No abstract available.
Hypothyroidism* ; Myasthenia Gravis*

Aspergillus funigatus and other pathogenic fungi synthesize a toxic epidithi-odiopiperzine (ETP) metabolite, namely gliotoxin. Gliotoxin commonly react with sulfhydryl groups, and then, forms hydrogen peroxide. These fungal toxins induce apoptotic cell death in various cells. Apoptosis induced by gliotoxin need calcium. Effect of calcium preconditioning was not reported in gliotoxin-induced apoptosis. To examine the effect of protein kinase C (PKC) and calcium which was regulate caspase-3, PKC and calcium preconditioning before gliotoxin treatment, apoptotic agents such as bcl-2 family, caspase-3 and DNA fragmentation in A7r5 cell line from rat smooth muscle cell were studied. These results showed that gliotoxin induces the expression of bad of bcl-2 family, caspase-3 activation and DNA fragmentation in A7r5 cells. Gliotoxin treatment followed by calcium and PKC preconditioning suppress the Bad of bcl-2 family, and inhibited caspase-3 activation, respectively. These results suggest that PKC and calcium preconditioning protect the gliotoxin-induced apoptosis, through the protection of pro-apoptotic bcl-2 family in A7r5 cells.
Animals ; Apoptosis ; Aspergillus ; Calcium ; Caspase 3 ; Cell Death ; Cell Line ; DNA Fragmentation ; Fungi ; Gliotoxin ; Humans ; Hydrogen Peroxide ; Muscle, Smooth* ; Mycotoxins ; Myocytes, Smooth Muscle* ; Protein Kinase C ; Rats*

Paclitaxel (Taxol) is known as effective drug for inhibition of cell cycle encouraging in human cancer cells. This drug named an antimicrotubule agent which simulate the mitotic arrest towards an apoptosis. The influence of phorbol 12 myristate 13 acetate (PMA) activated protein kinase C (PKC) and nitric oxide (NO) on taxol-induced apoptosis, is poorly understood. To investigate the effects of PMA and NO on the signal transduction in taxol-induced apoptosis in C6-glial cells, the viability and caspase-3 activity of C6-glial cells were analyzed. Pretreatement with PKC activatior (PMA) protected taxol-induced cell death in C6-glial cells, by inhibited caspases-3 activity. On the other hand, the taxol-induced apoptosis was highly enhanced by sodium nitroprusside (SNP) and lipopolysaccharide (LPS), as NO activator. These results suggest that PMA strongly blocks the apoptotic effect of taxol, while nitric oxide has no protective effects in the process of toxol-induced apoptosis in C6-glial cells.
Apoptosis ; Caspase 3 ; Cell Cycle ; Cell Death ; Hand ; Humans ; Myristic Acid ; Nitric Oxide* ; Nitroprusside ; Paclitaxel ; Protein Kinase C ; Signal Transduction