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Dr. Marisol Orozco-Ibarra
Instituto Nacional de Neurología y Neurocirugía "Manuel Velasco Suárez"

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0 Mitochondria
0 Neuroscience
0 Oxidative Stress
0 Parkinson disease
0 glia

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Oxidative Stress
Mitochondria
Parkinson disease
Glial cells

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Journal article
Published: 23 July 2021 in International Journal of Molecular Sciences
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Idiopathic pulmonary fibrosis (IPF) is a devastating disease characterized by increased activation of fibroblasts/myofibroblasts. Previous reports have shown that IPF fibroblasts are resistant to apoptosis, but the mechanisms remain unclear. Since inhibition of the mitochondrial permeability transition pore (mPTP) has been implicated in the resistance to apoptosis, in this study, we analyzed the role of mitochondrial function and the mPTP on the apoptosis resistance of IPF fibroblasts under basal conditions and after mitomycin C-induced apoptosis. We measured the release of cytochrome c, mPTP opening, mitochondrial calcium release, oxygen consumption, mitochondrial membrane potential, ADP/ATP ratio, ATP concentration, and mitochondrial morphology. We found that IPF fibroblasts were resistant to mitomycin C-induced apoptosis and that calcium, a well-established activator of mPTP, is decreased as well as the release of pro-apoptotic proteins such as cytochrome c. Likewise, IPF fibroblasts showed decreased mitochondrial function, while mPTP was less sensitive to ionomycin-induced opening. Although IPF fibroblasts did not present changes in the mitochondrial membrane potential, we found a fragmented mitochondrial network with scarce, thinned, and disordered mitochondria with reduced ATP levels. Our findings demonstrate that IPF fibroblasts are resistant to mitomycin C-induced apoptosis and that altered mPTP opening contributes to this resistance. In addition, IPF fibroblasts show mitochondrial dysfunction evidenced by a decrease in respiratory parameters.

ACS Style

Erika Luis-García; Carina Becerril; Alfonso Salgado-Aguayo; Omar Aparicio-Trejo; Yair Romero; Edgar Flores-Soto; Criselda Mendoza-Milla; Martha Montaño; Victoria Chagoya; José Pedraza-Chaverri; Mohammed El Hafidi; Marisol Orozco-Ibarra; Annie Pardo; Moisés Selman. Mitochondrial Dysfunction and Alterations in Mitochondrial Permeability Transition Pore (mPTP) Contribute to Apoptosis Resistance in Idiopathic Pulmonary Fibrosis Fibroblasts. International Journal of Molecular Sciences 2021, 22, 7870 .

AMA Style

Erika Luis-García, Carina Becerril, Alfonso Salgado-Aguayo, Omar Aparicio-Trejo, Yair Romero, Edgar Flores-Soto, Criselda Mendoza-Milla, Martha Montaño, Victoria Chagoya, José Pedraza-Chaverri, Mohammed El Hafidi, Marisol Orozco-Ibarra, Annie Pardo, Moisés Selman. Mitochondrial Dysfunction and Alterations in Mitochondrial Permeability Transition Pore (mPTP) Contribute to Apoptosis Resistance in Idiopathic Pulmonary Fibrosis Fibroblasts. International Journal of Molecular Sciences. 2021; 22 (15):7870.

Chicago/Turabian Style

Erika Luis-García; Carina Becerril; Alfonso Salgado-Aguayo; Omar Aparicio-Trejo; Yair Romero; Edgar Flores-Soto; Criselda Mendoza-Milla; Martha Montaño; Victoria Chagoya; José Pedraza-Chaverri; Mohammed El Hafidi; Marisol Orozco-Ibarra; Annie Pardo; Moisés Selman. 2021. "Mitochondrial Dysfunction and Alterations in Mitochondrial Permeability Transition Pore (mPTP) Contribute to Apoptosis Resistance in Idiopathic Pulmonary Fibrosis Fibroblasts." International Journal of Molecular Sciences 22, no. 15: 7870.

Journal article
Published: 24 June 2021 in Free Radical Biology and Medicine
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Renal fibrosis is a well-known mechanism that favors chronic kidney disease (CKD) development in obstructive nephropathy, a significant pathology worldwide. Fibrosis induction involves several pathways, and although mitochondrial alterations have recently emerged as a critical factor that triggers renal damage in the obstructed kidney, the temporal mitochondrial alterations during the fibrotic induction remain unexplored. Therefore, in this work, we evaluated the time course of mitochondrial mass and bioenergetics alterations induced by a unilateral ureteral obstruction (UUO), a widely used model to study the mechanism involved in kidney fibrosis induction and progression. Our results show a marked reduction in mitochondrial oxidative phosphorylation (OXPHOS) in the obstructed kidney on days 7 to 28 of obstruction without significant mitochondrial coupling changes. Besides, we observed that mitochondrial mass was reduced, probably due to decreased biogenesis and mitophagy induction. OXPHOS impairment was associated with decreased mitochondrial biogenesis markers, the peroxisome proliferator-activated receptor γ co-activator-1alpha (PGC-1α), and nuclear respiratory factor 1 (NRF1); and also, with the induction of mitophagy in a PTEN-induced kinase 1 (PINK1) and Parkin independent way. It is concluded that the impairment of OXPHOS capacity may be explained by the reduction in mitochondrial biogenesis and the induction of mitophagy during fibrotic progression.

ACS Style

Alexis Paulina Jiménez-Uribe; Belen Bellido; Omar Emiliano Aparicio-Trejo; Edilia Tapia; Laura Gabriela Sánchez-Lozada; José Antonio Hernández-Santos; Francisca Fernández-Valverde; Estefani Yaquelin Hernández-Cruz; Marisol Orozco-Ibarra; José Pedraza-Chaverri. Temporal characterization of mitochondrial impairment in the unilateral ureteral obstruction model in rats. Free Radical Biology and Medicine 2021, 172, 358 -371.

AMA Style

Alexis Paulina Jiménez-Uribe, Belen Bellido, Omar Emiliano Aparicio-Trejo, Edilia Tapia, Laura Gabriela Sánchez-Lozada, José Antonio Hernández-Santos, Francisca Fernández-Valverde, Estefani Yaquelin Hernández-Cruz, Marisol Orozco-Ibarra, José Pedraza-Chaverri. Temporal characterization of mitochondrial impairment in the unilateral ureteral obstruction model in rats. Free Radical Biology and Medicine. 2021; 172 ():358-371.

Chicago/Turabian Style

Alexis Paulina Jiménez-Uribe; Belen Bellido; Omar Emiliano Aparicio-Trejo; Edilia Tapia; Laura Gabriela Sánchez-Lozada; José Antonio Hernández-Santos; Francisca Fernández-Valverde; Estefani Yaquelin Hernández-Cruz; Marisol Orozco-Ibarra; José Pedraza-Chaverri. 2021. "Temporal characterization of mitochondrial impairment in the unilateral ureteral obstruction model in rats." Free Radical Biology and Medicine 172, no. : 358-371.

