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Titolo:
Amphetamine-induced toxicity in dopamine terminals in CD-1 and C57BL/6J mice: Complex roles for oxygen-based species and temperature regulation
Autore:
Krasnova, IN; Ladenheim, B; Jayanthi, S; Oyler, J; Moran, TH; Huestis, MA; Cadet, JL;
Indirizzi:
NIDA, Mol Neuropsychiat Sect, NIH, Intramural Res Program, Baltimore, MD 21224 USA NIDA Baltimore MD USA 21224 tramural Res Program, Baltimore, MD 21224 USA NIDA, Chem & Drug Metab Sect, NIH, Baltimore, MD 21224 USA NIDA BaltimoreMD USA 21224 Drug Metab Sect, NIH, Baltimore, MD 21224 USA Johns Hopkins Univ, Sch Med, Dept Psychiat & Behav Sci, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 av Sci, Baltimore, MD 21205 USA
Titolo Testata:
NEUROSCIENCE
fascicolo: 2, volume: 107, anno: 2001,
pagine: 265 - 274
SICI:
0306-4522(2001)107:2<265:ATIDTI>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
METHAMPHETAMINE-INDUCED NEUROTOXICITY; DISMUTASE TRANSGENIC MICE; VESICULAR MONOAMINE TRANSPORTER; HYDROXYL RADICAL FORMATION; SUPEROXIDE-DISMUTASE; OXIDATIVE STRESS; BODY-TEMPERATURE; GLUTATHIONE-PEROXIDASE; INDUCED HYPERTHERMIA; DRUG TREATMENTS;
Keywords:
amphetamine; dopamine; superoxide radicals; antioxidant enzymes; caudate-putamen;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
60
Recensione:
Indirizzi per estratti:
Indirizzo: Cadet, JL NIDA, Mol Neuropsychiat Sect, NIH, Intramural Res Program, 5500 Nathan Shock Dr, Baltimore, MD 21224 USA NIDA 5500 Nathan Shock Dr Baltimore MD USA 21224 e, MD 21224 USA
Citazione:
I.N. Krasnova et al., "Amphetamine-induced toxicity in dopamine terminals in CD-1 and C57BL/6J mice: Complex roles for oxygen-based species and temperature regulation", NEUROSCIENC, 107(2), 2001, pp. 265-274

Abstract

In order to examine differential strain susceptibility to neurotoxic effects of amphetamine and to assess the potential role of superoxide radicals in am phetamine-induced dopaminergic damage, the drug was injected to mice with different levels or copper/zinc superoxide dismutase (Cu/Zn SOD) enzyme. Administration of amphetamine (10 mg/kg, i.p.. given every 2 h, a total of four times) to wild-type CD-I and C57BL/6J mice caused significant decreases in dopamine and 3,4-dihydroxyphenylacetic acid levels, in [I-125]RTI-121-labeled dopamine transporters as well as a significant depletion in the concentration of dopamine transporter and vesicular monoamine transporter 2 proteins. The amphetamine-induced toxic effects were less prominent in CD-1mice, which have much higher levels of Cu/Zn SOD activity (0.69 units/mg of protein) in their striata than C57BL/6J animals (0.007 units/mg of protein). Transgenic mice on CD-1 and C57BL/6J background, which had striatal levels of Cu/Zn SOD 2.57 and 1.67 units/mg of protein, respectively, showed significant protection against all the toxic effects of amphetamine. The attenuation of toxicity observed in transgenic mice was not caused by differences in amphetamine accumulation in wild-type and mutant animals. However, CD-1-SOD transgenic mice showed marked hypothermia to amphetamine whereas C57-SOD transgenic mice did not show a consistent thermic response to the drug. The data obtained demonstrate distinctions in the neurotoxic profile of amphetamine in CD-I and C57BL/6J mice, which show some differences in Cu/Zn SOD activity and in their thermic responses to amphetamine administration. Thus, these observations provide evidence for possible complex interactions between thermoregulation and free radical load in the long-term neurotoxic effects of this illicit drug of abuse. Published by Elsevier Science Ltd onbehalf of IBRO.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/04/20 alle ore 18:47:02