Intramitochondrial K+ as activator of car☐yatractyloside-induced Ca2+ release

Chávez, Edmundo; Moreno‐Sánchez, Rafael; Zazueta, Cecilia; Reyes‐Vivas, Horacio; Arteaga, Diana

doi:10.1016/0005-2736(91)90087-o

Cited by 30 publications

(11 citation statements)

References 52 publications

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“…The adverse effects of high were associated with mitochondrial accumulation (Fig. Cellular was also found to affect Cytotoxicity ): Low intracellular levels decreased loss of and viability, consistent with the finding that isolated mitochondria depleted of were resistant to damage (Chavez et al, 1991). This may have interesting implications in cell toxicity, because depletion of intracellular ATP, a common event in toxic cell injury, increases cellular phosphate concentrations (Park et al, 1992).…”

Section: Role Of Mitochondrial Damage In Cytotoxicitysupporting

confidence: 66%

“…This may have interesting implications in cell toxicity, because depletion of intracellular ATP, a common event in toxic cell injury, increases cellular phosphate concentrations (Park et al, 1992). Based on studies in isolated mitochondria, that mitochondria have been proposed to have a higher binding capacity for leading to lower (Chavez et al, 1991). The recent introduction of a method to estimate mitochondrial free suggests that low levels also decrease Cytotoxicity in intact cells by preventing a rise in (Fig.…”

Section: Role Of Mitochondrial Damage In Cytotoxicitymentioning

confidence: 99%

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Mitochondria in Pathogenesis

Lemasters¹,

Nieminen²

2002

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Preface Surprisingly, the mitochondrion has emerged as a center of attention in pathophysiology, generating both excitement and controversy. Old controversies concerning the mechanism of mitochondrial energy transduction subsided with the acceptance of Peter Mitchell's hypothesis of oxidative phosphorylation, first proposed in 1961. The chemiosmotic hypothesis elegantly described how mitochondrial respiration creates an electrochemical gradient of protons across the mitochondrial inner membrane, which in turn drives ATP synthesis through the mitochondrial ATP synthase. Tight coupling of this process requires that the mitochondrial inner membrane have an exceptionally low nonspecific permeability to protons and other charged solutions. In several pathological conditions, however, the mitochondrial permeability barrier fails, leading to cell death. Indeed, in programmed cell death (apoptosis) mitochondrial membrane failure may be a key signaling event. Moreover, the same respiratory processes that generate the proton electrochemical gradient driving oxidative phosphorylation may also lead to formation of toxic reactive oxygen species that cause cellular injury. Such oxygen radicals may contribute to the decline of bioenergetic capacity with advancing age.Among the organelles of animal cells, mitochondria are unique in that they contain their own DNA. The complete nucleotide sequence of human mtDNA is established, and it encodes genes for several hydrophobic subunits of complexes I, III, IV, and V, as well as genes for ribosomal proteins and tRNA. Mutations of mtDNA have wide-ranging consequences for mitochondrial respiration and bioenergetics. Because scores of mtDNA copies are maternally inherited, in contrast to the single maternal and paternal copies of nuclear DNA, mitochondrial diseases have unusual features of incomplete penetrance, delayed expression, and heterogeneous tissue involvement. In addition, possible links between mtDNA mutations, mitochondrial free radical generation, and several neurodegenerative diseases, including Huntington, Parkinson, and Alzheimer diseases, are under investigation by several laboratories.Toxic chemicals have long been known to disrupt mitochondrial metabolism and lead to cellular injury, but the mechanisms causing the injury are turning out to be more complex than expected. For instance, calcium, oxidant chemicals, ischemia/reperfusion, and a range of other agents promote onset of the mitochondrial permeability transition ix x Preface (MPT) in mitochondria from liver, heart, and other tissues, as first characterized by Hunter and Haworth in the mid-1970s. The significance of the MPT to pathophysiological processes, however, is only now being recognized. Besides involvement of the transition in necrotic cell death, new findings implicate it in apoptosis as well. Indeed, it may be the exceptional form of cell death that does not involve transition.This book attempts to provide an overview of recent major advances in the understanding of mitochondria's numerous roles in pathop...