Journal article
Published: 08 February 2021
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Decreased levels of repressor element-1 silencing transcription (REST) factor in the brain, plasma, and neuronderived exosomes are associated with Alzheimer's disease (AD). The objective of the study was to test the viability of serum REST as a possible blood-based biomarker for AD, comparing serum REST levels in AD patients from a National Institute of Health in Mexico City (with different levels of severity and comorbidities), with elderly controls (EC) and young controls (YC). We used an enzyme-linked immunosorbent assay to determine serum REST levels in AD patients (n = 28), EC (n = 19), and YC (n = 24); the AD patients were classified by dementia severity and comorbidities (depression and microangiopathy) using clinimetric tests and magnetic resonance imaging. Mean serum REST levels did not differ between AD patients, EC, and YC. The severity of AD and the presence of depression or microangiopathy were not associated with serum REST levels. Our results differ from previously published patterns found for plasma and cerebral REST levels. Free serum REST levels may not be a viable AD blood-based biomarker.

ACS Style

Francisco L. Ramírez-Cuapio; Mónica A. Torres-Ramos; Marisol Orozco-Ibarra; Isaac Acosta; Ana L. Sosa-Ortiz. Serum Repressor Element-1 Silencing Transcription Factor Levels in Alzheimer's Patients from a National Institute of Health in Mexico City, Elderly and Young Controls. 2021, 73, 1 .

AMA Style

Francisco L. Ramírez-Cuapio, Mónica A. Torres-Ramos, Marisol Orozco-Ibarra, Isaac Acosta, Ana L. Sosa-Ortiz. Serum Repressor Element-1 Silencing Transcription Factor Levels in Alzheimer's Patients from a National Institute of Health in Mexico City, Elderly and Young Controls. . 2021; 73 (1):1.

Chicago/Turabian Style

Francisco L. Ramírez-Cuapio; Mónica A. Torres-Ramos; Marisol Orozco-Ibarra; Isaac Acosta; Ana L. Sosa-Ortiz. 2021. "Serum Repressor Element-1 Silencing Transcription Factor Levels in Alzheimer's Patients from a National Institute of Health in Mexico City, Elderly and Young Controls." 73, no. 1: 1.

Journal article
Published: 04 February 2021 in Brain Research
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Cobalt protoporphyrin (CoPP) is a potent heme oxygenase-1 inductor that produces temporary hypophagia and chronic weight loss. A complete description of this effect and the underlying mechanisms are unknown. In this work, we challenged the ability of CoPP to produce changes in rat behavior and cellular alterations in the Nucleus Accumbens that would explain those effects. We subcutaneously administered 25 µmol/kgbody weight CoPP in female rats and determined body weight, food intake, hyperactivity, and anxiety-like behavior, as well as the number of neurons and glial cells in the Nucleus Accumbens. CoPP significantly reduced food intake, water consumption, and body weight. Behavioral tests showed that anxiety-like behaviors and locomotor activity were not modified five days after the administration of CoPP. We also found a reduced number of neurons in the Nucleus Accumbens Shell. The above results could be relevant to diseases like anorexia, so it is necessary to deepen the study about the molecular mechanisms involved in reducing the food intake and weight loss elicited by CoPP.

ACS Style

Luis Fernando Rubio-Atonal; Norma Serrano-García; Jorge Humberto Limón-Pacheco; José Pedraza-Chaverri; Marisol Orozco-Ibarra. Cobalt protoporphyrin decreases food intake, body weight, and the number of neurons in the Nucleus Accumbens in female rats. Brain Research 2021, 1758, 147337 .

AMA Style

Luis Fernando Rubio-Atonal, Norma Serrano-García, Jorge Humberto Limón-Pacheco, José Pedraza-Chaverri, Marisol Orozco-Ibarra. Cobalt protoporphyrin decreases food intake, body weight, and the number of neurons in the Nucleus Accumbens in female rats. Brain Research. 2021; 1758 ():147337.

Chicago/Turabian Style

Luis Fernando Rubio-Atonal; Norma Serrano-García; Jorge Humberto Limón-Pacheco; José Pedraza-Chaverri; Marisol Orozco-Ibarra. 2021. "Cobalt protoporphyrin decreases food intake, body weight, and the number of neurons in the Nucleus Accumbens in female rats." Brain Research 1758, no. : 147337.

Journal article
Published: 29 July 2020 in Toxics
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Some studies have shown that silicon dioxide nanoparticles (SiO2-NPs) can reach different regions of the brain and cause toxicity; however, the consequences of SiO2-NPs exposure on the diverse brain cell lineages is limited. We aimed to investigate the neurotoxic effects of SiO2-NP (0–100 µg/mL) on rat astrocyte-rich cultures or neuron-rich cultures using scanning electron microscopy, Attenuated Total Reflection-Fourier Transform Infrared spectroscopy (ATR-FTIR), FTIR microspectroscopy mapping (IQ mapping), and cell viability tests. SiO2-NPs were amorphous particles and aggregated in saline and culture media. Both astrocytes and neurons treated with SiO2-NPs showed alterations in cell morphology and changes in the IR spectral regions corresponding to nucleic acids, proteins, and lipids. The analysis by the second derivative revealed a significant decrease in the signal of the amide I (α-helix, parallel β-strand, and random coil) at the concentration of 10 µg/mL in astrocytes but not in neurons. IQ mapping confirmed changes in nucleic acids, proteins, and lipids in astrocytes; cell death was higher in astrocytes than in neurons (10–100 µg/mL). We conclude that astrocytes were more vulnerable than neurons to SiO2-NPs toxicity. Therefore, the evaluation of human exposure to SiO2-NPs and possible neurotoxic effects must be followed up.

ACS Style

Jorge Humberto Limón-Pacheco; Natalie Jiménez-Barrios; Alejandro Déciga-Alcaraz; Adriana Martínez-Cuazitl; Mónica Maribel Mata-Miranda; Gustavo Jesús Vázquez-Zapién; Jose Pedraza-Chaverri; Yolanda Irasema Chirino; Marisol Orozco-Ibarra. Astrocytes Are More Vulnerable than Neurons to Silicon Dioxide Nanoparticle Toxicity in Vitro. Toxics 2020, 8, 51 .

