Decreased in vivo protein and phospholipid methylation after in vivo elevation of brain S-adenosyl-homocysteine.

نویسندگان

  • R A Schatz
  • T E Wilens
  • O Z Sellinger
چکیده

The administration of adenosine together with homocysteine resulted in a dose-related elevation of cerebral S-adenosyl-Lhomocysteine without concomitant perturbation of S-adenosyl-Lmethionine levels. The adenosine + homocysteine treatment also decreased the incorporation of labjle and stable methyl groups into brain protrjins. Brain [ HI-phosphatidyl N,N-dimethylethanolamine and [ HI-phgsphatidylcholine were also significantly decreased while [ HI-phosphatidyl-N-monomethylethanolamine remained unchanged. The data indicate that elevated brain S-adenosylhomocysteine can markedly and selectively inhibit the in vivo methylation of brain proteins and phospholipids.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

S-adenosyl-L-homocysteine hydrolase, key enzyme of methylation metabolism, regulates phosphatidylcholine synthesis and triacylglycerol homeostasis in yeast: implications for homocysteine as a risk factor of atherosclerosis.

In eukaryotes, S-adenosyl-L-homocysteine hydrolase (Sah1) offers a single way for degradation of S-adenosyl-L-homocysteine, a product and potent competitive inhibitor of S-adenosyl-L-methionine (AdoMet)-dependent methyltransferases. De novo phosphatidylcholine (PC) synthesis requires three AdoMet-dependent methylation steps. Here we show that down-regulation of SAH1 expression in yeast leads to...

متن کامل

Decreased transmethylation of biogenic amines after in vivo elevation of brain S-adenosyl-l-homocysteine.

The ability of S-adenosyl-L-homocysteine (AdoHcy) to inhibit biologic transmethylation reactions in vitro has led us to explore the possibility of pharmacologically manipulating AdoHcy levels in vivo and examining the consequences of these alterations on the transmethylation of some biogenic amines. Swiss-Webster mice were injected intraperitoneally with different doses of adenosine (Ado) and D...

متن کامل

Effect of phospholipid methylation on beta-adrenergic receptors in the normal and hypertrophied rat myocardium.

Abdominal aortic constriction in rats results in mild cardiac hypertrophy (20% increase in left ventricular weight compared to sham-operated controls) which is associated with increased numbers of beta-adrenergic receptors (123 +/- 7.3 fmol/mg protein (mean +/- SE) vs. 87 +/- 4.3 fmol/mg in controls, P < 0.01) without changes in their affinities for dihydroalprenolol. In vitro synthesis of phos...

متن کامل

Homocysteine as a Risk Factor for Atherosclerosis: Is Its Conversion to S-Adenosyl-L-Homocysteine the Key to Deregulated Lipid Metabolism?

Homocysteine (Hcy) has been recognized for the past five decades as a risk factor for atherosclerosis. However, the role of Hcy in the pathological changes associated with atherosclerosis as well as the pathological mechanisms triggered by Hcy accumulation is poorly understood. Due to the reversal of the physiological direction of the reaction catalyzed by S-adenosyl-L-homocysteine hydrolase Hc...

متن کامل

Insulin stimulation of phospholipid methylation in isolated rat adipocyte plasma membranes.

Partially purified plasma membranes prepared from rat adipocytes contain N-methyltransferase(s) that utilize(s) S-adenosyl-L-methionine to synthesize phosphatidylcholine from phosphatidylethanolamine. The incorporation of [3H]methyl from S-adenosyl-L-[methyl-3H]methionine into plasma membrane phospholipids was linear with incubation time and plasma membrane protein concentration and was inhibit...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • Biochemical and biophysical research communications

دوره 98 4  شماره 

صفحات  -

تاریخ انتشار 1981