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Biomedical subjects

E B Rodriguez de Turco

Publications and source records attributed to E B Rodriguez de Turco.

At least 37 records · Page 2Linked to original sources
PubMed1992

Docosahexaenoic acid uptake and metabolism in photoreceptors: retinal conservation by an efficient retinal pigment epithelial cell-mediated recycling process.

After 18:3 omega 3 is obtained from the diet, it is accumulated by the liver, where it is esterified and temporarily stored as triacylglycerols. As it is required, 18:3 omega 3 is elongated and desaturated to 22:6 omega 3, then released into the circulation with lipoprotein carriers. RPE cells remove the 22:6 omega 3 from the choriocapillaris and subsequently release it to the retina proper. In the frog, all 22:6 omega 3 input to the photoreceptors occurs by way of the RPE cells. After passing through the interphotoreceptor matrix, it is selectively taken into the myoid region of photoreceptor cells where it is immediately activated and esterified onto position 2 (and sometimes also position 1) of a glycerol molecule. Some phospholipids are passed through the endoplasmic reticulum and Golgi apparatus, while others are not. Generally, transport to the outer segments seems to be independent of the Golgi apparatus. Addition to rod outer segments occurs in two ways: i) a general diffuse pathway, probably common to all fatty acids, which rapidly labels the entire outer segment; and ii) a specific dense pathway, utilized only by 22:6 omega 3-containing phospholipids, which become locked into the matrix of disc membranes along with opsin. There appears to be no exchange between these two forms of label. Accumulation of newly synthesized basal discs pushes older, 22:6 omega 3-laden discs apically until the outer segment tips, high in 22:6 omega 3-phospholipids (the dense form of outer segment label), are shed into the RPE cytoplasm. There, as the 22:6 omega 3 fatty acids are released from the disc membranes during degradation, a recycling mechanism immediately directs these essential fatty acids back into the interphotoreceptor matrix, thus conserving this molecule in the retina, and permitting it to be again selectively taken up by the photoreceptors for photomembrane synthesis. The process of 22:6 omega 3 handling and trafficking by the retina is specifically orchestrated around a conservation mechanism that is regulated by the RPE cells and that ensures, through a short feedback loop from the phagosomes to the interphotoreceptor matrix, adequate levels of 22:6 omega 3 for photoreceptors at all times.

Animals↗
PubMed1992

Light stimulates in vivo inositol lipid turnover in frog retinal pigment epithelial cells at the onset of shedding and phagocytosis of photoreceptor membranes.

We have developed an experimental model to study in vivo inositol lipid metabolism in frog retinal pigment epithelial (RPE) cells, including the effect of light on phospholipase C-mediated hydrolysis of phosphatidylinositol 4,5-bisphosphate. RPE cells were rapidly isolated after either brief light or dark periods. Light and electron microscopy showed complete detachment of the retina from the RPE cells, and that the RPE cell suspensions were devoid of photoreceptor cell outer segments. Frog tissues were labeled in vivo for 20 hr by intravitreal injection of [3H]inositol (4 microCi, 4 microliters per eye) within a 24-hr constant illumination period. Following 1 hr of darkness (priming period), frogs were intravitreally injected with LiCl (0.5 M, 4 microliters per eye) 15 min before the onset of either 30-min light stimulation or an additional 30 min of darkness (controls). In order to preserve endogenous inositol phosphate pools present after dark and light exposure, the RPE cells were harvested in the shortest time possible, at low temperatures (18-20 degrees C), and in the presence of 10 mM LiCl. Total [3H]inositol-labeled water-soluble products (inositol plus inositol phosphates) were increased by 86% after 30 min of light. Inositol trisphosphate (IP3) showed the highest accumulation (a 5.5-fold increase), followed by inositol bisphosphate (1.9-fold increase) and inositol monophosphate (1.4-fold increase). Free [3H]inositol also accumulated (2.8-fold increase), reflecting only a partial inhibition of phosphomonoesterase by LiCl. These changes were paralleled by a 12% decrease in 3H-labeled phosphatidylinositol with no significant difference in the labeling of polyphosphoinositides.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Retinal pigment epithelial cells play a central role in the conservation of docosahexaenoic acid by photoreceptor cells after shedding and phagocytosis.