AMA Style

Jorge Humberto Limón-Pacheco, Natalie Jiménez-Barrios, Alejandro Déciga-Alcaraz, Adriana Martínez-Cuazitl, Mónica Maribel Mata-Miranda, Gustavo Jesús Vázquez-Zapién, Jose Pedraza-Chaverri, Yolanda Irasema Chirino, Marisol Orozco-Ibarra. Astrocytes Are More Vulnerable than Neurons to Silicon Dioxide Nanoparticle Toxicity in Vitro. Toxics. 2020; 8 (3):51.

Chicago/Turabian Style

Jorge Humberto Limón-Pacheco; Natalie Jiménez-Barrios; Alejandro Déciga-Alcaraz; Adriana Martínez-Cuazitl; Mónica Maribel Mata-Miranda; Gustavo Jesús Vázquez-Zapién; Jose Pedraza-Chaverri; Yolanda Irasema Chirino; Marisol Orozco-Ibarra. 2020. "Astrocytes Are More Vulnerable than Neurons to Silicon Dioxide Nanoparticle Toxicity in Vitro." Toxics 8, no. 3: 51.

Journal article
Published: 14 March 2020 in International Journal of Molecular Sciences
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One of the characteristics of the cerebral aging process is the presence of chronic inflammation through glial cells, which is particularly significant in neurodegeneration. On the other hand, it has been demonstrated that the aryl hydrocarbon receptor (AHR) participates in the inflammatory response. Currently, evidence in animal models shows that the hallmarks of aging are associated with changes in the AHR levels. However, there is no information concerning the behavior and participation of AHR in the human aging brain or in Alzheimer’s disease (AD). We evaluated the expression of AHR in human hippocampal post-mortem tissue and its association with reactive astrocytes by immunohistochemistry. Besides this, we analyzed through ELISA the AHR levels in blood serum from young and elder participants, and from AD patients. The levels of AHR and glial fibrillar acid protein were higher in elder than in young post-mortem brain samples. AHR was localized mainly in the cytosol of astrocytes and displayed a pattern that resembles extracellular vesicles; this latter feature was more conspicuous in AD subjects. We found higher serum levels of AHR in AD patients than in the other participants. These results suggest that AHR participates in the aging process, and probably in the development of neurodegenerative diseases like AD.

ACS Style

Nicte Alaide Ramos-García; Marisol Orozco-Ibarra; Enrique Estudillo; Guillermo Elizondo; Erick Gómez Apo; Laura Graciela Chávez Macías; Ana Luisa Sosa-Ortiz; Mónica Adriana Torres-Ramos. Aryl Hydrocarbon Receptor in Post-Mortem Hippocampus and in Serum from Young, Elder, and Alzheimer’s Patients. International Journal of Molecular Sciences 2020, 21, 1983 .

AMA Style

Nicte Alaide Ramos-García, Marisol Orozco-Ibarra, Enrique Estudillo, Guillermo Elizondo, Erick Gómez Apo, Laura Graciela Chávez Macías, Ana Luisa Sosa-Ortiz, Mónica Adriana Torres-Ramos. Aryl Hydrocarbon Receptor in Post-Mortem Hippocampus and in Serum from Young, Elder, and Alzheimer’s Patients. International Journal of Molecular Sciences. 2020; 21 (6):1983.

Chicago/Turabian Style

Nicte Alaide Ramos-García; Marisol Orozco-Ibarra; Enrique Estudillo; Guillermo Elizondo; Erick Gómez Apo; Laura Graciela Chávez Macías; Ana Luisa Sosa-Ortiz; Mónica Adriana Torres-Ramos. 2020. "Aryl Hydrocarbon Receptor in Post-Mortem Hippocampus and in Serum from Young, Elder, and Alzheimer’s Patients." International Journal of Molecular Sciences 21, no. 6: 1983.

Journal article
Published: 19 October 2018 in Neurochemistry International
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Rotenone, a classic mitochondrial complex I inhibitor, leads to dopaminergic neuronal death resulting in a Parkinson's-like-disease. Docosahexaenoic acid (DHA) has shown neuroprotective effects in other experimental models of Parkinson's disease, but its effect on the rotenone-induced parkinsonism is still unknown. We tested whether DHA in vivo exerts a neuroprotective effect on rotenone-induced parkinsonism and explored the mechanisms involved, including mitochondrial function and ultrastructure as well as the expression of tubulin and synaptophysin. We pretreated eighty male Wistar rats with DHA (35 mg/kg/day) for 7 days and then administered rotenone for either 8 or 14 days. We then measured rearing behavior, number of dopaminergic neurons, tyrosine hydroxylase content, tubulin and synaptophysin expression, mitochondrial complex I, respiratory control ratio, mitochondrial transmembrane potential, ATP production activity and mitochondrial ultrastructure. We found that in vivo DHA supply exerted a neuroprotective effect, evidenced by decreased dopaminergic neuron cell death. Although we detected rotenone induced mitochondrial ultrastructure alterations, these were not associated with mitochondrial dysfunction. Rotenone had no effect on mitochondrial complex I, respiratory control ratio, mitochondrial transmembrane potential or ATP production activity. DHA also prevented a rotenone-induced decrease in tubulin and synaptophysin expression. Our results support the neuroprotective effect of DHA on rotenone-induced parkinsonism, and a possible effect on early stage Parkinson's disease. This protective effect is not associated with mitochondrial function improvement, but rather with preventing loss of tubulin and synaptophysin, proteins relevant to synaptic transmission.

ACS Style

Norma Serrano-García; Francisca Fernández-Valverde; Erika Rubi Luis-Garcia; Leticia Granados-Rojas; Tarsila Elizabeth Juárez-Zepeda; Sandra Adela Orozco-Suárez; José Pedraza-Chaverri; Marisol Orozco-Ibarra; Anabel Jiménez-Anguiano. Docosahexaenoic acid protection in a rotenone induced Parkinson's model: Prevention of tubulin and synaptophysin loss, but no association with mitochondrial function. Neurochemistry International 2018, 121, 26 -37.

AMA Style

Norma Serrano-García, Francisca Fernández-Valverde, Erika Rubi Luis-Garcia, Leticia Granados-Rojas, Tarsila Elizabeth Juárez-Zepeda, Sandra Adela Orozco-Suárez, José Pedraza-Chaverri, Marisol Orozco-Ibarra, Anabel Jiménez-Anguiano. Docosahexaenoic acid protection in a rotenone induced Parkinson's model: Prevention of tubulin and synaptophysin loss, but no association with mitochondrial function. Neurochemistry International. 2018; 121 ():26-37.

Chicago/Turabian Style

Norma Serrano-García; Francisca Fernández-Valverde; Erika Rubi Luis-Garcia; Leticia Granados-Rojas; Tarsila Elizabeth Juárez-Zepeda; Sandra Adela Orozco-Suárez; José Pedraza-Chaverri; Marisol Orozco-Ibarra; Anabel Jiménez-Anguiano. 2018. "Docosahexaenoic acid protection in a rotenone induced Parkinson's model: Prevention of tubulin and synaptophysin loss, but no association with mitochondrial function." Neurochemistry International 121, no. : 26-37.

