Effect of cholesterol content on some physical and functional properties of mitochondria isolated from adult rat liver, fetal liver, cholesterol-enriched liver and hepatomas AH-130, 3924A and 5123

Feo, Francesco; Canuto, Rosa Angela; Garcea, Renato; Gabriel, Ludovica

doi:10.1016/0005-2736(75)90063-2

Cited by 85 publications

(40 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…From our results, the decrease of cholesterol content appears to be involved, whereas farnesylation does not appear to be important in inducing apoptosis at the earlier treatment times. Cholesterol is increased in mitochondria of AH-130 hepatoma cells in comparison with normal liver, as also occurs in Morris hepatoma and hepatoma chemically induced in rats as we have shown elsewhere (27,28). The cholesterol increase in mitochondria causes changes in physical and functional properties (27), and could be involved in preventing apoptosis in hepatoma cells.…”

Section: Discussionsupporting

confidence: 53%

See 1 more Smart Citation

Apoptosis induced by clofibrate in Yoshida AH-130 hepatoma cells

Canuto

Muzio

Maggiora

et al. 2003

Journal of Lipid Research

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 53%

“…Isoprenoids are involved in farnesylation of proteins important for cell cycle progression (24)(25)(26). Our previous results evidenced that cholesterol content increases in mitochondria of hepatoma cells, altering the physical and functional properties of the membranes (27,28).…”

mentioning

confidence: 93%

Apoptosis induced by clofibrate in Yoshida AH-130 hepatoma cells

Canuto

Muzio

Maggiora

et al. 2003

Journal of Lipid Research

View full text Add to dashboard Cite

“…We would speculate that these conditions existing in certain tumor cells, e.g. Yoshida ascites and Morris hepatoma cells whose mitochondrial cholesterol levels are greater than in normal tissue (70,71), may determine resistance to apoptosis stimuli that work through ANT.…”

Section: Fig 5 Membrane Permeability Transition Induced By Atractylmentioning

confidence: 99%

Cholesterol Impairs the Adenine Nucleotide Translocator-mediated Mitochondrial Permeability Transition through Altered Membrane Fluidity

Colell¹,

Garcı́a-Ruiz

Lluis³

et al. 2003

Journal of Biological Chemistry

124

View full text Add to dashboard Cite

Mitochondrial permeability transition (MPT) has been proposed to play a key role in cell death. Downstream MPT events include the release of apoptogenic factors that sets in motion the mitochondrial apoptosome leading to caspase activation. The current work examined the regulation of MPT by membrane fluidity modulated upon cholesterol enrichment. Mitochondria enriched in cholesterol displayed increased microviscosity resulting in impaired MPT induced by atractyloside, a c-conformation stabilizing ligand of the adenine nucleotide translocator (ANT). This effect was dependent on the dose of cholesterol loaded and reversed upon the fluidization of mitochondria by the fatty acid derivative A 2 C. Mitoplasts derived from cholesterol-enriched mitochondria responded to atractyloside in a similar fashion as intact mitochondria, indicating that a significant amount of cholesterol is still found in the inner membrane. The effects of cholesterol on MPT induced by atractyloside were mirrored by the release of intermembrane proteins, cytochrome c, Smac/Diablo, and apoptosis inducing factor. However, cholesterol loading did not affect the uptake rate of adenine nucleotide hence dissociating the function of ANT as a MPT-mediated protein from its adenine nucleotide exchange function. Thus, these findings indicate that the ability of atractyloside to induce MPT via ANT requires an appropriate membrane fluidity range.

show abstract

“…In hepatoma mitochondria the discontinuities of activation energies are slight or absent. This could be due to the high cholesterol content of these organelles [ 12,131. Membranes of hepatoma AH-1 30 mitochondria contain 25 mol percent cholesterol to phospholipid (18.5 inner membrane, 41.7 outer membrane) versus 4.6 mol percent (3.8 inner, 10.9 outer) in liver mitochondria [13].…”

Section: Discussionmentioning

confidence: 99%

“…The medium and procedures for isolation of mitochondria and mitochondrial membranes (inner plus outer) were as published [ 12 ] . The concentrations of microsomes, from determinations of glucose-6-phosphatase and NADPH-cyt.…”

Section: Methodsmentioning

confidence: 99%