The involvement of retinal pigment epithelial (RPE) cells in the recycling of docosahexaenoic acid (DHA), from phagocytized disc membranes back to the retina, was studied in frogs subsequent to injection of [3H]DHA via the dorsal lymph sac. Rod outer segments (ROS) gradually accumulated [3H]DHA as a dense, heavily labeled region that arrived at the distal tips by 28 days post-injection. Autoradiographic analysis at the time of maximal shedding and phagocytosis (1-2 hr after the onset of light) showed diffusely (before 28 days) and heavily (after 28 days) labeled phagosomes in RPE cells. Biochemical analysis of the [3H]DHA-containing lipids of discs that contribute to the labeling of RPE cells after phagocytosis was also performed. Between 27 and 34 days, when 12% of retinal [3H]DHA-lipids present in disc membranes are phagocytized by RPE cells, total retinal labeling remained unchanged. Taken together, these data suggest that the [3H]DHA of the densely labeled region of the ROS was recycled back to the photoreceptor cells only after it had reached the RPE cells following 28 days post-injection. We conclude that, following daily phagocytosis of ROS tips, RPE cells play a central role in the conservation and redelivery of ROS-derived DHA back to photoreceptor cells through the interphotoreceptor matrix.

Animals↗
PubMed1991

Hepatic phosphatidylinositol kinase activity in continuously endotoxemic rats.

The activity of phosphatidylinositol (PI) kinase and the content and fatty acid composition of inositol phospholipids (IPLs) were analyzed in the livers of rats that had been continuously infused with Escherichia coli endotoxin (ET) or saline for 30 h. Maximal enzymatic activity in total liver membrane fractions was observed in the presence of 1 mM ATP, 20 mM MgCl2, exogenously added 0.3 mM PI and Triton X-100 (0.25%). The activity of PI kinase for endogenous and exogenous PI was 43 and 79% higher respectively, in ET- as compared with saline-infused rats. The Km of the enzyme for ATP was not altered (0.175 mM), while the apparent Vmax was higher for ET- as compared with saline-infused rats (0.48 and 0.38 nmol of phosphatidylinositol 4-phosphate formed/mg protein per min, respectively). The ET-induced higher activity of PI kinase was paralleled by a 68-78% increase in the content of polyphosphoinositides (PPI), while PI content was unchanged. All IPLs from livers of endotoxemic rats had a lower content of arachidonic acid. We demonstrate for the first time that ET can directly and/or indirectly stimulate the net synthesis of PPI in liver cells. This effect could serve to modulate the PPI derived signals by increasing the availability of the substrate phosphatidylinositol 4,5-bisphosphate.

1-Phosphatidylinositol 4-Kinase↗
PubMed1991

Effect of chronic endotoxemia on concanavalin A-stimulated inositol lipid metabolism in rat splenocytes.

The effect of a chronic, nonlethal infusion of endotoxin (ET) on the phosphatidylinositol (PI) cycle in rat splenocytes was evaluated. Rats were infused intravenously with sterile saline or Escherichia coli ET (0.1 mg/100 g body weight/24 hr) for 30 hr via subcutaneously implanted osmotic pumps. The splenocytes were then labeled in vitro for 90 min with [32P]PO4 or for 3 hr with [3H]myoinositol to assess the status of the resynthesis and degradative parts of the PI cycle, respectively. PI cycle activity was depressed in splenocytes of ET-infused rats as evidenced by a 25% reduction in the incorporation of [32P]PO4 into phosphatidic acid (PA), PI, and the polyphosphoinositides and by a similar decrease in the production of [3H]inositol phosphates. Stimulation of splenocytes with concanavalin A (Con A) resulted in dose-dependent increases in the incorporation of [32P]PO4 into PA and PI and in the production of [3H]inositol phosphates, indicating that Con A stimulates the PI cycle in these cells. The Con A-stimulated increase in inositol phosphate production was higher in splenocytes from ET-infused rats. We have previously shown that splenocytes from rats infused for 30 hr with ET exhibit a decreased blastogenic responsiveness to Con A and lipopolysaccharide [Spitzer et al., Proc. Soc. Exp. Biol. Med. 186,27, 1987]. The present data do not support the notion that inositol lipid-mediated signaling mechanisms are solely responsible for the expression of the appropriate functional response and suggest that in ET-infused rats there is an uncoupling of the initial response to Con A (i.e., the production of inositol lipid-derived second messengers) and the long-term (i.e., mitogenic) response.

