Monoamine Oxidase-B Mediates Ecstasy-Induced Neurotoxic Effects to Adolescent Rat Brain Mitochondria

Alves, Emanuele Amorim; Summavielle, Teresa; Alves, Cecília J.; Gomes‐Da‐Silva, Joana; Barata, José Custódio; Fernandes, Eduarda; Bastos, Maria de Lourdes; Tavares, M. A.; Carvalho, Félix

doi:10.1523/jneurosci.2645-07.2007

Cited by 62 publications

(67 citation statements)

References 46 publications

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“…Furthermore, depletion of GSH upon MDMA exposure was observed in vitro in rat cortical neurons (Capela et al, 2007a) and in vivo in the mouse hippocampus, along with a decrease in Cu/Zn SOD activity (Frenzilli et al, 2007). In vivo exposure to MDMA was also reported to induce an increase in lipoperoxides and protein carbonyls, accompanied by mitochondrial DNA deletions, in isolated mitochondria from adolescent rat brains (Alves et al, 2007). In addition, lipoperoxides were detected by other authors in the brains of rats exposed to MDMA (Sprague and Nichols, 1995;Colado et al, 1997).…”

Section: 4mentioning

confidence: 98%

Cellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs

Cunha‐Oliveira

Rego

Oliveira

2008

Brain Research Reviews

189

136

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Section: 4mentioning

confidence: 98%

Cellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs

Cunha‐Oliveira

Rego

Oliveira

2008

Brain Research Reviews

189

136

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“…Aunque las sobredosis y las enfermedades infecciosas provocan altas tasas de mortalidad, los efectos físicos a largo da-Silva, Barata, Fernandes, et al, 2007). Methamphetamine was also shown to induce a decrease in mtDNA copy number and mitochondrial proteins per mitochondrion, as well as apoptosis in a human dopaminergic neuroblastoma SH-SY5Y cell line (Wu, Ping, Yen, Chang, Wang, Yeh, et al, 2007).…”

Section: Signos De Envejecimiento Acelerado En Los Consumidores De Drmentioning

confidence: 98%

“…It was recently demonstrated that the exposure of an adolescence rat model to a neurotoxic binge administration of methylenedioxymethamphetamine ("ecstasy") induces an oxidative stress status in brain mitochondria accompanied by deletion of mtDNA (Alves, Summavielle, Alves, Gomes-acompañado por deterioro del ADNmt (Alves, Summavielle, Alves, Gomes-da-Silva, Barata, Fernandes, et al 2007). Asimismo, la metanfetamina produce un descenso en el número de copias de ADNmt y de proteínas mitocondriales por mitocondrio, además de apoptosis en la línea cellular SH-SY5Y del neuroblastoma dopaminérgico humano (Wu, Ping, Yen, Chang, Wang, Yeh, et al, 2007).…”

Section: Acceleration Of the Aging Process By Drug Abusementioning

confidence: 99%

¿Existe envejecimiento precoz entre los consumidores de drogas de abuso?

Carvalho¹

2009

Adicciones

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The aging or senescence process that follows maturation is characterized by time-related functional decline due to genetic, biochemical, physiological and anatomical degeneration in tissues and organ systems with time. Oxidative damage to mitochondrial DNA (mtDNA) in the heart and brain is inversely related to maximum life span of mammals, suggesting that accumulation of mtDNA damage is involved in the various disorders associated with aging, cancer and neurodegeneration. The suppression of stem/progenitor cell proliferation also contributes to the aging process, by reducing tissue regeneration and repair and ultimately reducing longevity. Another important factor is the intracellular deposition of lipofuscin granules (age pigment), a non-degradable polymeric material accumulated within lysosomes, which ultimately exacerbate oxidative stress levels in senescent cells. Drugs of abuse can strongly contribute to these senescence accelerating factors in the brain. Methylenedioxymethamphetamine ("ecstasy") and methamphetamine were shown to promote deletions in brain mtDNA. Concerning stem/ progenitor cells, it has been shown that several opiates and psychostimulants, including ecstasy, decrease the self-renewal capacity of the hippocampus by diminishing the rate of proliferation of neural progenitors and/or by impairing the long-term survival of neural precursors. Chronic alcohol consumption induces lipofuscin deposition in neurons and heart cells. These facts provide interesting hints on the potential of these drugs in accelerating brain senescence. While the extent and severity of the contribution of drugs of abuse for accelerated senescence remain uncertain, these putative aging effects add up to the dark side of drug addiction and undoubtedly require a strong research effort in the near future. RESUMEN ABSTRACTEl proceso de envejecimiento que sigue a la madurez se caracteriza por una decadencia funcional vinculada a la edad y cuyo origen es la degeneración anatómica, fisiológica, bioquímica y genética de los tejidos y de los órganos. El daño oxidativo del ADN mitocondrial (ADNmt) en el corazón y el cerebro es inversamente proporcional a la longevidad máxima de los mamíferos, lo cual indica que la acumulación de daño de ADNmt participa en diversas enfermedades relacionadas con el envejecimiento, el cáncer y la neurodegeneración. La menor proliferación de células madre/progenitoras también contribuye al proceso de envejecimiento reduciendo la regeneración y reparación de los tejidos y, en consecuencia, recortando la longevidad. Otro factor importante es la deposición intracelular de los gránulos de lipofuscina (pigmentos de la edad), un polímero no degradable concentrado en los lisosomas, que acelera los niveles de estrés oxidativo en las células seniles. Las drogas contribuyen en gran medida a estos factores de aceleración del envejecimiento en el cerebro. Se ha demostrado que la metilenedioximetanfetamina (éxtasis) y la metafentamina provocan deterioro del ADNmt. Con respecto a las células madre/progenitoras se ...

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“…METH and MDMA are known to decrease the levels and activity of mitochondrial complexes I, II, and IV in the striatum (Burrows et al, 2000;Brown et al, 2005;Klongpanichapak et al, 2006;Puerta et al, 2010). MDMA was also shown to cause deletions in mitochondrial DNA coding for subunits of complexes I and IV (Alves et al, 2007). More recently it was shown that even relatively low doses of both AMPH and METH (2 mg/kg or less) decrease complex I, II, or IV activity in various brain regions, including the striatum, FC, and amygdala, obtained from animals killed while still under the influence of the drugs (Feier et al, 2012).…”

Section: Action Of Substituted Amphetamines and Cathinonesmentioning

confidence: 99%