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1.
Antioxidants (Basel) ; 10(11)2021 Nov 08.
Artigo em Inglês | MEDLINE | ID: mdl-34829656

RESUMO

Coenzyme Q is a unique lipidic molecule highly conserved in evolution and essential to maintaining aerobic metabolism. It is endogenously synthesized in all cells by a very complex pathway involving a group of nuclear genes that share high homology among species. This pathway is tightly regulated at transcription and translation, but also by environment and energy requirements. Here, we review how coenzyme Q reacts within mitochondria to promote ATP synthesis and also integrates a plethora of metabolic pathways and regulates mitochondrial oxidative stress. Coenzyme Q is also located in all cellular membranes and plasma lipoproteins in which it exerts antioxidant function, and its reaction with different extramitochondrial oxidoreductases contributes to regulate the cellular redox homeostasis and cytosolic oxidative stress, providing a key factor in controlling various apoptosis mechanisms. Coenzyme Q levels can be decreased in humans by defects in the biosynthesis pathway or by mitochondrial or cytosolic dysfunctions, leading to a highly heterogeneous group of mitochondrial diseases included in the coenzyme Q deficiency syndrome. We also review the importance of coenzyme Q levels and its reactions involved in aging and age-associated metabolic disorders, and how the strategy of its supplementation has had benefits for combating these diseases and for physical performance in aging.

2.
Biogerontology ; 16(5): 599-620, 2015 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-26105157

RESUMO

Ageing is accompanied by the accumulation of damaged molecules in cells due to the injury produced by external and internal stressors. Among them, reactive oxygen species produced by cell metabolism, inflammation or other enzymatic processes are considered key factors. However, later research has demonstrated that a general mitochondrial dysfunction affecting electron transport chain activity, mitochondrial biogenesis and turnover, apoptosis, etc., seems to be in a central position to explain ageing. This key role is based on several effects from mitochondrial-derived ROS production to the essential maintenance of balanced metabolic activities in old organisms. Several studies have demonstrated caloric restriction, exercise or bioactive compounds mainly found in plants, are able to affect the activity and turnover of mitochondria by increasing biogenesis and mitophagy, especially in postmitotic tissues. Then, it seems that mitochondria are in the centre of metabolic procedures to be modified to lengthen life- or health-span. In this review we show the importance of mitochondria to explain the ageing process in different models or organisms (e.g. yeast, worm, fruitfly and mice). We discuss if the cause of aging is dependent on mitochondrial dysfunction of if the mitochondrial changes observed with age are a consequence of events taking place outside the mitochondrial compartment.


Assuntos
Envelhecimento/metabolismo , Autofagia , Metabolismo Energético , Mitocôndrias/metabolismo , Estresse Oxidativo , Fatores Etários , Envelhecimento/efeitos dos fármacos , Envelhecimento/patologia , Animais , Antioxidantes/uso terapêutico , Autofagia/efeitos dos fármacos , Restrição Calórica , Metabolismo Energético/efeitos dos fármacos , Humanos , Mitocôndrias/efeitos dos fármacos , Mitocôndrias/patologia , Dinâmica Mitocondrial , Modelos Animais , Estresse Oxidativo/efeitos dos fármacos , Espécies Reativas de Oxigênio/metabolismo
3.
Mitochondrion ; 9(5): 353-63, 2009 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-19616644

RESUMO

A mutation in the Drosophila gene technical knockout (tko(25t)), encoding mitoribosomal protein S12, phenocopies human mitochondrial disease. We isolated three spontaneous X-dominant suppressors of tko(25t) (designated Weeble), exhibiting almost wild-type phenotype and containing overlapping segmental duplications including the mutant allele, plus a second mitoribosomal protein gene, mRpL14. Ectopic, expressed copies of tko(25t) and mRpL14 conferred no phenotypic suppression. When placed over a null allele of tko, Weeble retained the mutant phenotype, even in the presence of additional transgenic copies of tko(25t). Increased mutant gene dosage can thus compensate the mutant phenotype, but only when located in its normal chromosomal context.


Assuntos
Drosophila/genética , Duplicação Gênica , Doenças Mitocondriais/genética , Proteínas Mitocondriais/genética , Proteínas Ribossômicas/genética , Supressão Genética , Animais , Feminino , Dosagem de Genes , Humanos , Masculino
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