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Section: Role Of Mitochondrial Damage In Cytotoxicitysupporting

confidence: 66%

Section: Role Of Mitochondrial Damage In Cytotoxicitymentioning

confidence: 99%

Mitochondria in Pathogenesis

Lemasters¹,

Nieminen²

2002

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“…The hyperpermeable state is mainly characterized by efflux of Ca 2+ [15,16]. The effect of kCh on CATinduced permeability transition is illustrated in Fig.…”

Section: Resultsmentioning

confidence: 99%

On the mechanism by which 6‐ketocholestanol protects mitochondria against uncoupling‐induced Ca²⁺ efflux

et al. 1996

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This work shows that 6-ketocholestanol (kCh) inhibits the effect of carbonyl cyanide-m-chlorophenyl hydrazone (CCP) on mitochondrial Ca 2÷ efflux. Such an effect proved to be caused by diminution of membrane fluidity, therefore, it is affected by the incubation temperature. Furthermore, kCh reversed CCPinduced Ca 2+ efflux depending on the accumulation of phosphate. It is also shown that kCh enhances the effect of carboxyatractyloside on membrane permeability transition.

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“…Therefore, in mitochondria with low content of cardiolipin, Ca 2+ fails to induce membrane leakage. It should be noted that cardiolipin content in kidney mitochondria from hypothyroid rats was about 60% of those isolated from control rats [25]. …”

Section: Hypothyroidism and Mitochondriamentioning

confidence: 99%

Pleiotropic Effects of Thyroid Hormones: Learning from Hypothyroidism

Franco

Chávez

Pérez-Méndez

2011

Journal of Thyroid Research

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Hypothyroidism induces several metabolic changes that allow understanding some physiopathological mechanisms. Under experimental hypothyroid conditions in rats, heart and kidney are protected against oxidative damage induced by ischemia reperfusion. An increased resistance to opening of the permeability transition pore seems to be at the basis of such protection. Moreover, glomerular filtration rate of hypothyroid kidney is low as a result of adenosine receptors-induced renal vasoconstriction. The vascular tone of aorta is also regulated by adenosine in hypothyroid conditions. In other context, thyroid hormones regulate lipoprotein metabolism. High plasma level of LDL cholesterol is a common feature in hypothyroidism, due to a low expression of the hepatic LDL receptor. In contrast, HDL-cholesterol plasma levels are variable in hypothyroidism; several proteins involved in HDL metabolism and structure are expressed at lower levels in experimental hypothyroidism. Based on the positive influence of thyroid hormones on lipoprotein metabolism, thyromimetic drugs are promising for the treatment of dyslipidemias. In summary, hypothyroid status has been useful to understand molecular mechanisms involved in ischemia reperfusion, regulation of vascular function and intravascular metabolism of lipoproteins.

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Intramitochondrial K+ as activator of car☐yatractyloside-induced Ca2+ release

Cited by 30 publications

References 52 publications

Mitochondria in Pathogenesis

Mitochondria in Pathogenesis

On the mechanism by which 6‐ketocholestanol protects mitochondria against uncoupling‐induced Ca²⁺ efflux

Pleiotropic Effects of Thyroid Hormones: Learning from Hypothyroidism

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Intramitochondrial K+ as activator of car☐yatractyloside-induced Ca2+ release

Cited by 30 publications

References 52 publications

Mitochondria in Pathogenesis

Mitochondria in Pathogenesis

On the mechanism by which 6‐ketocholestanol protects mitochondria against uncoupling‐induced Ca2+ efflux

Pleiotropic Effects of Thyroid Hormones: Learning from Hypothyroidism

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Product

Resources

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On the mechanism by which 6‐ketocholestanol protects mitochondria against uncoupling‐induced Ca²⁺ efflux