Animals↗
PubMed1991

Rapid and selective uptake, metabolism, and cellular distribution of docosahexaenoic acid among rod and cone photoreceptor cells in the frog retina.

The uptake, metabolism, and cellular distribution of 3H-docosahexaenoic acid (3H-22:6) in the frog retina during in vitro incubation were studied. An initial diffuse labeling throughout the retina was detected by autoradiography and was followed by an active steady increase in labeled photoreceptor cells. After 6 hr of incubation, 92% of the label was concentrated in photoreceptor cells. Among these cells, 435-rods (green rods) labeled heavily and showed two to three times higher uptake than the 502-rods (red rods). Cone uptake labeling was the lowest, showing negligible labeling throughout the cytoplasm. However, oil droplets of the 575-cones actively concentrated 22:6. The high uptake of 3H-22:6 by photoreceptor cells was followed by its rapid esterification into phospholipids. After 6 hr of labeling, only 5% of the radioactivity in the retina was free 22:6, whereas 88% was esterified into phospholipids. The remaining 22:6 was distributed equally in triacylglycerols (TAGs) and diacylglycerols. When 3H-22:6 (0.11 microM) of high specific activity was used, early incubation times showed phosphatidylinositol (PI) labeling to be of the same order of magnitude or greater than that of phosphatidylcholine (PC) or phosphatidylethanolamine (PE). Although the amount of endogenous 22:6 esterified into PI accounted for less than 2% of the 22:6 in retinal phospholipids, 27% of 3H-22:6 labeling was recovered in this phospholipid. When 14C-22:6 at a final concentration of 70 microM was used, a different profile of lipid labeling was observed. Forty percent of the labeling remained in the free fatty acid pool, followed by TAG (24%), PC (14%), and PE (12%). PI showed the smallest increase in picomoles of 14C-22:6 incorporated, when compared with 3H-22:6. In conclusion, a selective and differential uptake of 3H-22:6 by photoreceptor cells is coupled to its active utilization for phospholipid biosynthesis, mainly that of PC, PE, and PI. The differential uptake of 3H-22:6 among photoreceptor cells may reflect involvement of this fatty acid in cell-specific functions.

Animals↗
PubMed1990

Eicosanoid production in nonparenchymal liver cells isolated from rats infused with E. coli endotoxin.

Continuous i.v. infusion of a nonlethal dose of Escherichia coli endotoxin induced an early (3-h) accumulation of neutrophils in the rat liver followed by a later (30-h) greater extravasation of mononuclear phagocytes (MNP). These inflammatory cells, recovered together by centrifugal elutriation, were analyzed for their potential capacity to metabolize [1-14C]-AA. Ca2+ ionophore A23187 (5 microM) stimulated the release of [1-14C]-AA from PC and PI both in cells from saline- and ET-infused rats, the latter showing a higher capacity to further metabolize AA to eicosanoids. LTB4 and 5-HETE were the major metabolites accumulated in cells from rats infused with ET for 3 h, while PGD2 played the main role in cells from saline-infused rats. This could reflect [1-14C]-AA metabolism by PMNP and Kupffer cells, respectively. By 30 h of ET-infusion, a shift from PGD2 to PGE2 release was observed. These results suggest that eicosanoids released by nonparenchymal cells (i.e., Kupffer and endothelial cells) and PMNP in the liver of ET-infused rats may alter the normal intercellular information flow between parenchymal and nonparenchymal cells, contributing to the severe impairment in liver function and metabolism during endotoxicosis and sepsis.

Animals↗
PubMed1990

Preferential uptake and metabolism of docosahexaenoic acid in membrane phospholipids from rod and cone photoreceptor cells of human and monkey retinas.

