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dc.date.accessioned | 2022-08-08T18:23:20Z | |
dc.date.available | 2022-08-08T18:23:20Z | |
dc.date.issued | 2007-04 | |
dc.identifier.uri | http://sedici.unlp.edu.ar/handle/10915/140165 | |
dc.description.abstract | We studied lipid metabolism and the antioxidant defense system in plasma and liver of rats fed diets supplemented with Lω-nitro-L-arginine methyl ester (L-NAME), isosorbide dinitrate (DIS), L-arginine (Arg), or the associations of these drugs. Liver hydroperoxide and thiobarbituric-acid-reactive substance (TBARS) levels were decreased by Arg and increased by L-NAME or DIS treatments. Oxidized glutathione and conjugated dienes were increased by DIS. Nitrate + nitrite levels and serum calcium ([Ca⁺⁺]) were incremented by Arg or DIS and reduced by L-NAME. Superoxide dismutase and catalase activities decreased under Arg treatment, while L-NAME or DIS caused stimulation. Liver high-density lipoprotein (HDL) cholesterol was increased by DIS or NAME (alone or associated with Arg). Free fatty acids and neutral and polar lipids were increased by Arg, L-NAME, and DIS. However, predominating phospholipid synthesis increased the neutral/polar ratio. Decreased levels of nitric oxide (NO) (low [Ca⁺⁺]) was directly associated with increased fatty acid synthetase, decreased phospholipase A₂, carnitine-palmitoyl transferase, and fatty acid desaturase activities. Raised NO (high [Ca⁺⁺]) inversely correlated with increased phospholipase-A₂ and acyl-coenzyme A (CoA) synthetase and decreased fatty acid synthetase and β-oxidation rate. Arg or DIS produced changes that were partially reverted by association with L-NAME. Based on these observations, prolonged therapeutical approaches using drugs that modify NO availability should be carefully considered. | en |
dc.format.extent | 211-228 | es |
dc.language | en | es |
dc.subject | Oxidative stress | es |
dc.subject | Calcium | es |
dc.subject | Lipid metabolism | es |
dc.subject | Rat liver | es |
dc.subject | Nitric oxide | es |
dc.title | Lipid Metabolism in Rats is Modified by Nitric Oxide Availability Through a Ca⁺⁺-Dependent Mechanism | en |
dc.type | Articulo | es |
sedici.identifier.other | doi:10.1007/s11745-006-3004-6 | es |
sedici.identifier.other | pmid:17393227 | es |
sedici.identifier.issn | 0024-4201 | es |
sedici.identifier.issn | 1558-9307 | es |
sedici.creator.person | Marra, Carlos Alberto | es |
sedici.creator.person | Nella, Julio | es |
sedici.creator.person | Manti, Damián | es |
sedici.creator.person | Tacconi de Alaniz, María Josefa | es |
sedici.subject.materias | Ciencias Médicas | es |
sedici.subject.materias | Bioquímica | es |
sedici.description.fulltext | true | es |
mods.originInfo.place | Instituto de Investigaciones Bioquímicas de La Plata | es |
sedici.subtype | Articulo | es |
sedici.rights.license | Creative Commons Attribution 4.0 International (CC BY 4.0) | |
sedici.rights.uri | http://creativecommons.org/licenses/by/4.0/ | |
sedici.description.peerReview | peer-review | es |
sedici.relation.journalTitle | Lipids | es |
sedici.relation.journalVolumeAndIssue | vol. 42, no. 3 | es |