Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.1.3.5 (
5'-nucleotidase
)
3,167
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Saturated and monounsaturated fatty acids are mainly synthetized in the brain, but some of them could originate from the diet; in contrast polyunsaturated fatty acids are derived from dietary linoleic and linolenic acid. Saturated fatty acid biosynthesis occurs via three main pathways in mammalian cells. One is de novo synthesis of fatty acids from
acetyl-CoA
via malonyl-CoA; this system has been isolated in soluble form (the soluble system) from various animal tissues including brain. The second and third pathways involve elongation: in the mitochondrial system, acetyl CoA is the principal substrate in extracts from all organs, even brain; in the microsomal system, however, malonyl-CoA acts as donor of the 2 carbon fragments. In vivo studies in brain have shown that very long chain fatty acids are synthesized by elongation rather than by a than by a de novo mechanism. Feeding animals with oils that have a low n-3 acid content (linolenic series) results in all brain cells and organelles reduced amounts of 22:6 n-3 which is compensated for by an increase in 22:5 n-6. The speed of recuperation from these anomalies is extremely slow for brain cells, organelles and microvessels, in contrast with other organs. Essential fatty acids for the brain could be those with very long chains as shown with cell culture. They are probably synthesized in the liver from linolenic acid. They can also be supplied directly by food. During the period of cerebral development there is a linear relation between the n-3 acid content of the brain and that of food until linolenic acid represents approx. 200 mg per 100 g of food (for 1200 mg linoleic acid). A decrease in acids of the linolenic series in the membranes results in a 40% reduction of Na-K-ATPase in nerve terminals and a 20% reduction in
5'-nucleotidase
in whole brain homogenate. A diet low in linolenic acid leads to anomalies in the electroretinogram which disappear partially with age, it seriously affects learning tasks. The presence of linolenic acid in the diet confers a greater resistance to certain neurotoxic agents.
...
PMID:Control of brain fatty acids. 207 91
In view of its vasodilatory effect on the coronary circulation (probably mediated by adenosine) and its metabolic compartmentalization (intramitochondrial activation to form
acetyl-CoA
), the metabolic effects of acetate were studied in isolated rat heart mitochondria. Acetate caused conversion of adenylates to AMP and the formation of adenosine. Adenylate efflux was inhibited by carboxyatractyloside but not by N-ethylmaleimide. The intramitochondrial accumulation of AMP was enhanced by carboxyatractyloside during acetate metabolism and the formation of extramitochondrial adenosine inhibited. A carboxyatractyloside-sensitive unidirectional AMP influx with a Km of 50 microM and Vmax of 11 nmol/min per mg mitochondrial protein was also observed. The mitochondrial adenosine content was high and constant during the experiments. The steep apparent concentration gradient of adenosine indicates that most of the mitochondrial adenosine is tightly bound to protein. Adenosine formation was proportional to the extramitochondrial AMP concentration, showing that the
5'-nucleotidase
activity of cardiac mitochondrial preparations is extramitochondrial in origin. The data suggest that the mitochondrial ATP/ADP carrier is capable of transporting AMP and that intramitochondrial AMP is recycled during acetate metabolism in the myocardium partially by means of the ATP/ADP translocator, leading to an increase in extramitochondrial AMP and adenosine formation.
...
PMID:Adenine nucleotide transport and adenosine production in isolated rat heart mitochondria during acetate metabolism. 254 56