The uptake, metabolism, and cellular distribution of [3H]docosahexaenoic acid (DHA) in human and monkey retinas were studied with biochemical and autoradiographic techniques. In specimens from two human retina biopsies, incubated for 4 hr or 6 hr with [3H]docosahexaenoic acid (110 nM), 80% of the esterified [3H]fatty acid was recovered in phospholipids and the remainder in triacylglycerols and diacylglycerols. The distribution of [3H]DHA in individual phospholipids (PL) was similar in both retinas, with phosphatidylcholine (PC) and phosphatidylethanolamine (PE) accounting for most of the label. A similar labeling profile was observed in glycerolipids from monkey retina, and after 1 hr of incubation, high labeling of phosphatidic acid (PA, 11%) and phosphatidylinositol (PI, 20%) was observed. In both human and monkey retinas, a preferential uptake of [3H]DHA by photoreceptor cells was revealed by autoradiography. Cone photoreceptors showed a slightly higher density of silver grains in their inner segments than did rod photoreceptors. Photoreceptors accounted for 59% and 79% of the total [3H]DHA taken up by the human and monkey retinas, respectively, the remainder being distributed throughout the neural retina. In conclusion, this study shows for the first time that in human and monkey retinas, DHA is taken up with a high degree of selectivity by photoreceptor cells, and then becomes esterified mainly into phospholipids that will be subsequently utilized for the synthesis of new disc membranes.

Aged↗
PubMed1989

Inositol lipid metabolism in vasopressin stimulated hepatocytes from rats infused with tumor necrosis factor.

We studied the effect of i.v. infusion of human recombinant tumor necrosis factor alpha (rHuTNF alpha, Cetus, 15 micrograms/100 g bw over 3 h) on vasopressin (VP)-stimulated 32P-inositol lipid turnover and the release of 3H-inositol phosphates in isolated rat hepatocytes. The early VP-induced decrease (within 30 s) in 32P-phosphatidylinositol 4-phosphate and 32P-phosphatidylinositol 4,5-bisphosphate labeling was significantly reduced (-40%) and at the same time the uptake of 32P into phosphatidic acid was 50% lower than in saline-infused (matched control) rats. Within 5 min of VP-stimulation, lower 32P phosphatidylinositol (-40%) and higher 32P-phosphatidic acid (+30%) labeling were observed in rHuTNF alpha-infused rats. Infusion of rHuTNF alpha also affected the VP-induced release of 3H-inositol phosphates. The accumulation of 3H-inositol-labeled water soluble products was decreased by 25% and 17% at 30 s and 10 min, respectively. These data show that rHuTNF alpha mimics early perturbations induced by Escherichia coli endotoxin infusion in VP-stimulated inositol lipid metabolism in rat hepatocytes.

Animals↗
PubMed1989

Modification of adrenergic and vasopressin receptor-linked lipid metabolism during endotoxemia.

Our studies addressing various aspects of lipid metabolism linked to the activation of alpha 1-adrenergic and vasopressin receptors suggest the following conclusions: 1) Adjustments in lipid metabolic flux seem to compensate for catabolic processes known to be triggered by endotoxin; 2) the diminished DG signal generation for vasopressin1 receptor-linked transduction mechanisms is likely to underlie some concomitant functional impairments and 3) defective acylation of AA may contribute to cellular metabolic perturbations by affecting the turnover of PI, a phospholipid involved in signal transmission, and leading to increased availability of AA for eicosanoid synthesis.

Animals↗
PubMed1989

Modification of protein kinase C (PKC) activity and diacylglycerol (DAG) accumulation in hepatocytes in continuous endotoxemia.

On the basis of our work, the status of PKC-mediated signal transduction in hepatocytes in chronic endotoxemia can be summarized as follows: 1. Vasopressin (10(-8) M)-induced DAG accumulation is delayed and reduced by 50%, as compared with the response of cells of saline-infused rats. 2. Under basal conditions, total PKC activity (cytosol + pellet) is elevated due to a tendency for higher cytosolic fractional activity. 3. Both TPA- and hormonally-induced (in response to VP and PE) translocation are impaired. 4. Quantitative receptor autoradiography reveals a selective decrease in [3H-PDBu] binding sites in hepatic membranes. We conclude that modulation in endotoxemia of the DAG signal elicited by VP stimulation in hepatocytes could lead to altered transmembrane control of PKC-mediated protein phosphorylation, thereby contributing to the mechanism of impairments in the regulation of cellular metabolism.

Animals↗
PubMed1988

Early effects of Escherichia coli endotoxin infusion on vasopressin-stimulated breakdown and metabolism of inositol lipids in rat hepatocytes.