Journal article
Published: 01 December 2017 in Archivos de Neurociencias
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Antecedente: la mitocondria se daña en la isquemia cerebral focal (ICF). Dada su participación en la producción de ATP y los procesos de muerte celular, es relevante caracterizar el proceso de daño. Objetivo: evidenciar el daño tisular y los cambios en el perfil proteómico mitocondrial del cuerpo estriado e hipocampo en la ICF. Material y métodos: en ratas Wistar macho, se indujo ICF por 15’ o 1h, y se obtuvieron muestras de inmediato o a las 24 h de reperfusión (rpf). Se realizó valoración neurológica, análisis histológico y análisis proteómico mitocondrial. Resultados: se presentó déficit neurológico a partir de los 15’ de ICF. Consistentemente, se detectó daño tisular mediante H&E; además, se encontró muerte celular a 1h-ICF/rpf mediante la tinción de TTC. En el perfil proteómico se observaron 20 puntos candidato de proteínas, de los cuales, varios mostraron cambios cualitativos (seis en estriado y cuatro en hipocampo) a partir de los 15’ de ICF en comparación con el control. Dos de estos puntos mostraron claro aumento en su expresión en ambas regiones. Conclusión: con este estudio se muestra que desde los primeros minutos del evento isquémico la mitocondria sufre cambios en la expresión de proteínas como respuesta al daño producido por la ICF. La identificación y caracterización de las proteínas que se alteran permitirá estudiar con mayor profundidad los procesos bioquímicos que se presentan ante la ICF, lo cual contribuirá a ampliar el conocimiento básico de la secuencia de eventos que se dan como respuesta a la ICF.

ACS Style

Luis Enrique Villafuerte-Morquecho; Marisol Orozco-Ibarra; Jorge Daniel Corzo-Toledo; Febe Elena Cázares-Raga; Fidel De La Cruz Hernández-Hernández; Alma Ortiz-Plata. Respuesta de la mitocondria en un modelo de isquemia cerebral focal en rata. Archivos de Neurociencias 2017, 22, 26 -32.

AMA Style

Luis Enrique Villafuerte-Morquecho, Marisol Orozco-Ibarra, Jorge Daniel Corzo-Toledo, Febe Elena Cázares-Raga, Fidel De La Cruz Hernández-Hernández, Alma Ortiz-Plata. Respuesta de la mitocondria en un modelo de isquemia cerebral focal en rata. Archivos de Neurociencias. 2017; 22 (4):26-32.

Chicago/Turabian Style

Luis Enrique Villafuerte-Morquecho; Marisol Orozco-Ibarra; Jorge Daniel Corzo-Toledo; Febe Elena Cázares-Raga; Fidel De La Cruz Hernández-Hernández; Alma Ortiz-Plata. 2017. "Respuesta de la mitocondria en un modelo de isquemia cerebral focal en rata." Archivos de Neurociencias 22, no. 4: 26-32.

Retraction of publication
Published: 01 September 2017 in Toxicology
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ACS Style

Julio C. Tobón-Velasco; Jorge H. Limón-Pacheco; Marisol Orozco-Ibarra; Marina Macías-Silva; Genaro Vázquez-Victorio; Elvis Cuevas; Syed F. Ali; Antonio Cuadrado; José Pedraza-Chaverrí; Abel Santamaría. Retraction notice to "6-OHDA-induced apoptosis and mitochondrial dysfunction are mediated by early modulation of intracellular signals and interaction of Nrf2 and NF-κB factors" [Toxicology (2013) 109 - 119]. Toxicology 2017, 390, 167 .

AMA Style

Julio C. Tobón-Velasco, Jorge H. Limón-Pacheco, Marisol Orozco-Ibarra, Marina Macías-Silva, Genaro Vázquez-Victorio, Elvis Cuevas, Syed F. Ali, Antonio Cuadrado, José Pedraza-Chaverrí, Abel Santamaría. Retraction notice to "6-OHDA-induced apoptosis and mitochondrial dysfunction are mediated by early modulation of intracellular signals and interaction of Nrf2 and NF-κB factors" [Toxicology (2013) 109 - 119]. Toxicology. 2017; 390 ():167.

Chicago/Turabian Style

Julio C. Tobón-Velasco; Jorge H. Limón-Pacheco; Marisol Orozco-Ibarra; Marina Macías-Silva; Genaro Vázquez-Victorio; Elvis Cuevas; Syed F. Ali; Antonio Cuadrado; José Pedraza-Chaverrí; Abel Santamaría. 2017. "Retraction notice to "6-OHDA-induced apoptosis and mitochondrial dysfunction are mediated by early modulation of intracellular signals and interaction of Nrf2 and NF-κB factors" [Toxicology (2013) 109 - 119]." Toxicology 390, no. : 167.

Journal article
Published: 01 June 2017 in Chemico-Biological Interactions
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Intrastriatal injection of 1-methyl-4-phenylpyridinium (MPP) is considered a model to reproduce some biochemical alterations observed in Parkinson's disease (PD) patients. Among those alterations, inhibition of mitochondrial complex I activity, increased free radical production and reduced antioxidant responses have been reported. Copper (Cu) plays an important role in the metabolism and antioxidative responses through its participation as a cofactor in the cytochrome c oxidase enzyme (COX), Cu/Zn-superoxide dismutase (Cu/Zn-SOD), and metallothioneins. We tested the effect of copper sulfate (CuSO) pretreatment on the mitochondrial electron transport chain (METC) in the striatum after MPP toxicity in rats. The results showed that the MPP intrastriatal injection reduced mitochondrial complex I, II, IV and V activities; while 10 μmol of CuSO pretreatment counteracted this damage. Activities of complexes I, II and IV, were coincident with ATP recovery. Moreover, Cu/Zn-SOD activity was reduced as a consequence of MPP damage; however, copper pre-treatment kept the striatal Cu/Zn-SOD activity unchanged in MPP-damaged animals. We observed that MPP also reduced the metallothionein (MT) content and that CuSO pretreatment maintained baseline values. CuSO pretreatment also reduced the striatal caspase-3 and caspase-9 activities that were increased three days after MPP-induced damage. The present study provided evidence that copper pretreatment reduced MPP-induced apoptotic damage, probably through direct action on copper-dependent proteins or indirectly on proteins in the apoptotic pathway.

