Signaling for ethanol-induced apoptosis and repair in vitro.

Abstract:

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.

journal_name

Clin Biochem

journal_title

Clinical biochemistry

authors

Katz GG,Shear NH,Malkiewicz IM,Valentino K,Neuman MG

doi

10.1016/s0009-9120(01)00218-1

subject

Has Abstract

pub_date

2001-05-01 00:00:00

pages

219-27

issue

3

eissn

0009-9120

issn

1873-2933

pii

S0009-9120(01)00218-1

journal_volume

34

pub_type

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