The turnover of vasopressin-stimulated 32P-phosphoinositides and 32P-phosphatidic acid and accumulation of [2-3H]-inositol phosphates were examined in hepatocytes from rats infused i.v. with saline and E. coli endotoxin for 3 hrs. Within 60s of VP stimulation the decrease in phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate labeling as well as the increased uptake of 32P into phosphatidic acid were similar in both groups. However, at a later time (300s) the 32P-phosphatidylinositol turnover was greatly decreased concomitantly with a higher labeling of phosphatidic acid. The accumulation of [2-3H]-inositol phosphates in ET-cells was significantly decreased both at 30s and 600s after VP addition. The distribution of [2-3H]-inositol labeling accumulated in the different inositol phosphate fractions over the first 30s of VP stimulation showed a tendency to lower accumulation of inositol trisphosphate, and a significantly lower accumulation of inositol bisphosphate simultaneously with a higher labeling of the inositol tetrakisphosphate fraction. These observations reflect an early effect of ET-infusion on VP-stimulated inositol lipid turnover and on the subsequent metabolism of the released inositol phosphates.

Animals↗
PubMed1988

Kinetics of diacylglycerol accumulation in response to vasopressin stimulation in hepatocytes of continuously endotoxaemic rats.

The content and composition of 1,2-diacyl-sn-glycerol (1,2-DAG) was determined in hepatocytes from saline (0.9% NaCl)- and Escherichia coli endotoxin (ET)-infused rats upon continuous vasopressin (VP) (10(-8) M) stimulation. In both experimental groups the accumulation of 1,2-DAG was detected after a lag period (2-5 min), was sustained up to the last time analysed (10 min), and C18:0- and C20:4-fatty-acid-containing-DAG accumulation preceded that of DAG containing other acyl groups. In hepatocytes from ET-infused rats the VP-induced accumulation of DAG was delayed and was decreased by 50%, showing a C18:0/C20:4 molar ratio of 1.6 as compared with 1.1 for cells from saline-infused rats. A similar lower cellular response to VP stimulation was observed in cells prelabelled with [14C]C20:4 fatty acid. The accumulation of [14C]C20:4-DAG (lower in ET than in saline-infused rats) was paralleled by a decrease in phosphatidylinositol (PI) labelling, whereas phosphatidic acid showed a transient increase by 5 min in saline- but not in ET-infused rats. The present results demonstrate that the previously reported impairment in the early degradation of poly-PI and later in the 'PI cycle' during VP stimulation [Rodriguez de Turco & Spitzer (1987) Metab. Clin. Exp. 36, 753-760] is also reflected at the level of their phosphodiesteratic product, DAG. Moreover, the kinetics of the accumulation of DAG acyl groups is consistent with the idea that the initial release of C18:0- and C20:4-DAG (possibly derived from inositol lipids) could regulate the subsequent enlargement of this pool by stimulating a phospholipase C-mediated degradation of other phospholipids (e.g. phosphatidylcholine).

Animals↗
PubMed1988

Perturbation of glycerolipid content and biosynthesis in hepatocytes of rats continuously infused with Escherichia coli endotoxin.

The effect of chronic, nonlethal endotoxemia on the endogenous content and de novo biosynthesis of glycerolipids was investigated in rat hepatocytes. Continuous E. coli endotoxin (ET) infusion for 30 hours through a subcutaneously implanted mini-pump greatly altered the composition of membrane phospholipids. Sphingomyelin (SPH) and phosphatidylserine (PS) content increased by 56% and 29%, respectively, while the content of phosphatidylcholine (PC) decreased slightly (6%) as compared with saline-infused rats. These effects contrasted with those observed in pair-fed rats (whose food intake was matched to that voluntarily consumed by ET-infused animals). Food restriction induced a great depletion of phospholipid content, mainly phosphatidylethanolamine (PE), PC, phosphatidylinositol (PI), and PS, with no changes at the level of SPH as compared with control (fed ad libitum) rats. Triacylglycerol (TG) content was greatly decreased (66%) in ET-infused rats and the magnitude of the change and the fatty acid composition followed a pattern similar to that observed in pair-fed rats. The kinetics of [2-3H]-glycerol incorporation reflected efficient utilization of the precursor for de novo biosynthesis of glycerolipids. Labeling of the intermediate metabolite phosphatidic acid (PA) peaked at an earlier time (1 min) in ET-infused, and in pair-fed rats, as compared with saline-infused and control rats (3 min) respectively, and was followed by a later peak in diacylglycerol (DG) labeling. The metabolic flux thereafter in endotoxemia reflected a redirection toward the synthesis of TG and PI, while in pair-fed animals the label went mainly to PC, concomitantly with a great reduction in the uptake of label into PI.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Metabolic fate of arachidonic acid in hepatocytes of continuously endotoxemic rats.