ACS Style

Moisés Rubio-Osornio; Marisol Orozco-Ibarra; Araceli Diaz-Ruiz; Eduardo Brambila; Marie-Catherine Boll; Antonio Monroy Noyola; Jorge Guevara; Sergio Montes; Camilo Ríos. Copper sulfate pretreatment prevents mitochondrial electron transport chain damage and apoptosis against MPP + -induced neurotoxicity. Chemico-Biological Interactions 2017, 271, 1 -8.

AMA Style

Moisés Rubio-Osornio, Marisol Orozco-Ibarra, Araceli Diaz-Ruiz, Eduardo Brambila, Marie-Catherine Boll, Antonio Monroy Noyola, Jorge Guevara, Sergio Montes, Camilo Ríos. Copper sulfate pretreatment prevents mitochondrial electron transport chain damage and apoptosis against MPP + -induced neurotoxicity. Chemico-Biological Interactions. 2017; 271 ():1-8.

Chicago/Turabian Style

Moisés Rubio-Osornio; Marisol Orozco-Ibarra; Araceli Diaz-Ruiz; Eduardo Brambila; Marie-Catherine Boll; Antonio Monroy Noyola; Jorge Guevara; Sergio Montes; Camilo Ríos. 2017. "Copper sulfate pretreatment prevents mitochondrial electron transport chain damage and apoptosis against MPP + -induced neurotoxicity." Chemico-Biological Interactions 271, no. : 1-8.

Journal article
Published: 01 April 2017 in The Journal of Nutritional Biochemistry
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This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief as it contains inappropriately manipulated images in Figure 7B. As such this article represents a severe abuse of the scientific publishing system. The scientific community takes a very strong view on this matter, and apologies are offered to the readers of the journal that this problem was not detected during the submission process.

ACS Style

Iván Carmona-Ramírez; Abel Santamaría; Julio C. Tobón-Velasco; Marisol Orozco-Ibarra; Irma G. González-Herrera; José Pedraza-Chaverrí; Perla D. Maldonado. Retraction notice to “Curcumin restores Nrf2 levels and prevents quinolinic acid-induced neurotoxicity “ [JNB 24 (2013) 14-24]. The Journal of Nutritional Biochemistry 2017, 42, 203 .

AMA Style

Iván Carmona-Ramírez, Abel Santamaría, Julio C. Tobón-Velasco, Marisol Orozco-Ibarra, Irma G. González-Herrera, José Pedraza-Chaverrí, Perla D. Maldonado. Retraction notice to “Curcumin restores Nrf2 levels and prevents quinolinic acid-induced neurotoxicity “ [JNB 24 (2013) 14-24]. The Journal of Nutritional Biochemistry. 2017; 42 ():203.

Chicago/Turabian Style

Iván Carmona-Ramírez; Abel Santamaría; Julio C. Tobón-Velasco; Marisol Orozco-Ibarra; Irma G. González-Herrera; José Pedraza-Chaverrí; Perla D. Maldonado. 2017. "Retraction notice to “Curcumin restores Nrf2 levels and prevents quinolinic acid-induced neurotoxicity “ [JNB 24 (2013) 14-24]." The Journal of Nutritional Biochemistry 42, no. : 203.

Journal article
Published: 28 September 2016 in Nutritional Neuroscience
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Our results show that FO exerts a beneficial prophylactic effect against mitochondrial damage. Elucidating the mechanisms linking the effects of FO with its prevention of neurodegeneration could be the key to developing recommendations for FO consumption in neurological pathologies.

ACS Style

Marisol Orozco-Ibarra; Jazmín García-Morales; Francisco José Calvo-Silva; Francisca Fernández-Valverde; Norma Serrano-García. Striatal mitochondria response to 3-nitropropionic acid and fish oil treatment. Nutritional Neuroscience 2016, 21, 132 -142.

AMA Style

Marisol Orozco-Ibarra, Jazmín García-Morales, Francisco José Calvo-Silva, Francisca Fernández-Valverde, Norma Serrano-García. Striatal mitochondria response to 3-nitropropionic acid and fish oil treatment. Nutritional Neuroscience. 2016; 21 (2):132-142.

Chicago/Turabian Style

Marisol Orozco-Ibarra; Jazmín García-Morales; Francisco José Calvo-Silva; Francisca Fernández-Valverde; Norma Serrano-García. 2016. "Striatal mitochondria response to 3-nitropropionic acid and fish oil treatment." Nutritional Neuroscience 21, no. 2: 132-142.

Article
Published: 02 September 2016 in Journal of Biochemical and Molecular Toxicology
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Quinolinic acid (QA) triggers striatal neuronal death by an excitotoxic cascade that involves oxidative stress, which in turns is tightly linked to mitochondria. Mitochondrial dysfunction is a molecular feature described in several brain pathologies. In this work, we determined whether the sulforaphane-neuroprotective effect in the rodent experimental model of Huntington's disease induced by QA is associated with mitochondrial function preservation. We found that QA impaired mitochondrial function within 24 h post-lesion. Sulforaphane effectively disrupted the mitochondrial dysfunction by preventing the decrease in respiratory control ratio, transmembrane potential, ability to synthetize ATP, and the activity of mitochondrial complexes I, II, and IV.

ACS Style

Erika Rubí Luis-García; Jorge Humberto Limón-Pacheco; Norma Serrano-García; Alma Delia Hernández-Pérez; José Pedraza-Chaverri; Marisol Orozco-Ibarra. Sulforaphane prevents quinolinic acid-induced mitochondrial dysfunction in rat striatum. Journal of Biochemical and Molecular Toxicology 2016, 31, e21837 .

AMA Style

Erika Rubí Luis-García, Jorge Humberto Limón-Pacheco, Norma Serrano-García, Alma Delia Hernández-Pérez, José Pedraza-Chaverri, Marisol Orozco-Ibarra. Sulforaphane prevents quinolinic acid-induced mitochondrial dysfunction in rat striatum. Journal of Biochemical and Molecular Toxicology. 2016; 31 (2):e21837.

Chicago/Turabian Style

Erika Rubí Luis-García; Jorge Humberto Limón-Pacheco; Norma Serrano-García; Alma Delia Hernández-Pérez; José Pedraza-Chaverri; Marisol Orozco-Ibarra. 2016. "Sulforaphane prevents quinolinic acid-induced mitochondrial dysfunction in rat striatum." Journal of Biochemical and Molecular Toxicology 31, no. 2: e21837.

