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  • 1975-1979  (2)
  • calcium  (1)
  • plasma membrane  (1)
  • 1
    ISSN: 1573-4919
    Keywords: regucalcin ; (Ca2+-Mg2+)-ATPase ; calcium pump ; carbon tetrachloride ; liver injury ; plasma membrane ; rat liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The alteration of the plasma membrane (Ca2+-Mg2+)-ATPase activity in the liver of rats administered orally carbon tetrachloride (CCl4) solution was investigated. Rats received a single oral administration of CCl4 (10, 25 and 50%, 1.0 ml/100 g body weight), and 3 or 24 h later they were sacrificed. CCl4 administration caused a remarkable elevation of liver calcium content and a corresponding increase in liver plasma membrane (Ca2+-Mg2+)-ATPase activity, indicating that the increased Ca2+ pump activity is partly involved in calcium accumulation in liver cells. Moreover, the participation in regucalcin, which is an intracellular activating factor on the enzyme, was examined by using anti-regucalcin IgG. The plasma membrane (Ca2+-Mg2+)-ATPase activity increased by CCl4 administration was not entirely inhibited by the presence of anti-regucalcin IgG (1.0 and 2.5 ug/ml) in the enzyme reaction mixture. However, the effect of regucalcin (0.25–1.0 uM) to activate (Ca2+-Mg2+)-ATPase in the liver plasma membranes of normal rats was not revealed in the liver plasma membranes obtained from CCl4-administered rats. Also, the effect of regucalcin was not seen when the plasma membranes were washed with 1.0 mM EGTA, indicating that the disappearance of regucalcin effect is not dependent on calcium binding to the plasma membranes due to liver calcium accumulation. Now, the presence of dithiothreitol (5 mM) or heparin (20 ug/ml) caused a remarkable elevation of the plasma membrane (Ca2+-Mg2+)-ATPase activity in the liver obtained from CCl4-administered rats. Thus, the regucalcin effect differed from that of dithiothreitol or heparin. The present study suggests that the impairment of regucalcin effect on Ca2+ pump activity in liver plasma membranes is partly contribute to hepatic calcium accumulation induced by liver injury with CCl4 administration.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-4919
    Keywords: calcium ; calcium transport ; brain ; calcium-regulating hormone ; calcium-antagonist ; energy dependency
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract The characterization of calcium accumulation in the brain of rats administered orally calcium chloride solution was investigated. Rats received a single oral administration of calcium (15–50 mg/100 g body weight), and they were sacrificed by bleeding-between 15 and 120 min after the administration. The administration of calcium (50 mg/100 g) produced a significant increase in serum calcium concentration and a corresponding elevation of brain calcium content, indicating that the transport of calcium into the brain is associated with the elevation of serum calcium levels. The increase in brain calcium content by calcium administration was not appreciably altered by the pretreatment with Ca2+ channel blockers (verapamil or diltiazem with the doses of 1.5 and 3.0 mg/100 g). In thyroparathyroidectomized rats, the administration of calcium (50 mg/100 g) caused a significant increase in brain calcium content, indicating that calcium-regulating hormones do not participate in the brain calcium transport. Now, brain calcium content was clearly elevated by fasting (overnight), although serum calcium level was not significantly altered. Calcium administration to fasted rats induced a further elevation of brain calcium content as compared with that of control (fasted) rats. The fasting-induced increase in brain calcium content was appreciably restored by refeeding. This restoration was also seen by the oral administration of glucose (0.4 g/100 g) to fasted rats. The present study demonstrates that serum calcium is transported to brain, and that the increased brain calcium is released promptly. The release of calcium from brain may be involved in energy metabolism, and this release may be weakened by the reduction of glucose supply into brain. The finding suggests a physiological significance of energy-dependent mechanism in the regulation of brain calcium.
    Type of Medium: Electronic Resource
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