The present experiments were designed to characterize the kinetics of [1-14C]arachidonic acid (AA) metabolism as a function of time in hepatocytes obtained from rats infused continuously for 30 h with a nonlethal dose of Escherichia coli endotoxin (ET). Chronic endotoxemia greatly reduces the ability of hepatocytes to utilize [1-14C]AA, which is reflected from the earliest times of incubation in very low labeling of intermediates in the biosynthetic pathways of glycerolipids (phosphatidic acid and diacylglycerol) and slower removal of [1-14C]AA from the free fatty acid pool as compared with saline-infused rats. At later times of incubation, the labeling of phospholipids (especially phosphatidylethanolamine and phosphatidylinositol [PI]), but not of triacylglycerides is decreased. Analysis of fatty acid composition of individual phospholipids from cells of ET-infused rats reveals that the content of AA is significantly reduced only in PI. Hence an impairment in activation/acylation enzymatic mechanisms could affect the turnover of metabolically active phospholipid pools, i.e., PI, involved in signal transmission processes, and result in increased availability of 20:4 for eicosanoid synthesis, contributing to cellular metabolic perturbations in endotoxicosis.

Animals↗
PubMed1988

Impairments in vasopressin-stimulated inositol lipid metabolism in hepatocytes of septic rats.

Vasopressin (VP)-stimulated 32P-inositol lipid metabolism was studied in hepatocytes obtained from rats rendered septic by cecal ligation and puncture. Basal 32P-phosphatidylinositol (PI) labeling, as well as its hormone-stimulated turnover, were greatly reduced in septic rats compared with sham-operated rats. The earliest VP-induced degradation of 32P-polyphosphoinositides (poly-PI) was greatly attenuated in septic rats. Moreover, while 32P-poly-PI labeling reached its lowest value by 60 sec of VP stimulation in cells from sham-operated rats, maximal changes in 32P-phosphatidylinositol 4,5-bisphosphate (32PIP2) occurred within 30 sec in septic rats. In contrast, the recovery of 32PIP2 labeling was more active in cells from septic rats, overcoming the impairment in its resynthesis triggered by surgical trauma in cells from sham-operated rats. The lower uptake of 32P into phosphatidic acid (PA) at the different time points analyzed was a sensitive indicator of the lower production of diacylglycerols from the VP-induced degradation of inositol phospholipids in septic rats. These observations support the idea that sepsis is associated with perturbations in the earliest events of the hepatocyte signal transmission pathway, namely, at the level of a receptor coupled to inositol lipid metabolism. Such perturbations are likely to be involved in the previously reported defective cell physiologic response to external hormone stimulation.

Animals↗
PubMed1986

Reduced labeling of brain phosphatidylinositol, triacylglycerols, and diacylglycerols by [1-14C]arachidonic acid after electroconvulsive shock: potentiation of the effect by adrenergic drugs and comparison with palmitic acid labeling.

The effect of electroconvulsive shock on the labeling of phospholipids and neutral lipids in mice brains was examined after intracerebral injection of [1-14C] arachidonic acid or [1-14C]palmitic acid. Electroconvulsive shock reduced greatly the removal of radiolabeled arachidonic acid from the free fatty acid pool. At the same time, the incorporation of arachidonic acid was partially inhibited in triacylglycerol, diacylglycerol, and phosphatidylinositol, whereas the incorporation of [1-14C]palmitic acid was not affected. Pretreatment with desipramine and pargyline potentiated the lipid effect of electroconvulsive shock in neutral glycerides. These electroconvulsive shock-induced changes reflect alterations in the metabolism of intracerebrally injected arachidonic acid, but not of similarly injected palmitic acid. From the available data whether decreased ATP, enzyme inhibition or other factors are involved cannot be ascertained. Moreover, the electroconvulsive shock-enhanced endogenous free arachidonic acid may possibly dilute the injected radiolabeled fatty acid, thus decreasing its availability for arachidonoyl-coenzyme A synthesis. Hence, a partial inhibition of the activation-acylation of these fatty acids, primarily arachidonic acid, also may be involved in the seizure-induced accumulation of free fatty acids in the brain.

Animals↗