Kardiolipiini eroaa muista fosfolipidirakenteista olennaisesti ja sen toimintapaikka on tosiaankin vain mitokodnria, jolla on erikoinen kalvorakenne, ulko kalvo ja sisäkalvo ja niitten välille jäänyt enregiatarkoituksiin tärkeä tila. Ulkokalvolla ja sisäkalvolla on erilaiset fosfolipidikoostumat.
KARDIOLIPIINI on tosi moduli joka on kondensoitu kolmesta glyserolirungosta. R tarkoittaa rasvahappoa.
Kuva
https://www.ncbi.nlm.nih.gov/pubmed/25627476
https://link.springer.com/article/10.1007%2Fs10863-015-9607-y
https://link.springer.com/article/10.1007%2Fs10863-015-9607-y
- Metabolisia mitokondrioita on tutkittu 2014, kardiolipiini, joka on mitokondrain sisäkalvossa. Kardiolipiinirakenteeseen vaikuttaa ihmisen elintapa ja dieetti ainakin osaltaan, herediteetti on tietysti vahvin vaikuttaja. muta ihminen voi elintavoillaan haitata kardiolipiinirakenteen pätevyyttä. Ala on yksi linkki, josas on kuvattu mitokondrian ulompaa kaksoislipidikerrosta joka suojaa sisäossaa, jonka ympärillä on poimuinen lipidikerros, ja siinä sisäkerroksessa on kardiolipiinin sijaintipaikka. Siihen sisäkerrokseen asettu kellumaan tämän "energialaitoksen" proteiiniketju, "hengitysketju" , joka kuljttaa elektroneja ja ottaa vastaan happea, tekee radikaalimuotoista happea ja muodostaa vesimolekyyliä, metabolista vettä H2O. ATP-pakkauksia tekevä järjestelmä sijaitsee myös siinä. Tuottuvia protoneja syötetään kalvovälitilaan ja sieltä ne virtaavat alas ja nergia otetaan fosfaattisidoksiin proiteiinissa : ATP-pakkauksiin.
- Alustana tälle järjestelmälle täytyy olla normaalia kardiolipiiniä.
J Bioenerg Biomembr. 2014 Oct;46(5):447-57. doi: 10.1007/s10863-014-9555-y. Epub 2014 Jun 21.
Impact
of high dietary lipid intake and related metabolic disorders on the
abundance and acyl composition of the unique mitochondrial phospholipid,
cardiolipin.
UMR 866, Dynamique Musculaire et Métabolisme, Centre INRA de Montpellier, 34060, Montpellier,Abstract
Excessive
dietary lipid intake, coupled with lack of exercise, are the major
causes of the development and progression of metabolic syndrome features
e. g. obesity, hepatic steatosis, insulin resistance, type 2 diabetes
and cardiovascular diseases. These metabolic diseases are associated
with both structural and functional alterations of mitochondria.
Cardiolipin (CL) is a unique phospholipid that is almost exclusively localized in the mitochondrial inner membrane.
Cardiolipin is at the heart of mitochondrial metabolism playing a key role in several processes of mitochondrial bioenergetics as well as in mitochondrial membrane stability and dynamics, and in many of the mitochondrial-dependent steps of apoptosis. Indeed, alterations to CL content and acyl chain profile have been associated with mitochondrial dysfunction in multiple tissues in Barth syndrome and in many other physio-pathological conditions. After a brief overview of the biological roles of CL, we highlight the consequences of lipid overload-related nutritional manipulations as well as related metabolic disorders on both CL content and its fatty acid composition in the major metabolic tissues, the heart, muscle and liver. The goal of this review is to fill a void in the CL literature concerning the effects of CL abundance and form that arise following high lipid supplementation and the related metabolic disorders.
Cardiolipin (CL) is a unique phospholipid that is almost exclusively localized in the mitochondrial inner membrane.
Cardiolipin is at the heart of mitochondrial metabolism playing a key role in several processes of mitochondrial bioenergetics as well as in mitochondrial membrane stability and dynamics, and in many of the mitochondrial-dependent steps of apoptosis. Indeed, alterations to CL content and acyl chain profile have been associated with mitochondrial dysfunction in multiple tissues in Barth syndrome and in many other physio-pathological conditions. After a brief overview of the biological roles of CL, we highlight the consequences of lipid overload-related nutritional manipulations as well as related metabolic disorders on both CL content and its fatty acid composition in the major metabolic tissues, the heart, muscle and liver. The goal of this review is to fill a void in the CL literature concerning the effects of CL abundance and form that arise following high lipid supplementation and the related metabolic disorders.
