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Your search keyword '"Rolo, Anabela Pinto"' showing total 4 results
Start Over Author "Rolo, Anabela Pinto" Publisher elsevier
4 results on '"Rolo, Anabela Pinto"'

1. List of contributors

Author

Ahmad, Abul H., primary, Akingbasote, James, additional, Anadón, Arturo, additional, Anand, Rashmi, additional, Anantharam, Vellareddy, additional, András, Csaba, additional, Ares, Irma, additional, Avdonin, Pavel V., additional, Ay, Muhammet, additional, Banerjee, Aryamitra, additional, Barnett, Reid E., additional, Belinskaia, Daria A., additional, Bertero, Alessia, additional, Bharti, Vijay K., additional, Bian, Wan-Ping, additional, Bischoff, Karyn L., additional, Caloni, Francesca, additional, Castela, Ana Catarina, additional, Chand, Naresh, additional, Chanderbhan, Ronald F., additional, Charli, Adhithiya, additional, Charrette, Andrew, additional, Chen, Si, additional, Chen, Tao, additional, Choudhuri, Supratim, additional, Choudhury, Soumen, additional, Coccini, Teresa, additional, Cope, Rhian B., additional, Coppock, Robert W., additional, Costa, Lucio G., additional, Damodaran, Tirupapuliyur, additional, Darvesh, Altaf S., additional, Dhruw, Leena, additional, Dormán, György, additional, Doss, Robin B., additional, DuBourdieu, Dan, additional, Dziwenka, Margitta, additional, Eades, Joshua, additional, Esch, Harald L., additional, Filazi, Ayhan, additional, Fitsanakis, Vanessa A., additional, Flachner, Beáta, additional, Fossati, Paola, additional, Gambaryan, Stepan P., additional, Garg, Ramesh C., additional, Garg, Satish K., additional, Gil, Fernando, additional, Goncharov, Nikolay V., additional, Gulati, Kavita, additional, Guo, Lei, additional, Guo, Xiaoqing, additional, Gupta, Bhanushree, additional, Gupta, Ramesh C., additional, Guthrie, Najla, additional, Gwaltney-Brant, Sharon M., additional, Hajdú, István, additional, Hartsel, Joshua A., additional, Hazzah, Trina, additional, Hernández, Antonio F., additional, Hickory, Brian, additional, Hilmas, Corey J., additional, Hoeng, Julia, additional, Jain, Amul, additional, Jenkins, Richard O., additional, Jin, Huajun, additional, Joshi, Jagdish Chandra, additional, Kalinovsky, Tatiana, additional, Kalpana, Starling, additional, Kalidindi, Sanyasi R., additional, Kanthasamy, Anumantha G., additional, Kanthasamy, Arthi, additional, Kaore, Navinchandra M., additional, Kaore, Shilpa N., additional, Kapoor, Vijay Kumar, additional, Kaur, Gurjot, additional, Kolanos, Renata, additional, Korf, Ekaterina A., additional, Krishna, Gopala, additional, Krishna, Mayur, additional, Kuča, Kamil, additional, Kudryavtsev, Igor V., additional, Kumar, Amit, additional, Kumar, Dinesh, additional, Kumar, Prafull, additional, Lall, Rajiv, additional, La Mesa, Camillo, additional, Latino, Diogo A.R.S., additional, Lehmann, Leane, additional, Li, Xilin, additional, Machado, Ivo F., additional, Makriyannis, Alexandros, additional, Malik, Jitendra K., additional, Martín-Domingo, M. Concepción, additional, Martínez, María-Aránzazu, additional, Martínez-Larrañaga, María-Rosa, additional, Mei, Nan, additional, Messinis, Dimitris E., additional, Mindukshev, Igor V., additional, Negi, Poonam, additional, Niedzwiecki, Aleksandra, additional, Ning, Baitang, additional, Novozhilov, Artem V., additional, Palmeira, Carlos Marques, additional, Papas, Andreas M., additional, Pei, De-Sheng, additional, Peitsch, Manuel C., additional, Peterson, Jeffrey D., additional, Pistollato, Francesca, additional, Pitt, Jason, additional, Pitt, Yiuka, additional, Pospisil, Pavel, additional, Poussin, Carine, additional, Pradhan, Aanchal, additional, Prakash, Atul, additional, Prasad, Sahdeo, additional, Rahal, Anu, additional, Rai, Nishant, additional, Raina, Rajinder, additional, Rath, Matthias, additional, Ray, Arunabha, additional, Rehman, Sana, additional, Richter, Gary, additional, Risuleo, Gianfranco, additional, Roberts, Ashley, additional, Rolo, Anabela Pinto, additional, Roomi, M. Waheed, additional, Sachana, Magdalini, additional, Satoh, Tetsuo, additional, Serebriakova, Maria K., additional, Sharma, Rahul, additional, Shukla, Amit, additional, Sinha, Anita, additional, Sinha, Priynak, additional, Spicer, Leon J, additional, Srivastava, Ajay, additional, Stice, Szabina A., additional, Sudnitsyna, Julia S., additional, Taku, Ila, additional, Talukder, Jamil, additional, Teodoro, João Soeiro, additional, Thokchom, Suresh Kumar, additional, Trulioff, Andrey S., additional, Ukolov, Anton I., additional, Umegaki, Keizo, additional, Verma, Pankaj, additional, Verma, Pawan K., additional, Wan, Dan, additional, Wilson-Frank, Christina, additional, Woldemeskel, Moges, additional, Wu, Qinghua, additional, Yang, Mildred S., additional, Yurdakok-Dikmen, Begum, additional, Zaja-Milatovic, Snjezana, additional, and Zoltani, Csaba K., additional

Published
2021
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3. Mitochondrial damage and apoptosis: Key features in BDE-153-induced hepatotoxicity.

