Activation of the ADP/ATP carrier from mitochondria by cationic effectors

Krämer, Reinhard; Mayr, Ursula; Heberger, Claudia; Tsompanidou, Stella

doi:10.1016/0005-2736(86)90166-5

Cited by 26 publications

(10 citation statements)

References 25 publications

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“…Polyamines are specifically transported into heart [32] and liver [33] mitochondria, where they appear to exert several functions, generally protective. For example, spermine regulates calcium transport [34], ATP synthesis [35], the ATP\ADP carrier [36], glutathione extrusion [37], transport of cytosolic enzymes [38,39] and is a strong inhibitor of MPT [30,34,37]. In the current report we have described a novel and unexpected effect of polyamines : the induction of cytochrome c release from heart mitochondria.…”

Section: Discussionmentioning

confidence: 85%

Polyamines directly induce release of cytochrome c from heart mitochondria

Stefanelli

Stanic

Zini

et al. 2000

Biochemical Journal

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Cytochrome c release from mitochondria to the cytosol represents a critical step in apoptosis, correlated to the activation of the caspase cascade. In this report, we show that addition of micromolar concentrations of polyamines to isolated rat heart mitochondria induces the release of cytochrome c. Spermine, which is effective at concentrations of 10-100 μM, is more potent than spermidine, whereas putrescine has no effect up to 1 mM. The release of cytochrome c caused by spermine is a rapid, saturable and selective process that is independent of mitochondria damage. Spermine, unlike polylysine, is able to release a discrete amount of cytochrome c from intact, functional mitochondria. The cytochrome c-releasing power of spermine is not affected by cyclosporin A, differently from the effect of permeability transition inducers. In a cardiac cell-free model of apoptosis, the latent caspase activity of cytosolic extracts from cardiomyocytes could be activated by cytochrome c released from spermine-treated heart mitochondria. These data indicate a novel mechanism of cytochrome c release from the mitochondrion, and suggest that prolonged and sustained elevation of polyamines, characteristic of some pathologies such as heart hypertrophy, could be involved in the development of apoptosis.

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Section: Discussionmentioning

confidence: 85%

Polyamines directly induce release of cytochrome c from heart mitochondria

Stefanelli

Stanic

Zini

et al. 2000

Biochemical Journal

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“…Magnesium concentration is known to regulate respiratory transitions in mitochondria (Masini et al, 1983). Moreover, any alterations in free and total magnesium may also affect other mitochondrial functions, such as activity of the ADP/ATP translocase, ATP synthase, and mitochondrial creatine kinase, all of which are influenced by divalent cations, particularly magnesium (Lee et al, 1970;Saks et al, 1975;Klingenberg, 1977;Moreno-Sanchez et al, 1985;Fagian et al, 1986;Kramer et al, 1986). Determining which of these processes are being affected, resulting in decreased bioenergetic state, requires further investigation.…”

Section: Discussionmentioning

confidence: 95%

Mitochondrial Metabolism Following Traumatic Brain Injury in Rats

Vink¹,

Head²,

Rogers³

et al. 1990

Journal of Neurotrauma

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Although a number of studies of traumatic brain injury have implicated mitochondrial dysfunction as a cause of altered posttraumatic energy metabolism, no studies to date have isolated mitochondria and measured their respiratory capacity following trauma. The present study sought to determine whether mitochondrial capacity for oxidative phosphorylation is adversely affected by fluid-percussion-induced traumatic brain injury in rats. Prior to brain injury, the mitochondrial respiratory control ratio was 4.3 +/- 0.2 and the ratio of nmoles of ADP phosphorylated per natom oxygen consumed (ADP/O ratio) was 2.66 +/- 0.09. After injury (2.8 atm; t = 4 h), there were slight but not significant alterations in ADP/O ratio (2.41 +/- 0.07) and state 3 respiratory rate (ADP stimulated); however, there were no changes in the respiratory control ratio. These data suggest that traumatic brain injury, unlike ischemia, does not cause uncoupling of ATP synthesis from respiration, and that brain mitochondria are quite resistant to trauma-induced injury.

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“…Polyamines at micromolar levels activated several-fold the ADP/ATP translocator from mitochondrial inner membranes. This effect, which was shared by other cationic species, showed some structural specificity and was observed on the carrier reconstituted in liposomes or with mitoplasts (Kramer et al, 1986). The polyamines could act, e.g., by binding to the cardiolipins which are tightly associated to the transporter.…”

Section: Polyamines and Transportmentioning

confidence: 91%