The influence of calcium channel blockers and ionophore on Cu2+-induced changes of the photosynthetic activity of runner bean plants (Phaseolus coccineus L.) was investigated. Excess Cu2+ was applied to leaves by injection or via the roots to examine a short/local or a long time/systemic effect of this metal, respectively. The changes in fluorescence parameters indicated that the mechanism of toxic action of Cu2+ ions on the photosynthetic apparatus was only partially connected with Ca2+ or Ca2+ channels. In young plants Ca2+ diminished especially photochemical and nonphotochemical dissipative processes induced by short- and long-term influence of excess Cu2+. Blocking of Ca2+ channels did not change direct Cu2+ action on the photosynthetic activity, however, their opening distinctly intensified the inhibitory effect of the metal. After a longer accumulation peri od the effect of Cu2+ ions did not change significantly due to modified Ca2+ penetration through membranes (except that caused by La3+). Copper directly introduced into older leaves diminished only at its highest concentration the activity both of the donor and acceptor sides of photosystem 2 (PS2) connected with Rfd decrease and increase of LNU. A similar effect was observed also after a long-term Cu2+ action, but disturbances on the acceptor side of PS2 were observed only at a higher Ca2+ content in the nutrient solution. Ca2+ ions, particularly after openning of channels, intensified direct inhibitory Cu2+ action on the photosynthetic activity expressed by decreased values of Fv/F0 and Rfd. Lanthanum and verapamil, at a lower Ca2+ content in the medium, decreased the photosynthetic activity of Cu2+-treated plants. This effect was also seen after additional Ca2+ supply to the leaves. and W. Maksymiec, T. Baszyński.
Calcium has been shown to control the proliferation of various cells in vitro and in vivo. In this study we have attempted to modify compensatory renal growth by pharmacological interventions in mice who have undergone uninephrectomy. The effect of a calcium channel blocker verapamil was investigated. Unilateral nephrectomy of intact male mice produced the expected increase in weight of the remaining kidney by 67.5 ±8.1 %. This rise was accompanied by a proportional increase in RNA. In mice, cell hypertrophy was found to be a major factor in compensatory renal growth. Verapamil given in a i.p. dose of 1.0 or 2.0 mg/day/mouse attenuated the growth of the remaining kidney so that its weight rose by only 48.2 ±6 % and 28.2 ±4.4 %, respectively. In vivo administration of verapamil decreased the degree of compensatory renal growth and this growth inhibiting effect was directly proportional to the dose.
The aim of this study was to investigate the effects of calcium channel blockers on tertbutyl hydroperoxide (TBH) induced liver injury using isolated perfused rat hepatocytes. Rat hepatocytes were immobilized in agarose threads and perfused with Williams E medium. Hepatocyte injury was induced by the addition of tertbutyl hydroperoxide (1 mM) to the perfusion medium 30 min after the addition of either verapamil or diltiazim. Hepatocyte injury was observed by monitoring the functional and metabolic competence of hepatocytes or by ultrastructural morphological examination of hepatocytes. Verapamil (0.5 mM) reduced lactate dehydrogenase leakage in TBH-injured hepatocytes as compared to the controls (154± 11 % vs. 247± 30 %). Lipid peroxides production was reduced after verapamil pretreatment as compared to the controls and oxygen consumption was increased by pretreatment of hepatocytes with verapamil. Verapamil pretreatment increased the protein synthesis activity at both levels of granular endoplasmic reticulum and free polysomes in cytoplasm and decreased ATPase activity. Diltiazem was qualitatively effective as verapamil. It is concluded that in hepatocyte oxidative injury, calcium channel blockers exhibited hepatoprotective properties. The hepatoprotective effect of calcium channel blockers was accompanied by a decrease in ATPase activity, which may implicate a normalization of Ca2+i after TBH intoxication., H. Farghali, E. Kmoníčková, H. Lotková, J. Martínek., and Obsahuje bibliografii