cell viability, which should be kept in mind as studies on proliferation and apoptosis are reviewed. [Pg.445]

King-Batoon et al. have found that the physiological concentrations of lycopene (2pM) partially demethylated the promoter for GSTP1 and restored its expression in the breast cancer cell line MDA-MB-468, but RAR0 was not demethylated. However, lycopene did induce the demethylation of RARp in MCF10A fibrocystic cells (King-Batoon et al. 2008). Genistein, in this study, was less active compared to lycopene. [Pg.455]


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See also in sourсe #XX -- [ Pg.264 ]




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