Author

Pereira LC, Cabral Miranda LF, Franco-Bernardes MF, Tasso MJ, Duarte FV, Inácio Varela AT, Rolo AP, Marques Palmeira CM, and Dorta DJ

Subjects
Adenosine Triphosphate metabolism, Animals, Calcium metabolism, Hep G2 Cells, Humans, Liver drug effects, Male, Membrane Potential, Mitochondrial drug effects, Mitochondria, Liver drug effects, Mitochondria, Liver metabolism, Mitochondrial Membranes drug effects, Mitochondrial Membranes metabolism, Mitochondrial Swelling drug effects, Oxidative Phosphorylation drug effects, Phosphatidylserines metabolism, Rats, Wistar, Reactive Oxygen Species metabolism, Apoptosis drug effects, Liver pathology, Mitochondria, Liver pathology, Polybrominated Biphenyls toxicity
Abstract

Brominated flame retardants are used in consumer goods to increase product resistance to fire and/or high temperatures. Polybrominated diphenyl ethers (PBDEs) are the most commonly employed class of brominated flame retardants because they are inexpensive and can effectively prevent flame from spreading. PBDEs are persistent, can bioaccumulate, are transported over long distances, and display toxicity. However, their toxic mechanisms of action have not been well established. Because mitochondria are recognized as the main energy-producing cell organelle and play a vital role in cellular function maintenance, here we apply mitochondria as an experimental model to evaluate the toxic effects of the PBDE congener BDE-153 (Hexa-BDE) at concentrations ranging from 0.1 to 25 μM. We also assess BDE-153 cytotoxicity to HepG2 cells in order to elucidate its mechanisms of toxicity. Exposure to BDE-153 affects isolated mitochondria: this congener can interact with the mitochondrial membrane, to dissipate the membrane potential and to induce significant ATP depletion. Furthermore, BDE-153 can diminish MTT reduction and cell proliferation and can interfere in cell cycle, as evaluated in cell cultures. These cytotoxic effects are related to mitochondrial dysfunction due to mitochondrial membrane potential dissipation and reactive oxygen species accumulation. These effects result in apoptotic cell death, as demonstrated by phosphatidylserine maintenance on the cell membrane external surface, nuclear condensation and fragmentation, and presence of pro-apoptotic factors such as cytochrome c and Apoptosis-inducing Factor (AIF) plus caspase 3 activation in the cytosol. Together, our results show PBDEs can induce cytotoxicity, reinforcing the idea that these compounds pose a risk to the exposed population., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Published
2018
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4. An autophagic process is activated in HepG2 cells to mediate BDE-100-induced toxicity.

Author

Pereira LC, Duarte FV, Varela AT, Rolo AP, Palmeira CM, and Dorta DJ

Subjects
Dose-Response Relationship, Drug, Hep G2 Cells, Humans, Microtubule-Associated Proteins biosynthesis, Autophagy drug effects, Autophagy physiology, Polybrominated Biphenyls toxicity
Abstract

To reduce flammability and meet regulatory requirements, Brominated Flame Retardants (BFRs) are added to a wide variety of consumer products including furniture, textiles, electronics, and construction materials. Exposure to polybrominated phenyl ethers (PBDEs) adversely affects the human health. Bearing in mind that (i) PBDEs are potentially toxic, (ii) the mechanism of PBDE toxicity is unclear, and (iii) the importance of the autophagy to the field of toxicology is overlooked, this study investigates whether an autophagic process is activated in HepG2 cells (human hepatoblastoma cell line) to mediate BDE-100-induced toxicity. HepG2 cells were exposed with BDE-100 at three concentrations (0.1, 5, and 25μM), selected from preliminary toxicity tests, for 24 and 48h. To assess autophagy, immunocytochemistry was performed after exposure of HepG2 cells to BDE-100. Labeling of HepG2 cells with 100nM LysoTracker Red DND-99 aided examination of lysosome distribution. Proteins that are key to the autophagic process (p62 and LC3) were evaluated by western blotting. DNA was isolated and quantified to assess mitochondrial DNA copy number by qPCR on the basis of the number of DNA copies of a mitochondrial encoded gene normalized against a nuclear encoded gene. Conversion of LC3-I to LC3-II increased in HepG2 cells. Pre-addition of 100nM wortmannin decreased the amount of LC3 in the punctuate form and increased nuclear fragmentation (apoptotic feature). HepG2 cells exposed to BDE-100 presented increased staining with the lysosomal dye and had larger LC3 and p62 content after pre-treatment with ammonium chloride. The mitochondrial DNA copy number decreased, which probably constituted an attempt of the cell to manage mitochondrial damage by selective mitochondrial degradation (mitophagy). In conclusion, an autophagic process is activated in HepG2 cells to mediate BDE-100-induced toxicity., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Published
2017
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