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Biomedical subjects

F Lermioglu

Publications and source records attributed to F Lermioglu.

5 recordsLinked to original sources

An investigation of household product labels in Turkey.

One hundred ninety-nine household product labels were evaluated for Turkish marking and labeling requirements and the adequacy for management of high dose exposures. Fifty-six percent of the products were proper. The rest had inadequate information or did not have warning instructions, an ingredients list and/or other requirements. The requirements do not provide adequate consumer warning and management of overdose ingestions. Household product labeling standards on Turkey should be reviewed and improved by collaboration with poison centers and manufacturers.

Consumer Product Safety

Cell density modulates the decrease of cytosolic free Ca2+ induced by atrial natriuretic hormone, S-nitroso-N-acetylpenicillamine and 8-bromo cyclic GMP in cultured rat mesangial cells.

Cyclic GMP-elevating agents, including atrial natriuretic hormone and NO-generating vasodilators, decrease cytosolic free Ca2+ levels in mesangial cells. We have investigated the role of cell density as a modulator of the decrease in cytosolic free Ca2+ induced by the cyclic GMP (cGMP)-elevating vasodilators atrial natriuretic peptide (99-126) [ANP (99-126); 'atriopeptin 28'] and the NO-generating vasodilator S-nitroso-N-acetylpenicillamine (SNAP), in cultured rat mesangial cells. Increasing cell density was significantly correlated with the decrease in cytosolic free Ca2+ induced by ANP (99-126) or SNAP. Moreover, this effect was independent of the cells' proliferative status. ANP (99-126) and SNAP induced greater fold stimulation of cGMP accumulation in high-density cells, but the levels of cGMP elicited by high concentrations of ANP (99-126) or SNAP were similar in high- and low-density cells. 8-Bromo cGMP was more effective in decreasing cytosolic free Ca2+ in high- than in low-density cells, suggesting that the greater effectiveness of ANP (99-126) and SNAP was, in part, due to greater effectiveness of endogenous cGMP in high-density cells. The results document that cell density, but not proliferative status, plays an important role in the modulation of intracellular Ca2+ dynamics in rat mesangial cells by atriopeptins, NO-generating vasodilators and cGMP.

Animals

Modulation of Ca by agents affecting voltage-sensitive Ca channels in mesangial cells.

The purpose of this study was to investigate the effects of depolarizing media and of Ca-channel activators and blockers on cytosolic free Ca in cultured rat mesangial cells. Membrane depolarizing media, containing 10-100 mM K+, dose dependently increased cytosolic Ca, and this effect was sustained and reversible. Nifedipine and lanthanum ion inhibited this increase, whereas verapamil was ineffective. A Ca-channel activator, BAY K 8644, dose dependently increased resting Ca levels, and nifedipine inhibited this effect. Moreover, the increase of Ca induced by maximally effective high K+ and BAY K 8644 was additive, suggesting differential mechanisms of action for the two channel activators. Nifedipine and verapamil decreased resting Ca levels by up to 35-40%. The results support the idea that mesangial cells have spontaneously active Ca channels that can be further activated by membrane depolarization or by the Ca-channel activator, BAY K 8644, and inhibited by the Ca-channel blockers, nifedipine or verapamil. Voltage-sensitive Ca channels in mesangial cells may play a role in the regulation of the glomerular filtration rate.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy

A novel biological effect of atrial natriuretic hormone: inhibition of mesangial cell mitogenesis.

We have investigated the effect of atrial natriuretic hormone on serum-induced mitogenesis in cultured rat mesangial cells. Synthetic peptides, atriopeptin 28 and atriopeptin 24, dose-dependently decreased thymidine incorporation, with a half-maximal effect at approximately 1 nM and a maximal inhibition of approximately 60%. Moreover, atriopeptin 28 significantly decreased the clonal proliferation of mesangial cells. Atriopeptin 28 also decreased resting cytosolic Ca but had no effect on the increase induced by serum, relative to the lower baseline established by atriopeptin 28. Nevertheless, the overall effect of atriopeptin 28 on Ca was to attenuate the serum-induced increase, relative to the original resting level. These results therefore provide evidence for a novel biological effect of atrial natriuretic hormone and suggest that the antimitogenic effect may be mediated by atriopeptin-induced alterations of intracellular Ca dynamics. We speculate that atrial natriuretic hormone may be a modulator of mesangial cell mitogenesis in vivo.

Animals