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Biomedical subjects

D Benalal

Publications and source records attributed to D Benalal.

6 recordsLinked to original sources
PubMed1985

Opiates and cultured neuroblastoma x glioma cells. Effect on cyclic AMP and polyamine levels and on ornithine decarboxylase and protein kinase activities.

In cultured NG 108-15 neuroblastoma x glioma cells, opiates decreased cellular cyclic AMP and polyamine levels. This decrease was related to the inhibition of ornithine decarboxylase and cyclic AMP-dependent protein kinase activities during the acute exposure of the cells to the drugs. Growing the cells in the presence of opiates for several days led to drug addiction. In the tolerant-addicted cells, polyamine and cyclic AMP levels were close to normal values as were the activities of ornithine decarboxylase and cyclic AMP-dependent protein kinase. Removal of the opiate from 'addicted' cells, by either washing or by adding the antagonist naloxone, resulted in an increase in cyclic AMP and polyamine levels and the activities of ornithine decarboxylase and cyclic AMP-dependent protein kinase. The effect of opiates was closely related to their biological activities. Inactive enantiomorphs did not affect cyclic AMP or polyamine levels; neither did they decrease ornithine decarboxylase and cyclic AMP-dependent protein kinase activities.

Cell Line↗
PubMed1984

Acute effect of prenatal pethidine administration on human fetal brain cyclic AMP levels and ornithine decarboxylase activity.

The acute effect of pethidine administration on cAMP levels and ornithine decarboxylase (ODC) activity of fetal human brain from mid trimester abortion was studied. Both activities remained at the low level up to 9 h after intravenous injection of the drug to the pregnant mother. Our data suggest that pethidine causes at least temporary alterations in the cAMP levels and ODC activity of the fetal developing brain.

Abortion, Induced↗
PubMed1982

Inhibition by lithium of PGE1-sensitive adenylate cyclase in neuroblastoma X glioma hybrid cells: approach to the attenuation of the opiate withdrawal syndrome.

Exposure of neuroblastoma X glioma hybrid cells to LiCl (Li+) for 48 h significantly reduces prostaglandin E1 (PGE1)-dependent cyclic adenosine monophosphate (AMP) accumulation. When applied simultaneously with morphine for the same period, Li+ inhibits the excessive accumulation of cyclic AMP in response to PGE1 characteristically exhibited by these cells upon opiate withdrawal. Likewise, Li+ inhibits, in vitro, PGE1-dependent cyclic AMP accumulation in tissue slices from rat corpus striatum. Prophylactic administration of Li+ in the diet attenuates the withdrawal symptoms in morphine-addicted rats. These findings support clinical reports that suggest that prophylactic treatment with Li+ attenuates the severity of the opiate withdrawal syndrome.

Adenylyl Cyclase Inhibitors↗
PubMed1979

Polyamines and cellular adenosine 3' :5'-cyclic monophosphate.

The effect of polyamines on the cellular concentrations of cyclic AMP was studied. It was shown that 1 microM-spermine caused a decrease in cyclic AMP in chick-embryo heart cells, chick-embryo fibroblasts, neuroblastoma, glioma and neuroblastoma-glioma hybrid cells, grown in culture. A similar decrease was observed when polyamines were added to cells in the presence of a phosphodiesterase inhibitor or after stimulating the cells with various hormones. Noradrenaline was used in cultures of heart cells, prostaglandin E1 and adenosine for neuroblastoma and neuroblastoma-glioma hybrids, whereas isoproterenol was used for the stimulation of glioma cells. Polyamines at higher concentrations were either without effect or caused a slight increase in cyclic AMP. Spermidine (10 microM) also caused a decrease in cellular cyclic AMP, as did 0.1 microM-putrescine. It is suggested that the effect of polyamines on cellular cyclic AMP may be explained by the effect of these polycations on the activity of cellular phosphodiesterase.

Adenosine↗