Journal article
Published: 01 February 2016 in Biological Research
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Aged garlic extract (AGE) and its main constituent S-allylcysteine (SAC) are natural antioxidants with protective effects against cerebral ischemia or cancer, events that involve hypoxia stress. Cobalt chloride (CoCl2) has been used to mimic hypoxic conditions through the stabilization of the α subunit of hypoxia inducible factor (HIF-1α) and up-regulation of HIF-1α-dependent genes as well as activation of hypoxic conditions such as reactive oxygen species (ROS) generation, loss of mitochondrial membrane potential and apoptosis. The present study was designed to assess the effect of AGE and SAC on the CoCl2-chemical hypoxia model in PC12 cells. We found that CoCl2 induced the stabilization of HIF-1α and its nuclear localization. CoCl2 produced ROS and apoptotic cell death that depended on hypoxia extent. The treatment with AGE and SAC decreased ROS and protected against CoCl2-induced apoptotic cell death which depended on the CoCl2 concentration and incubation time. SAC or AGE decreased the number of cells in the early and late stages of apoptosis. Interestingly, this protective effect was associated with attenuation in HIF-1α stabilization, activity not previously reported for AGE and SAC. Obtained results show that AGE and SAC decreased apoptotic CoCl2-induced cell death. This protection occurs by affecting the activity of HIF-1α and supports the use of these natural compounds as a therapeutic alternative for hypoxic conditions.

ACS Style

Marisol Orozco-Ibarra; Jorge Muñoz-Sánchez; Martín E. Zavala-Medina; Benjamín Pineda; Roxana Magaña-Maldonado; Edgar Vázquez-Contreras; Perla D. Maldonado; José Pedraza-Chaverri; María Elena Chánez-Cárdenas. Aged garlic extract and S-allylcysteine prevent apoptotic cell death in a chemical hypoxia model. Biological Research 2016, 49, 1 -10.

AMA Style

Marisol Orozco-Ibarra, Jorge Muñoz-Sánchez, Martín E. Zavala-Medina, Benjamín Pineda, Roxana Magaña-Maldonado, Edgar Vázquez-Contreras, Perla D. Maldonado, José Pedraza-Chaverri, María Elena Chánez-Cárdenas. Aged garlic extract and S-allylcysteine prevent apoptotic cell death in a chemical hypoxia model. Biological Research. 2016; 49 (1):1-10.

Chicago/Turabian Style

Marisol Orozco-Ibarra; Jorge Muñoz-Sánchez; Martín E. Zavala-Medina; Benjamín Pineda; Roxana Magaña-Maldonado; Edgar Vázquez-Contreras; Perla D. Maldonado; José Pedraza-Chaverri; María Elena Chánez-Cárdenas. 2016. "Aged garlic extract and S-allylcysteine prevent apoptotic cell death in a chemical hypoxia model." Biological Research 49, no. 1: 1-10.

Comparative study
Published: 01 September 2013 in Food Chemistry
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Antioxidant properties and protective effect of aged garlic extract (AGE) and of 20% hydroethanolic fresh extracts from garlic clove (GCE) and skin (GSE) on cerebral ischemia were evaluated by administering extracts at the beginning of reperfusion in a rat model of stroke. All three extracts scavenged superoxide anion, peroxynitrite anion, and peroxyl radicals, but with different efficiencies; furthermore, GCE and GSE scavenged hydroxyl radicals and GSE scavenged singlet oxygen. These extracts significantly prevented reduction of neuronal nuclear antigen in the infarcted area, although no improvement in neurological function was observed. Importantly, GCE and GSE contained S-allylcystein, a compound associated with AGE's neuroprotective effect against damage induced by cerebral ischemia. Extracts decreased mRNA expression of NR1- and NR2B-NMDA-receptor subunits and prevented ischemia-induced reduction in mitochondrial potential and in ATP synthesis. These results indicate that antioxidants present in garlic extracts may regulate ROS concentrations during ischemia, favour pro-survival pathways, and attenuate mitochondrial dysfunction.

ACS Style

Maria Isabel Cervantes; Pavel Montes De Oca Balderas; José De Jesús Gutiérrez-Baños; Marisol Orozco-Ibarra; Berenice Fernández Rojas; Omar Noel Medina-Campos; Mónica Espinoza-Rojo; Martha Ruiz-Tachiquín; Alma Ortiz-Plata; Ma. Isabel Salazar; Moisés Rubio-Osornio; Eduardo Castañeda-Saucedo; José Pedraza-Chaverri; Fernando Calzada; Penelope Aguilera. Comparison of antioxidant activity of hydroethanolic fresh and aged garlic extracts and their effects on cerebral ischemia. Food Chemistry 2013, 140, 343 -352.

AMA Style

Maria Isabel Cervantes, Pavel Montes De Oca Balderas, José De Jesús Gutiérrez-Baños, Marisol Orozco-Ibarra, Berenice Fernández Rojas, Omar Noel Medina-Campos, Mónica Espinoza-Rojo, Martha Ruiz-Tachiquín, Alma Ortiz-Plata, Ma. Isabel Salazar, Moisés Rubio-Osornio, Eduardo Castañeda-Saucedo, José Pedraza-Chaverri, Fernando Calzada, Penelope Aguilera. Comparison of antioxidant activity of hydroethanolic fresh and aged garlic extracts and their effects on cerebral ischemia. Food Chemistry. 2013; 140 (1-2):343-352.

Chicago/Turabian Style

Maria Isabel Cervantes; Pavel Montes De Oca Balderas; José De Jesús Gutiérrez-Baños; Marisol Orozco-Ibarra; Berenice Fernández Rojas; Omar Noel Medina-Campos; Mónica Espinoza-Rojo; Martha Ruiz-Tachiquín; Alma Ortiz-Plata; Ma. Isabel Salazar; Moisés Rubio-Osornio; Eduardo Castañeda-Saucedo; José Pedraza-Chaverri; Fernando Calzada; Penelope Aguilera. 2013. "Comparison of antioxidant activity of hydroethanolic fresh and aged garlic extracts and their effects on cerebral ischemia." Food Chemistry 140, no. 1-2: 343-352.

Review article
Published: 29 July 2013 in Evidence-Based Complementary and Alternative Medicine
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Ginkgo bilobaextracts have long been used in Chinese traditional medicine for hundreds of years. The most significant extract obtained fromGinkgo bilobaleaves has been EGb 761, a widely used phytopharmaceutical product in Europe. EGb 761 is a well-defined mixture of active compounds, which contains two main active substances: flavonoid glycosides (24–26%) and terpene lactones (6–8%). These compounds have shown antiapoptotic effects through the protection of mitochondrial membrane integrity, inhibition of mitochondrial cytochrome c release, enhancement of antiapoptotic protein transcription, and reduction of caspase transcription and DNA fragmentation. Other effects include the reduction of oxidative stress (which has been related to the occurrence of vascular, degenerative, and proliferative diseases), coupled to strong induction of phase II-detoxifying and cellular defense enzymes by Nrf2/ARE activation, in addition to the modulation of transcription factors, such as CREB, HIF-1α, NF-κB, AP-1, and p53, involved in the apoptosis process. This work reviews experimental results about the antiapoptotic effects induced by the standardized extract ofGinkgo bilobaleaves (EGb 761).