- PMID:
- DOI:
- 10.1007/s10863-014-9555-y
- [Indexed for MEDLINE]
https://qph.fs.quoracdn.net/main-qimg-17d708fb1ead71db48b33e79ec6a05bf-c
- Viime vuodelta löytyy selvitystä kardiolipidin molekulaarisesta koostumuskesta.
Proc Natl Acad Sci U S A. 2018 Apr 17;115(16):4158-4163. doi: 10.1073/pnas.1719407115. Epub 2018 Apr 4.Molecular structural diversity of mitochondrial cardiolipins.Oemer G1, Lackner K1, Muigg K1, Krumschnabel G2, Watschinger K3, Sailer S3, Lindner H4, Gnaiger E2, Wortmann SB5,6, Werner ER3, Zschocke J1, Keller MA7.Abstract
Current strategies used to quantitatively describe the biological diversity of lipids by mass spectrometry are often limited in assessing the exact structural variability of individual molecular species in detail. A major challenge is represented by the extensive isobaric overlap present among lipids, hampering their accurate identification. This is especially true for cardiolipins, a mitochondria-specific class of phospholipids, which are functionally involved in many cellular functions, including energy metabolism, cristae structure, and apoptosis. Substituted with four fatty acyl side chains, cardiolipins offer a particularly high potential to achieve complex mixtures of molecular species. Here, we demonstrate how systematically generated high-performance liquid chromatography-mass spectral data can be utilized in a mathematical structural modeling approach, to comprehensively analyze and characterize the molecular diversity of mitochondrial cardiolipin compositions in cell culture and disease models, cardiolipin modulation experiments, and a broad variety of frequently studied model organisms.Copyright © 2018 the Author(s). Published by PNAS.KEYWORDS:cardiolipin; lipids; mass spectrometry; mathematical modeling; mitochondria- PMID:
- 29618609
- PMCID:
- PMC5910844
- DOI:
- 10.1073/pnas.1719407115
- [Indexed for MEDLINE]
- ENTÄ SITtEN AIVOJEN mitokondrioitten kardiolipiinin piirteet?
J Alzheimers Dis. 2015;43(4):1375-92. doi: 10.3233/JAD-141002.Cardiolipin profile changes are associated to the early synaptic mitochondrial dysfunction in Alzheimer's disease.
Monteiro-Cardoso VF1, Oliveira MM1, Melo T2, Domingues MR2, Moreira PI3, Ferreiro E4, Peixoto F5, Videira RA1.- l. Abstract
Alzheimer's disease; brain bioenergetics; cardiolipin; mitochondrial lipidomics.Brain mitochondria are fundamental to maintaining healthy functional brains, and their dysfunction is involved in age-related neurodegenerative disorders such as Alzheimer's disease (AD). In this study, we conducted a research on how both non-synaptic and synaptic mitochondrial functions are compromised at an early stage of AD-like pathologies and their correlation with putative changes on membranes lipid profile, using 3 month-old nontransgenic and 3xTg-AD mice, a murine model of experimental AD. Bioenergetic dysfunction in 3xTg-AD brains is evidenced by a decrease of brain ATP levels resulting, essentially, from synaptic mitochondria functionality disruption as indicated by declined respiratory control ratio associated with a 50% decreased complex I activity. Lipidomics studies revealed that synaptic bioenergetic deficit of 3xTg-AD brains is accompanied by alterations in the phospholipid composition of synaptic mitochondrial membranes, detected either in phospholipid class distribution or in the phospholipids molecular profile. Globally, diacyl- and lyso-phosphatidylcholine lipids increase while ethanolamine plasmalogens and cardiolipins content drops in relation to nontransgenic background
However, the main lipidomic mark of 3xTg-AD brains is that cardiolipin cluster-organized profile is lost in synaptic mitochondria due to a decline of the most representative molecular species.
In contrast to synaptic mitochondria, results support the idea that non-synaptic mitochondria function is preserved at the age of 3 months. Although the genetically construed 3xTg-AD mouse model does not represent the most prevalent form of AD in humans, the present study provides insights into the earliest biochemical events in AD brain, connecting specific lipidomic changes with synaptic bioenergetic deficit that may contribute to the progressive synapses loss and the neurodegenerative process that characterizes AD. KEYWORDS:
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