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Fatty acids resources:

Fatty acids research abs 1 || Fatty acids research abs 2 || Fatty acids research abs 3 || Fatty acids research abs 4

Biochem Pharmacol. 2003 Jul 15;66(2):297-306.
Acetyl-L-carnitine cytoprotection against 1-methyl-4-phenylpyridinium toxicity in neuroblastoma cells.

Mazzio E, Yoon KJ, Soliman KF.

College of Pharmacy and Pharmaceutical Sciences, Florida A & M University, Tallahassee, FL 32307, USA.

Acetyl-L-carnitine (ALCAR) plays an integral role in the transport of long chain fatty acids across the inner mitochondrial membrane for oxidative phosphorylation. In non-human primates, administration of ALCAR was reported to prevent 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced neurological injury to the substantia nigra. The present study investigates the effects of ALCAR against the toxicity of 1-methyl-4-phenylpyridinium (MPP(+)), the neurotoxic metabolite of MPTP, in murine brain neuroblastoma cells. MPP(+), a potent mitochondrial toxin, induced a dose-dependent reduction in mitochondrial oxygen consumption and cell viability, corresponding to an accelerated rate of cellular glucose utilization. Treatment with ALCAR, but not L-carnitine, prevented MPP(+) toxicity and partially restored intracellular ATP concentrations, but did not reverse the MPP(+)-induced loss of mitochondrial oxygen consumption. These data indicate that protective effects are independent of oxidative phosphorylation. ALCAR had a substantial glucose sparing effect in both controls and MPP(+)-treated groups, demonstrating a potential role in enhancing glucose utilization through glycolysis. Antagonizing the entry of fatty acids into the mitochondria, with either insulin or malonyl CoA, did not interfere with ALCAR protection against MPP(+). On the contrary, insulin potentiated the protective effects of ALCAR. In conclusion, these data indicate that ALCAR protects against MPP(+) toxicity, independent of mitochondrial oxidative capacity or beta-oxidation of fatty acids. In contrast, the protective effects of ALCAR appear to involve potentiation of energy derived from glucose through anaerobic glycolysis.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12826272&dopt=Abstract

Biochem Pharmacol. 2003 Jul 15;66(2):307-13.
Effects of troglitazone on intracellular cholesterol distribution and cholesterol-dependent cell functions in MA-10 Leydig tumor cells.

Freeman DA, Romero A.

Department of Internal Medicine, University of Louisville School of Medicine, 800 Zorn Avenue, Louisville, KY 40206, USA. dale.freemaed.va.gov

Troglitazone treatment of MA-10 Leydig tumor cells resulted in cellular cholesteryl esters decreasing and cell free cholesterol increasing. This was not an effect unique to this chemical entity; rosiglitazone and pioglitazone caused these changes also. The excess free cholesterol was recovered largely in the cholesterol oxidase susceptible, plasma membrane cholesterol pool. This effect of troglitazone probably is not mediated by activation of peroxisome proliferator activated receptors since it immediately reversed with washing and did not occur at all in cells treated with the peroxisome proliferator activated receptor agonist, 15-deoxy Delta 12,14 prostaglandin J-2. Plasma membrane cholesterol esterification was inhibited by troglitazone in a dose-dependent manner. Plasma membrane cholesterol esterification was inhibited half-maximally by 14 microM troglitazone and by more than 90% by 40 microM troglitazone. This effect was not unique for MA-10 cells. Similar results were found using fibroblasts. Troglitazone was not simply inhibiting internalization of plasma membrane cholesterol. Dibutyryl-cAMP stimulation of troglitazone-treated cells resulted in more progesterone synthesis than in stimulated control cells; moreover, radioactive plasma membrane cholesterol was readily converted into progesterone in troglitazone-treated cells. Studies of LDL uptake in troglitazone-treated cells indicated that intracellular membranes were cholesterol replete. Troglitazone inhibited plasma membrane cholesterol esterification with kinetics similar to 58-035, a known inhibitor of the acyl coenzyme A: cholesterol acyltranserase (ACAT) enzyme. It is not likely an ACAT inhibitor since troglitazone did not block incorporation of exogenous free fatty acids into cholesteryl esters. Thus, it appears that troglitazone prevented presentation of free fatty acid to the ACAT enzyme.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12826273&dopt=Abstract

Cardiovasc Pathol. 2003 Jul-Aug;12(4):180-5.
Gene expression profiling--a new approach in the study of myocardial ischemia.

Simkhovich BZ, Kloner RA, Poizat C, Marjoram P, Kedes LH.

Heart Institute, Good Samaritan Hospital, USA.

Current technologies make it possible to study thousands of genes simultaneously in the same biological sample - an approach termed gene expression profiling. Several techniques, including (i) differential display, (ii) serial analysis of gene expression (SAGE), (iii) subtractive hybridization and (iv) gene microarrays (Gene Chips), have been developed. Recently, gene profiling was applied in studying the mechanisms of ischemic injury and ischemic preconditioning. In the case of reversible ischemia caused by one or several brief transient episodes of complete coronary occlusion (as with ischemic preconditioning), or with a more prolonged but partial coronary ligation, many up-regulated genes were related to the "cell survival program". Protective genes included mitogen-activated protein kinase-activated protein kinase 3 (MAPKAPK 3), heat shock proteins 70, 27, 22, B-crystalline, vascular endothelial growth factor, inducible nitric oxide synthase and plasminogen activator inhibitors 1 and 2. With permanent coronary occlusion lasting from 24 h to several weeks, and resulting in a true myocardial infarction (MI), the list of up-regulated genes included those related to remodeling (e.g., collagens I and III, fibronectin, laminin) and apoptosis (Bax), while many down-regulated genes were related to major energy-generating pathways in the heart, namely, fatty acid metabolism. Gene expression profiling experiments have resulted in the discovery of two different genetic programs in the heart, namely, a protective program activated upon brief episodes of transient ischemia and an injury-related one activated in response to irreversible ischemic injury. Searching for factors turning on protective genes, and turning down injury-related ones, is a justifiable approach in developing new therapeutic strategies aimed to fight ischemic heart disease.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12826286&dopt=Abstract [PubMed - in process]

Chem Senses. 2003 Jun;28(5):361-70.
Olfactory discrimination of short chain fatty acids in rats with large bilateral lesions of the olfactory bulbs.

Bisulco S, Slotnick B.

Department of Psychology, American University, Washington, DC 20016, USA.

Rats trained preoperatively to discriminate between acetic acid and caproic acid and between acetic acid and propionic acid were tested for their memory of these tasks and ability to discriminate between these odorants and between the enantiomers of carvone after receiving large bilateral bulbar lesions that included most of the fatty acid responsive areas identified in prior physiological studies. Concentrations of acid odorants were varied to insure that discrimination was based on the qualitative difference between acids. Experimental rats performed somewhat poorer than controls on the memory test but had no significant deficits in performing the acid discrimination tasks or discriminating between the enantiomers of carvone. These results demonstrate that removal of most bulbar sites identified as responsive to fatty acids and the consequent disruption of patterned input to the bulb is largely without effect on discriminating odor qualities of structurally similar acids.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12826532&dopt=Abstract [PubMed - in process]

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