ACS Style

Norma Serrano-García; José Pedraza-Chaverrí; José Juan Mares-Sámano; Marisol Orozco-Ibarra; Arturo Cruz-Salgado; Anabel Jiménez-Anguiano; Julio Sotelo; Cristina Trejo-Solis. Antiapoptotic Effects of EGb 761. Evidence-Based Complementary and Alternative Medicine 2013, 2013, 1 -18.

AMA Style

Norma Serrano-García, José Pedraza-Chaverrí, José Juan Mares-Sámano, Marisol Orozco-Ibarra, Arturo Cruz-Salgado, Anabel Jiménez-Anguiano, Julio Sotelo, Cristina Trejo-Solis. Antiapoptotic Effects of EGb 761. Evidence-Based Complementary and Alternative Medicine. 2013; 2013 ():1-18.

Chicago/Turabian Style

Norma Serrano-García; José Pedraza-Chaverrí; José Juan Mares-Sámano; Marisol Orozco-Ibarra; Arturo Cruz-Salgado; Anabel Jiménez-Anguiano; Julio Sotelo; Cristina Trejo-Solis. 2013. "Antiapoptotic Effects of EGb 761." Evidence-Based Complementary and Alternative Medicine 2013, no. : 1-18.

Journal article
Published: 01 February 2013 in Neuroscience
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Quinolinic acid (QA)-induced overactivation of N-methyl-d-aspartate receptors yields excitotoxicity, oxidative stress and mitochondrial dysfunction, which altogether contribute to trigger a wide variety of toxic pathways with biochemical, behavioral and neuropathological alterations similar to those observed in Huntington's disease. Noteworthy, in the brains of these patients, increased expression of heme oxygenase-1 (HO-1) levels can be found. It has been proposed that this enzyme can exert a dual role, as it can be either protective or deleterious to the CNS. While some evidence indicates that its overexpression affords cellular anti-oxidant protection due to decreased concentrations of its pro-oxidative substrate heme group, and increased bilirubin levels, other reports established that high HO-1 expression and activity may result in a pro-oxidizing atmosphere due to a release of Fe(2+). In this work, we examined the temporal evolution of oxidative damage to proteins, HO-1 expression, immunoreactivity, total activity, and cell death after 1, 3, 5 and 7 days of an intrastriatal QA infusion (240 nmol/μl). QA was found to induce cellular degeneration, increasing carbonylated proteins and generating a transitory response in HO-1 mRNA, protein content, and immunoreactivity and activity in nerve cells. In order to study the role of HO-1 in the QA-induced cellular death, the tin protoporphyrin IX (SnPP), a well-known HO inhibitor, was administered to rats (30 μmol/kg, i.p.). The administration of SnPP to animals treated with QA inhibited the HO activation, and exacerbated the striatal cell damage induced by QA. Our findings reveal a potential modulatory role of HO-1 in the toxic paradigm evoked by QA in rats. This evidence provides a valuable tool for further approaches on HO-1 regulation in neurotoxic paradigms.

ACS Style

A.L. Colín-González; Marisol Orozco-Ibarra; M.E. Chánez-Cárdenas; E. Rangel-López; A. Santamaría; J. Pedraza-Chaverri; D. Barrera-Oviedo; Perla D Maldonado. Heme oxygenase-1 (HO-1) upregulation delays morphological and oxidative damage induced in an excitotoxic/pro-oxidant model in the rat striatum. Neuroscience 2013, 231, 91 -101.

AMA Style

A.L. Colín-González, Marisol Orozco-Ibarra, M.E. Chánez-Cárdenas, E. Rangel-López, A. Santamaría, J. Pedraza-Chaverri, D. Barrera-Oviedo, Perla D Maldonado. Heme oxygenase-1 (HO-1) upregulation delays morphological and oxidative damage induced in an excitotoxic/pro-oxidant model in the rat striatum. Neuroscience. 2013; 231 ():91-101.

Chicago/Turabian Style

A.L. Colín-González; Marisol Orozco-Ibarra; M.E. Chánez-Cárdenas; E. Rangel-López; A. Santamaría; J. Pedraza-Chaverri; D. Barrera-Oviedo; Perla D Maldonado. 2013. "Heme oxygenase-1 (HO-1) upregulation delays morphological and oxidative damage induced in an excitotoxic/pro-oxidant model in the rat striatum." Neuroscience 231, no. : 91-101.

Retracted publication
Published: 01 February 2013 in Toxicology
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6-Hydroxydopamine (6-OHDA) is a neurotoxin that generates an experimental model of Parkinson's disease in rodents and is commonly employed to induce a lesion in dopaminergic pathways. The characterization of those molecular mechanisms linked to 6-OHDA-induced early toxicity is needed to better understand the cellular events further leading to neurodegeneration. The present work explored how 6-OHDA triggers early downstream signaling pathways that activate neurotoxicity in the rat striatum. Mitochondrial function, caspases-dependent apoptosis, kinases signaling (Akt, ERK 1/2, SAP/JNK and p38) and crosstalk between nuclear factor kappa B (NF-κB) and nuclear factor-erythroid-2-related factor 2 (Nrf2) were evaluated at early times post-lesion. We found that 6-OHDA initiates cell damage via mitochondrial complex I inhibition, cytochrome c and apoptosis-inducing factor (AIF) release, as well as activation of caspases 9 and 3 to induce apoptosis, kinase signaling modulation and NF-κB-mediated inflammatory responses, accompanied by inhibition of antioxidant systems regulated by the Nrf2 pathway. Our results suggest that kinases SAP/JNK and p38 up-regulation may play a role in the early stages of 6-OHDA toxicity to trigger intrinsic pathways for apoptosis and enhanced NF-κB activation. In turn, these cellular events inhibit the activation of cytoprotective mechanisms, thereby leading to a condition of general damage.

ACS Style

Julio C. Tobón-Velasco; Jorge H. Limón-Pacheco; Marisol Orozco-Ibarra; Marina Macías-Silva; Genaro Vázquez-Victorio; Elvis Cuevas; Syed F. Ali; Antonio Cuadrado; José Pedraza-Chaverrí; Abel Santamaría. RETRACTED: 6-OHDA-induced apoptosis and mitochondrial dysfunction are mediated by early modulation of intracellular signals and interaction of Nrf2 and NF-κB factors. Toxicology 2013, 304, 109 -119.

AMA Style

Julio C. Tobón-Velasco, Jorge H. Limón-Pacheco, Marisol Orozco-Ibarra, Marina Macías-Silva, Genaro Vázquez-Victorio, Elvis Cuevas, Syed F. Ali, Antonio Cuadrado, José Pedraza-Chaverrí, Abel Santamaría. RETRACTED: 6-OHDA-induced apoptosis and mitochondrial dysfunction are mediated by early modulation of intracellular signals and interaction of Nrf2 and NF-κB factors. Toxicology. 2013; 304 ():109-119.

