Lipids and lipolytic enzyme activities of rat heart mitochondria

Exercise-Induced Ultrastructural Changes in Skeletal Muscle*

“…5.2.2). Biochemical evidence mainly derived from heart muscle indicates that interfibrillar mitochondria oxidize substrates more rapidly than subsarcolemmal mitochondria, both populations having similar concentrations of cytochromes and cytochrome c oxidases (144,145). Similar findings are reported for mitochondria isolated from rat gastrocnemius muscle (108).…”

Characterization of trans‐monounsaturated alkenyl chains in total plasmalogens (1‐O‐alk‐1′‐enyl‐2‐acyl glycerophospholipids) from sheep heart

“…After flushing the tube with N 2 to remove residual HCl vapors, the lipids were dissolved in 5 mL chloroform. Transformation of the released aldehydes into TMDOA was performed according to a modification of the method devised by Palmer et al (14). To the preceding solution were added 10 mg of p-toluenesulfonic acid (Sigma-Aldrich Chimie S.à.r.l., Saint Quentin Fallavier, France) and 500 µL of 1,3-propanediol (Sigma-Aldrich).…”

The effect of superoxide generation on the ability of mitochondria to take up and retain Ca2+

“…Additionally there is accumulating evidence that the damage associated with Ca 2+ as measured by a general loss of internal components is due to a change to a generally permeable condition [5][6][7][8][27][28][29] apparently involving the activation of endogenous phospholipase by emergent Ca 2 +.…”

“…Evidence from studies with isolated mitochondria has shown that an excessive loading of Ca 2 +, such as may be expected on energising mitochondria in a high Ca 2+ environment, leads to a high efflux of the ion giving rise to stimulation of the endogenous phospholipase and consequent high permeability of the membrane. The lipase activity generates both fatty acids [4] and lysophospholipids [5][6][7][8] which themselves are known to cause mitochondrial swelling and loss of specific permeability. This proposed sequence of Present addresses: tDepartment of Biophysical Chemistry, Royal Free Hospital, Hunter St, London WCI; +Searle Research and Development, High Wycombe, Bucks; *Chester-Beatty Research Inst., Cranbrooke, Kent, England events does not take into account the possibility that active oxygen radicals, such as superoxide, 02- [9], may be generated from the reduced components [1] of the mitochondrial electron-transport chain when the oxygen supply is restored.…”