Effect of cardiolipin on functional properties of isolated rat liver mitochondria

Abstract

The specific involvement of cardiolipin in modulating and/or controlling the activity of a number of mitochondrial carriers, enzymes and receptors is well documented; however, comparatively less understood is its role for the integrated functions of intact mitochondria. The aim of the present research was to get a better insight into this problem by investigating the effect of in vitro addition of cardiolipin on the properties of isolated liver mitochondria.The results obtained show that cardiolipin induces extensive structural and functional perturbations at the level of the inner mitochondrial membrane. In fact, addition of cardiolipin to intact mitochondria causes a significant increase of proton leak associated with a parallel increase of respiratory rate in State 4. Concomitantly, a slight uncoupling of phosphorylation associated with a moderate increase in ATPase activity is observed. Furthermore, the pore-mediated membrane permeability to calcium is drastically modified, an effect that can be reversed by addition of cycIosporin.

Imeglimin Normalizes Glucose Tolerance and Insulin Sensitivity and Improves Mitochondrial Function in Liver of a High-Fat, High-Sucrose Diet Mice Model

“…In addition, we cannot exclude a role of imeglimin preventing other deleterious effects of oxidative stress, as previously reported (28,29). Cardiolipin content increases in mitochondrial membranes could contribute to the increase in the respiration rate during overfeeding because cardiolipins are known to induce nonphosphorylating energy wasting in mitochondria (16,30). Increases in ATP synthase and ANT content could also amplify mitochondrial respiration.…”

Decrease in mitochondrial energy coupling by thyroid hormones: a physiological effect rather than a pathological hyperthyroidism consequence

“…In order to check whether the treated rats changed their thyroid state, the rate of mitochondrial respiration was measured using α‐glycerol phosphate as respiratory substrate since the activity of mitochondrial α‐glycerol phosphate dehydrogenase (EC 1.1.99.5) is known to strictly correlate with the thyroid state of animals [29]. Mitochondria were prepared as described by Bobyleva et al [30]from 10% total liver homogenate. Mitochondrial respiration was measured at 30°C in a medium of the following composition: 100 mM KCl, 10 mM MgCl 2 , 10 mM Tris‐HCl, 10 mM Na,K phosphate buffer, pH 7.4, 10 mM dl ‐α‐glycerol phosphate and 3 μM rotenone.…”

Lack of Mitochondrial Anionic Phospholipids Causes an Inhibition of Translation of Protein Components of the Electron Transport Chain

“…In all carbon sources tested in three genetic backgrounds, PG levels remain elevated at least 5-fold in crd1⌬ strains. 2 Since lack of anionic phospholipids results in failure to translate components of the ETC, our biological reagent cannot be used to test whether components of the ETC require these lipids for function (2,3). However, in vitro reconstitution experiments show a necessity for CL for ATP synthase activity (67) and particularly the ADP/ATP translocase (68,69).…”

“…Due to their intracellular distribution, these anionic phospholipids have been postulated to be an essential component in many mitochondrial processes such as electron transport, ion permeability, membrane integrity, protein import, and solute transport (2,3).…”