Chicago/Turabian Style

Julio C. Tobón-Velasco; Jorge H. Limón-Pacheco; Marisol Orozco-Ibarra; Marina Macías-Silva; Genaro Vázquez-Victorio; Elvis Cuevas; Syed F. Ali; Antonio Cuadrado; José Pedraza-Chaverrí; Abel Santamaría. 2013. "RETRACTED: 6-OHDA-induced apoptosis and mitochondrial dysfunction are mediated by early modulation of intracellular signals and interaction of Nrf2 and NF-κB factors." Toxicology 304, no. : 109-119.

Retracted publication
Published: 31 January 2013 in The Journal of Nutritional Biochemistry
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Neurological diseases comprise a group of heterogeneous disorders characterized by progressive brain dysfunction and cell death. In the next years, these diseases are expected to constitute a world-wide health problem. Because excitotoxicity and oxidative stress are involved in neurodegenerative diseases, it becomes relevant to describe pharmacological therapies designed to activate endogenous cytoprotective systems. Activation of transcription factor Nrf2 stimulates cytoprotective vitagenes involved in antioxidant defense. In this work, we investigated the ability of the antioxidant curcumin to induce transcription factor Nrf2 in a neurodegenerative model induced by quinolinic acid in rats. Animals were administered with curcumin (400 mg/kg, p.o.) for 10 days, and then intrastriatally infused with quinolinic acid (240 nmol) on day 10 of treatment. Curcumin prevented rotation behavior (6 days post-lesion), striatal morphological alterations (7 days post-lesion) and neurodegeneration (1 and 3 days post-lesion) induced by quinolinic acid. Curcumin also reduced quinolinic acid-induced oxidative stress (measured as protein carbonyl content) at 6 h post-lesion. The protective effects of curcumin were associated to its ability to prevent the quinolinic acid-induced decrease of striatal intra-nuclear Nrf2 levels (30 and 120 min post-lesion), and total superoxide dismutase and glutathione peroxidase activities (1 day post-lesion). Therefore, results of this study support the concept that neuroprotection induced by curcumin is associated with its ability to activate the Nrf2 cytoprotective pathway and to increase the total superoxide dismutase and glutathione peroxidase activities.

ACS Style

Iván Carmona-Ramírez; Abel Santamaría; Julio Cesar Tobon-Velasco; Marisol Orozco-Ibarra; Irma G. Gonzalez-Herrera; José Pedraza-Chaverri; Perla D. Maldonado. RETRACTED: Curcumin restores Nrf2 levels and prevents quinolinic acid-induced neurotoxicity. The Journal of Nutritional Biochemistry 2013, 24, 14 -24.

AMA Style

Iván Carmona-Ramírez, Abel Santamaría, Julio Cesar Tobon-Velasco, Marisol Orozco-Ibarra, Irma G. Gonzalez-Herrera, José Pedraza-Chaverri, Perla D. Maldonado. RETRACTED: Curcumin restores Nrf2 levels and prevents quinolinic acid-induced neurotoxicity. The Journal of Nutritional Biochemistry. 2013; 24 (1):14-24.

Chicago/Turabian Style

Iván Carmona-Ramírez; Abel Santamaría; Julio Cesar Tobon-Velasco; Marisol Orozco-Ibarra; Irma G. Gonzalez-Herrera; José Pedraza-Chaverri; Perla D. Maldonado. 2013. "RETRACTED: Curcumin restores Nrf2 levels and prevents quinolinic acid-induced neurotoxicity." The Journal of Nutritional Biochemistry 24, no. 1: 14-24.

Journal article
Published: 26 October 2012 in Toxicologic Pathology
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Particulate matter, with a mean aerodynamic diameter of ≤10 µm (PM10), exposure is considered as a risk factor for cardiovascular and respiratory diseases. The mechanism of cell damage induced by PM10 exposure is related to mitochondrial alterations. The aim of this work was to investigate the detailed alterations induced by PM10 on mitochondrial function. Since lung tissue is one of the most important targets of PM10 inhalation, isolated mitochondria from lung rat tissue were exposed to PM10 and structural alterations were analyzed by transmission electron microscopy. Mitochondrial function was evaluated by respiratory control index (RCI), membrane potential, adenosine triphosphate (ATP) synthesis, and activity of respiratory chain. Results showed that exposure to PM10 in isolated mitochondria from lung tissue caused enlarged intermembrane spaces and shape alterations, disruption of cristae, and the decrease in dense granules. Oxygraphic traces showed a concentration-dependent decrease in oxygen consumption and RCI. In addition, mitochondrial membrane potential, ATP synthesis, and activity of complexes II and IV showed an increase and decrease, respectively, after PM10 exposure. PM10 exposure induced disruption in structure and function in isolated mitochondria from lung rat tissue.

ACS Style

Norma Laura Delgado-Buenrostro; Verónica Freyre-Fonseca; Claudia Maria Garcia-Cuellar; Yesennia Sánchez-Pérez; Emma Berta Gutiérrez Cirlos; Tecilli Cabellos-Avelar; Marisol Orozco-Ibarra; José Pedraza-Chaverri; Yolanda I. Chirino. Decrease in Respiratory Function and Electron Transport Chain Induced by Airborne Particulate Matter (PM 10 ) Exposure in Lung Mitochondria. Toxicologic Pathology 2012, 41, 628 -638.

AMA Style

Norma Laura Delgado-Buenrostro, Verónica Freyre-Fonseca, Claudia Maria Garcia-Cuellar, Yesennia Sánchez-Pérez, Emma Berta Gutiérrez Cirlos, Tecilli Cabellos-Avelar, Marisol Orozco-Ibarra, José Pedraza-Chaverri, Yolanda I. Chirino. Decrease in Respiratory Function and Electron Transport Chain Induced by Airborne Particulate Matter (PM 10 ) Exposure in Lung Mitochondria. Toxicologic Pathology. 2012; 41 (4):628-638.

Chicago/Turabian Style

Norma Laura Delgado-Buenrostro; Verónica Freyre-Fonseca; Claudia Maria Garcia-Cuellar; Yesennia Sánchez-Pérez; Emma Berta Gutiérrez Cirlos; Tecilli Cabellos-Avelar; Marisol Orozco-Ibarra; José Pedraza-Chaverri; Yolanda I. Chirino. 2012. "Decrease in Respiratory Function and Electron Transport Chain Induced by Airborne Particulate Matter (PM 10 ) Exposure in Lung Mitochondria." Toxicologic Pathology 41, no. 4: 628-638.