Review articleLactic acidosis and other mitochondrial disorders☆
References (222)
Lactic acidosis
Endocrinol Metab Clin North Am
(1993)- et al.
Natural history and course of acquired lactic acidosis in adults
Am J Med
(1994) Free radicals and myocardial ischemia: Overview and outlook
Free Radic Biol Med
(1988)Regulation of reductive processes by glutathione
Biochem Pharmacol
(1986)The significance of the structural and functional similarities of bacteria and mitochondria
Int Rev Cytol
(1969)- et al.
The mitochondrial receptor complex: A central role of MOM22 in mediating preprotein transfer from receptors to the general insertion pore
Cell
(1993) - et al.
Mitochondrial transcription initiation
J Biol Chem
(1993) - et al.
Age-dependent changes in rat brain mitochondria of synaptic and non-synaptic origins
Mech Aging Dev
(1987) Cytochrome oxidase: An endogenous metabolic marker for neuronal activity
Trends Neurosci
(1989)- et al.
Liver mitochondrial respiratory functions decline with age
Biochem Biophys Res Commun
(1989)
Decline in skeletal muscle mitochondrial respiratory chain function: Possible factor in aging
Lancet
Age-related modifications of cytochrome C oxidase activity in discrete brain regions
Mech Aging Dev
Age-related changes in the activity of the pyruvate carrier and in the lipid composition in rat-heart mitochondria
Biochim Biophys Acta
Pyruvate dehydrogenase dephosphorylation in rat brain synaptosomes and mitochondria: Evidence for a calcium-mediated effect in response to depolarization, and variations due to aging
Neurosci Lett
Analyses of mitochondrial respiratory chain function and mitochondrial DNA deletion in human skeletal muscle: Effect of ageing
J Neurol Sci
Effects of age on brain oxidative metabolism in vivo
Brain Res
Cytochrome C oxidase deficient fibres in the limb muscle and diaphragm of man without muscular disease: An age-related alteration
J Neurol Sci
Mitochondrial DNA mutations as an important contributor to aging and degenerative diseases
Lancet
Age-dependent increase in deleted mitochondrial DNA in the human heart: Possible contributory factor to presbycardia
Am Heart J
Age-associated accumulation of 8-hydroxydeoxyguanosine in mitochondrial DNA of human diaphragm
Biochem Biophys Res Commun
Diabetes mellitus associated with a pathogenic point mutation in mitochondrial DNA
Lancet
Japanese case of diabetes mellitus and deafness with mutation in mitochondrial tRNALeu(UUR) gene
Lancet
Diabetes mellitus is one of the heterogeneous phenotypic features of a mitochondrial DNA point mutation within the tRNALeu(UUR) gene
FEBS Lett
Mitochondrial gene mutation in islet-cell-antibody-positive patients who were initially non-insulin-dependent diabetics
Lancet
Diabetes mellitus is one of the heterogeneous phenotypic features of a mitochondrial DNA point mutation within the tRNALEU(UUR) gene
FEBS Lett
Oxygen-derived free radicals and postischemic myocardial dysfunction (“stunned myocardium”)
J Am Coll Cardiol
Role of toxic effects of oxygen in reperfusion damage
J Mol Cell Cardiol
Oxygen radicals and the nervous system
Trends Neurosci
Role of free radicals and catalytic metal ions in human disease: An overview
Methods Enzymol
Oxygen-mediated myocardial damage during ischaemia and reperfusion: Role of the cellular defenses against oxygen toxicity
J Mol Cell Cardiol
Lactic acidemia
A controlled clinical trial of dichloroacetate for treatment of lactic acidosis in adults
N Engl J Med
The mitochondrial electron transport and oxidative phosphorylation system
Annu Rev Biochem
A role of mitochondrial glutathione peroxidase in modulating mitochondrial oxidations in liver
Eur J Biochem
A different genetic code in human mitochondria
Nature
Sequence and organization of the human mitochondrial genome
Nature
Biogenesis of mitochondria
Annu Rev Cell Biol
Ten unorthodox perspectives on evolution prompted by comparative population genetic findings on mitochondrial DNA
Annu Rev Genet
Targeting proteins to mitochondria: A current overview
Biochem J
The reproductive organs and sex cells, in Developmental Anatomy
Mitochondrial genetics: A paradigm for aging and degenerative diseases?
Science
Diseases of the mitochondrial DNA
Annu Rev Biochem
Oxidative phosphorylation diseases
Reactive oxygen species and the central nervous system
J Neurochem
Mitochondrial DNA alterations as a source of human disorders
Neurology
Effect of sepsis on activity of pyruvate dehydrogenase complex in skeletal muscle and liver
Am J Physiol
Lactic acidosis complicating the acquired immunodeficiency syndrome
Ann Intern Med
Zidovudine myopathy: A distinctive disorder associated with mitochondrial dysfunction
Ann Neurol
The biologic clock: The mitochondria?
J Am Geriatr Soc
Cited by (77)
Hyperlactatemia and Lactic Acidosis
2019, Critical Care Nephrology: Third EditionTherapeutic applications of dichloroacetate and the role of glutathione transferase zeta-1
2017, Pharmacology and TherapeuticsMetabolic Acidosis
2017, National Kidney Foundation's Primer on Kidney DiseasesRapid quantification of metabolic intermediates in blood by liquid chromatography-tandem mass spectrometry to investigate congenital lactic acidosis
2016, Analytica Chimica ActaCitation Excerpt :It could be divided into two types: acquired and congenital lactic acidosis. Congenital lactic acidosis is caused by defects of enzymes in the pathways of pyruvate oxidation, Krebs cycle, gluconeogenesis and mitochondrial electron transport chain, which are all involved in energy metabolism [1,2]. Patients with congenital lactic acidosis have a wide variety of symptoms and signs.
Increased Procurement of Thoracic Donor Organs After Thyroid Hormone Therapy
2015, Seminars in Thoracic and Cardiovascular SurgeryCitation Excerpt :Experimental studies in the 1980s demonstrated that, following the induction of brain death in the baboon, an “autonomic storm” occurred, which was associated with rapid declines in plasma levels of thyroid hormones, cortisol, insulin, and ADH1 (reviewed in Cooper et al2). Brain-dead animals were no longer able to metabolize aerobically17 (reviewed in Cooper et al2), indicating that the mitochondrial aerobic pathways were inhibited and could no longer meet the ATP requirement to support cellular homeostasis18,19 (see Supplementary Discussion). The administration of T3/T4 (+/− other hormones) reversed the inhibition of the aerobic pathways, resulting in improved metabolic and hemodynamic status.
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Supported by National Institutes of Health Grants No. R01 ES07355, P42 ES07375, and RR00082.