Phosphorylation In Rats Research Articles

Chronic haloperidol treatment increased calcium-dependent phosphorylation in rat striatum

In previous studies, we observed that when rats were chronically treated with haloperidol, there was a significant increase of calmodulin activity in their striatal membranes. Calmodulin is knwon to modulate calcium-dependent protein phosphorylation in neural membranes. In the present study, we found that the total 32P-incorporation in the striatal proteins from chronic haloperidol-treated rats was significantly increased in comparison to saline-treated rats. A majority of the phosphorylation was attributed to the calcium-mediated activity, since it could be blocked by a calcium chelating agent (EGTA). By using EGTA to inhibit phosphorylation, the results indicated that the haloperidol-treated rats had approximately 3.5-fold greater Ca ++-dependent protein kinase activity than the saline-treated rats. Exogenous calcium alone was insufficient to stimulate phosphorylation in the haloperidol-treated rats to the same magnitude as in the saline-treated rats. Calmodulin may be required. 32P-incorporation of two striatal proteins at molecular weight 40 and 52 kilodaltons were markedly stimulated by calcium. Cyclic AMP-mediated phosphorylation seemed to take only a small part in the alteration of total phosphorylation. Therefore, the increase of calmodulin activity and calcium-dependent phosphorylation appears to play a major role in the drug-induced dopamine receptor supersensitivity in rat striatum.

Effects of chlorinated mono aromatic hydrocarbons on mitochondrial oxidative phosphorylation in rats liver.

The effects of chlorinated mono aromatic hydrocarbons on mitochondrial oxidative phosphorylation in rats were investigated. Of the chlorinated mono aromatic hydrocarbons examined, the tetra-and trichlorinated compounds strongly inhibited respiratory control with increasing state 4 respiration and decreasing state 3 respiration. The effect of the chlorinated mono aromatic hydro-carbons on the respiratory control of mitochondria was in the order of tetra ?? tri> di> mono chlorinated mono aromatic hydrocarbons, and the effect of isomers of the dichlorinated compounds was in the order of o-> m-> p-dichlorinated hydrocarbons. Chlorinated mono aromatic hydrocarbons also induced K+ release from mitochondria in the same order as the inhibitory effect on respiratory control, suggesting its interaction with the mitochondrial membrane and induction of a change in permeability to ions.It is concluded that chlorinated mono aromatic hydrocarbons act primarily as an uncoupler of the mitochondrial oxidative phosphorylation rather than as an electron transport or an energy transfer inhibitor. The destructive effect of the chlorinated mono aromatic hydrocarbons on the mitochondrial membrane was also demonstrated by the K+ release.

Comparative lipotropic and lipide phosphorylating effects of choline, betaine, and inositol.

The lipotropic and lipide phosphorylating effects of choline, betaine, and inositol were compared in rats maintained on low protein-low fat or low protein-high fat diets. All 3 agents (100 mg supplements/rat/day) were equally effective in causing a significant reduction of total lipides over controls in animals maintained on the low protein-low fat diet. Only choline and betaine supplements caused a substantial reduction of total liver fat in rats maintained on the high fat diet. Phospholipide synthesis was increased when choline, betaine, or inositol was administered as a single dose (0.4 mM) to animals maintained on the low protein-low fat diet. The order of effectiveness upon turnover rate was choline > betaine > inositol. Both choline and betaine, when administered as single doses, stimulated lipide phosphorylation in rats on the high fat diet, but inositol did not.