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Mitochondria hyperpolarization is an early event in oxidized low‐density lipoprotein‐induced apoptosis in Caco‐2 intestinal cells
Author(s) -
Giovannini Claudio,
Matarrese Paola,
Scazzocchio Beatrice,
Sanchez Massimo,
Masella Roberta,
Malorni Walter
Publication year - 2002
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(02)02972-1
Subject(s) - apoptosis , depolarization , mitochondrion , membrane potential , hyperpolarization (physics) , microbiology and biotechnology , chemistry , caspase , inner mitochondrial membrane , mitochondrial apoptosis induced channel , caco 2 , biochemistry , biophysics , programmed cell death , biology , cell , organic chemistry , nuclear magnetic resonance spectroscopy
We investigated the mechanisms underlying the pro‐apoptotic activity exerted by oxidized low‐density lipoproteins (oxLDL) in Caco‐2 intestinal cells, a cell line which retains many morphological and enzymatic features typical of normal human enterocytes. We found that: (i) oxLDL induced mitochondrial‐mediated apoptosis by provoking first an increase in mitochondrial membrane potential, followed, later, by the typical apoptosis‐associated depolarization (type II apoptosis); accordingly, (ii) caspase‐9 inhibition significantly hindered apoptosis while caspase‐8 inhibition did not; and finally (iii) dietary phenolic antioxidizing compounds exerted a significant protective antiapoptotic activity. These results point to mitochondrial hyperpolarization as ‘sensitizing feature’ in apoptotic proneness of Caco‐2 intestinal cells to oxLDL exposure.