Adenine sulfate

Adenine is a purine derivative and a nucleobase with a variety of roles in biochemistry. Adenine is a nucleobase with a variety of roles in biochemistry including cellular respiration, in the form of both the energy-rich adenosine triphosphate (ATP) and

Adenine sulfate improves cardiac function and the cardiac cholinergic system after myocardial infarction in rats.[Pubmed:21343668]

J Pharmacol Sci. 2011;115(2):205-13.

Recent studies have shown that vagal activation may have an important therapeutic implication for myocardial infarction (MI), but effective strategies remain unexplored. Here, we investigate whether Adenine sulfate can preserve cardiac function and the cholinergic system against MI. Rats were treated with Adenine sulfate for three weeks after coronary ligation. Cardiac function was assessed by hemodynamics. The muscarinic M(2) receptor and cholinesterase-positive nerves were semi-quantified by immunochemical and histochemical staining. The maximal binding capacity (B(max)) of muscarinic receptors, determined by radioligand binding assay, showed that cardiac function was impaired in MI rats. Adenine sulfate reversed MI-induced reduction of mean artery pressure and left ventricular systolic pressure and elevation of left ventricular end-diastolic pressure. Moreover, Adenine sulfate also increased nitric oxide (NO) and nitric oxide synthase (NOS) activity. The amelioration was accompanied by a reversal of the infarction-induced reduction of cholinesterase-positive nerves and M(2)-receptor expression and B(max) in the Adenine sulfate high dose group. Meanwhile, Adenine sulfate treatment corrected the disorder of cardiac redox state by reduction in maleic dialdehyde and increase in superoxide dismutase. In conclusion, Adenine sulfate exerts cardioprotection against MI and ameliorates NO production. Changes in cardiac vagal distribution density and M(2)-receptor expression raise the possibility that improvement of the cardiac cholinergic system is involved in Adenine sulfate-induced cardioprotective effects.

Heparin and chondroitin sulfate inhibit adenine nucleotide hydrolysis in liver and kidney membrane enriched fractions.[Pubmed:11606255]

Int J Biochem Cell Biol. 2001 Dec;33(12):1193-201.

The inhibition of adenine nucleotide hydrolysis by heparin and chondroitin sulfate (sulfated polysaccharides) was studied in membrane preparations from liver and kidney of adult rats. Hydrolysis was measured by the activity of NTPDase and 5'-nucleotidase. The inhibition of NTPDase by heparin was observed at three different pH values (6.0, 8.0 and 10.0). In liver, the maximal inhibition observed for ATP and ADP hydrolysis was about 80% at pH 8.0 and 70% at pH 6.0 and 10.0. Similarly to the effect observed in liver, heparin caused inhibition of ATP and ADP hydrolysis that reached a maximum of 70% in kidney (pH 8.0). Na(+), K(+) and Rb(+) changed the inhibitory potency of heparin, suggesting that its effects may be related to charge interaction. In addition to heparin, chondroitin sulfate also caused a dose-dependent inhibition in liver and kidney membranes. The maximal inhibition observed for ATP and ADP hydrolysis was about 60 and 50%, respectively. In addition, the hepatic and renal activity of 5'-nucleotidase was inhibited by heparin and chondroitin sulfate, except for kidney membranes where chondroitin sulfate did not alter AMP hydrolysis. On this basis, the findings indicate that glycosaminoglycans have a potential role as inhibitors of adenine nucleotide hydrolysis on the surface of liver and kidney cell membranes in vitro.

Adenine Inhibits TNF-alpha Signaling in Intestinal Epithelial Cells and Reduces Mucosal Inflammation in a Dextran Sodium Sulfate-Induced Colitis Mouse Model.[Pubmed:27166765]

J Agric Food Chem. 2016 Jun 1;64(21):4227-34.

Adenine (6-amino-6H-purine), found in molokheiya (Corchorus olitorius L.), has exerted vasorelaxation effects in the thoracic aorta. However, the mode of action of the anti-inflammatory effect of adenine is unclear. Thus, we investigated to clarify the effect of adenine on chronic inflammation of the gastrointestinal tract. In intestinal epithelial cells, adenine significantly inhibited tumor necrosis factor-alpha-induced interleukin-8 secretion. The inhibition of adenine was abolished under the treatment of inhibitors of adenyl cyclase (AC) and protein kinase A (PKA), indicating the effect of adenine was mediated through the AC/PKA pathway. Adenine (5, 10, and 50 mg/kg BW/day) was administered orally for 14 days to female BALB/c mice, and then 5% dextran sodium sulfate (DSS) was given to induce colitis. Adenine (5 mg/kg BW/day) significantly prevented DSS-induced colon shortening, expression of pro-inflammatory cytokines, and histological damage in the colon. These results suggest that adenine can be a promising nutraceutical for the prevention of intestinal inflammation.

Adenine hemisulfate (6-Aminopurine hemisulfate) is a purine derivative with a variety of roles in biochemistry, including cellular respiration, in the form of both the energy-rich adenosine triphosphate (ATP) and the cofactors nicotinamide adenine dinucleotide (NAD) and flavin adenine dinucleotide (FAD), and protein synthesis, as a chemical component of DNA and RNA.

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