OBJECTIVES: To evaluate whether caspases are involved in ethanol (EtOH)-induced apoptosis and if polyenylphosphatidylcholine (PPC) affects apoptosis, in vitro in Hep G2 cells. METHODS: Cells were treated with 100 mmol/L EtOH for 24 h and with 2 doses of 100 mmol/L EtOH (1/24 h) in the presence of absence of 20 mmol/L of PPC or 50 micromol/L caspase 3 inhibitor (IDN). Cells were analyzed for apoptosis by transmission electron microscopy (TEM) 6000 cells/treatment, DNA fragmentation by ELISA and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate (T dt-mediated d-UTP) nick-end-labeling, TUNEL. RESULTS: 100 mmol/L dose of EtOH resulted in 22 +/- 2.5% (p < 0.001) apoptosis (vs. control). Two consecutive doses of 100 mmol/L EtOH for 24 h each caused 36 +/- 3.0% (p < 0.001 vs. control and p < 0.05 vs. one dose). PPC significantly reduced apoptosis (vs. non exposed to PPC): 100 mmol/L -12 +/- 1.5% (p < 0.05) and 2 x 10(-)(0) mmol/L -20 +/- 2.0% (p < 0.001). Pretreatment with 50 micromol caspase inhibitor reduced EtOH-induced apoptosis in a similar proportion. CONCLUSIONS: PPC downregulates EtOH-apoptosis by a mechanism similar to caspase inhibition.
OBJECTIVES: To evaluate whether caspases are involved in ethanol (EtOH)-induced apoptosis and if polyenylphosphatidylcholine (PPC) affects apoptosis, in vitro in Hep G2 cells. METHODS: Cells were treated with 100 mmol/L EtOH for 24 h and with 2 doses of 100 mmol/L EtOH (1/24 h) in the presence of absence of 20 mmol/L of PPC or 50 micromol/L caspase 3 inhibitor (IDN). Cells were analyzed for apoptosis by transmission electron microscopy (TEM) 6000 cells/treatment, DNA fragmentation by ELISA and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate (T dt-mediated d-UTP) nick-end-labeling, TUNEL. RESULTS: 100 mmol/L dose of EtOH resulted in 22 +/- 2.5% (p < 0.001) apoptosis (vs. control). Two consecutive doses of 100 mmol/L EtOH for 24 h each caused 36 +/- 3.0% (p < 0.001 vs. control and p < 0.05 vs. one dose). PPC significantly reduced apoptosis (vs. non exposed to PPC): 100 mmol/L -12 +/- 1.5% (p < 0.05) and 2 x 10(-)(0) mmol/L -20 +/- 2.0% (p < 0.001). Pretreatment with 50 micromol caspase inhibitor reduced EtOH-induced apoptosis in a similar proportion. CONCLUSIONS:PPC downregulates EtOH-apoptosis by a mechanism similar to caspase inhibition.
Authors: Juliette Martin; Fabrice Magnino; Karin Schmidt; Anne-Christine Piguet; Ju-Seog Lee; David Semela; Marie V St-Pierre; Andrew Ziemiecki; Doris Cassio; Charles Brenner; Snorri S Thorgeirsson; Jean-François Dufour Journal: Gastroenterology Date: 2006-06 Impact factor: 22.682
Authors: Manuela G Neuman; Helmut K Seitz; Rolf Teschke; Stephen Malnick; Kamisha L Johnson-Davis; Lawrence B Cohen; Anit German; Nicolas Hohmann; Bernhardo Moreira; George Moussa; Mihai Opris Journal: Curr Issues Mol Biol Date: 2022-03-16 Impact factor: 2.976
Authors: Manuela G Neuman; Samuel W French; Barbara A French; Helmut K Seitz; Lawrence B Cohen; Sebastian Mueller; Natalia A Osna; Kusum K Kharbanda; Devanshi Seth; Abraham Bautista; Kyle J Thompson; Iain H McKillop; Irina A Kirpich; Craig J McClain; Ramon Bataller; Radu M Nanau; Mihai Voiculescu; Mihai Opris; Hong Shen; Brittany Tillman; Jun Li; Hui Liu; Paul G Thomes; Murali Ganesan; Steve Malnick Journal: Exp Mol Pathol Date: 2014-09-11 Impact factor: 3.362