1. Tiedetään että lipidiperoksidaatio tuottaa MDA:ta jo dieetin puolella ja sitten kehossa.
2. Sillä on reaktiivisuutta tumahappojen, proteiinien ja fosfolipidien funktionaalisiin ryhmiin,
3. Se on bakteerille mutageeninen.
4. Koe-eläimissä se on ihosyöpää ja maksasyöpää aiheuttava.
Artikkeli kuvaa eläinkokeita, joisa syötettiin malondialdehydin natriumenolisuolaa.se vaikutti maksasolutumien annoksesta riippuvia hyperplastisia ja neoplastisia muutoksia ja nosti mortaliteetin mitä korkeimmalle tasolle aiheutamatta kuitenkaan maksatuumoreita.
Ihofibroblastiviljelmään lisättynä se aiheutti epänormaaliutta tumiin.
(1,3,C14*) -merkattu MDA oxidoitui (C14*) asetaatiksi sekä C*O2 hiilidioksidiksi in vivo nopeasti koeläimen maksan mitokondrioissa. Kuitenkin radioaktiivisuudesta oli havaittavissa 10% virtsasta.
Kromotagrafisesti havaittiin useita tuoteita, joista tuli MDA:ta happohydrolyysissä.
MDA:n kokonaiseritys lisääntyi lipidiperoksidaatiota aiheuttavista seikoista, kuten E-vitamiinin puutteesta, raudasta, hiilitetrakloridista ja kudosten rikastamisesta PUFA-rasvahapoilla.
MDA:n päämetaboliittina virtsassa todettiin N-asetyl-e-(2-propenal)lysiiniä.
Kun MDA reagoi ensisijaisesti ravinnossa tulevien N-terminaalisten lysiinien epsilon-aminoryhmän kanssa, muodostuu yllämainittua tuotetta. Mutta sitä muodsotuu myös kehossa, sillä jos koe-eläimiä pidettiin MDA-vapaalla dieetillä tai paastossa, niin tuota molekyyliä esiintyi kuitenkin virtsassa.
Lipids. 1986 Apr;21(4):305-7.
The metabolism of malondialdehyde.
Abstract .Interest
in malondialdehyde (MDA) metabolism stems from its formation as a
product of lipid peroxidation in the diet and in the tissues; its
reactivity with functional groups of nucleic acid bases, proteins and
phospholipids; its mutagenicity in bacteria, and its reported skin and
liver carcinogenicity in animals.
Administration of the Na enol salt of
MDA in the drinking water of mice over a range of 0.1-10.0
micrograms/g/day for 12 mo produced dose-dependent hyperplastic and
neoplastic changes in liver nuclei and increased mortality at the
highest level but produced no gross hepatic tumors.
Addition of MDA to the medium of rat skin fibroblasts grown in culture caused nuclear abnormalities at concentrations as low as 10(-6) M despite an uptake of only 4%.
[1,3-14C] MDA was rapidly oxidized to [14C]acetate in rat liver mitochondria and to 14CO2 in vivo; however, approximately 10% of the radioactivity was recovered in the urine.
Chromatographic analysis of rat urine revealed the presence of several compounds which yield MDA on acid hydrolysis.
Total MDA excretion increased in response to conditions which stimulate lipid peroxidation in vivo, including vitamin E deficiency, Fe or CCl4 administration, and enrichment of the tissues with PUFA.
N-acetyl-e-(2-propenal)lysine was identified as a major urinary metabolite of MDA in rat and human urine. This compound is derived primarily from N-alpha-(2-propenal)lysine released in digestion as a product of reactions between MDA and the epsilon-amino groups of N-terminal lysine residues in food proteins. However, its presence in the urine of animals fasted or fed MDA-free diets indicates that it is also formed in vivo.(ABSTRACT TRUNCATED AT 250 WORDS).
Suomennos 22.1. 2018
Kommentti: Käytännössä tämä merkannee sitä,että PUFA- käytöllä on jokin suositeltu ylärajansa joka ehkä on individuelli.
Addition of MDA to the medium of rat skin fibroblasts grown in culture caused nuclear abnormalities at concentrations as low as 10(-6) M despite an uptake of only 4%.
[1,3-14C] MDA was rapidly oxidized to [14C]acetate in rat liver mitochondria and to 14CO2 in vivo; however, approximately 10% of the radioactivity was recovered in the urine.
Chromatographic analysis of rat urine revealed the presence of several compounds which yield MDA on acid hydrolysis.
Total MDA excretion increased in response to conditions which stimulate lipid peroxidation in vivo, including vitamin E deficiency, Fe or CCl4 administration, and enrichment of the tissues with PUFA.
N-acetyl-e-(2-propenal)lysine was identified as a major urinary metabolite of MDA in rat and human urine. This compound is derived primarily from N-alpha-(2-propenal)lysine released in digestion as a product of reactions between MDA and the epsilon-amino groups of N-terminal lysine residues in food proteins. However, its presence in the urine of animals fasted or fed MDA-free diets indicates that it is also formed in vivo.(ABSTRACT TRUNCATED AT 250 WORDS).
Suomennos 22.1. 2018
Kommentti: Käytännössä tämä merkannee sitä,että PUFA- käytöllä on jokin suositeltu ylärajansa joka ehkä on individuelli.
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