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Mechanisms of Nanotoxicity to Cells, Animals, and Humans
Published in Vineet Kumar, Nandita Dasgupta, Shivendu Ranjan, Nanotoxicology, 2018
Belinda Wong Shu Ee, Puja Khanna, Ng Cheng Teng, Baeg Gyeong Hun
As the energy house of the cell, mitochondria supply most of the energy required in the form of ATP during cellular respiration. Mitochondria are the site of basal ROS generation in which electrons escape from ETC and react with oxygen molecules to form free radicals. Nanoparticle exposure can cause mitochondrial dysfunction, which leads to decreased ATP production but increased ROS generation, culminating in oxidative stress (Valko et al. 2007). For instance, AgNPs reduced the ATP content in IMR-90 and U251 cells due to damaged mitochondria (AshaRani et al. 2009). Mitochondrial depolarization is one of the mechanisms by which nanoparticles induce mitochondrial dysfunction. Mitochondrial membrane potential is generated in the inner mitochondrial membrane when protons are pumped into the intermembrane space. These protons will later flow back into the mitochondria via ATP synthase to generate ATP. Hence, maintaining mitochondrial membrane potential is essential for consistent energy production (Chen 1988). Decreased mitochondrial membrane potential is an indicator for its depolarization and mitochondria malfunction. TiO2 NP exposure in primary rat cortical astrocytes reduced the mitochondrial membrane potential along with oxidative stress build-up in cells (Wilson et al. 2015). Similarly, iron oxide nanoparticles depolarized mitochondria membranes in a dose-dependent manner in A549 cells (Khan et al. 2012). These observations suggest that nanoparticles damage mitochondria. Decreased ATP contents and mitochondrial membrane depolarization are the signs of damaged mitochondria and can lead to oxidative stress. Following these events, the damaged mitochondria can be removed via mitophagy. Alternatively, affected cells can activate mitochondrial-mediated apoptosis.
Association of metabolic syndrome risk factors with activation of brown adipose tissue evaluated by infrared thermography
Published in Quantitative InfraRed Thermography Journal, 2023
Samir E. da Rosa, Eduardo B. Neves, Eduardo C. Martinez, Runer A. Marson, Victor M. Machado de Ribeiro dos Reis
MetS is linked to the accumulation of white adipose tissue (WAT), specifically VAT, which raises the risk of cardiometabolic disease, especially because it secrets various substances such as adipokines that are responsible for metabolic changes [2,6]. Furthermore, brown adipose tissue (BAT) has been identified as a major player in regulating the desired metabolism for the regulation of systemic GL, fatty acids and branched-chain amino acids (BCAA), improving GL homeostasis, reducing weight gain and consequently the MetS risk factors [7,8]. This is possible due to the BAT high ability to promote thermogenesis through uncoupling protein 1 (UCP-1), mitochondrial inner membrane protein, that is responsible for the transport of protons from the intermembrane space to the mitochondrial matrix, promoting the dissipation of the electrochemical gradient, normally used in the synthesis of ATP [8–10]. Thus, BAT, as opposed to WAT, is not directly related to the increase in CND but is related to an increase in the body’s metabolic rate, reducing body weight and even MetS risk factors [7,8,11].
Adverse Outcome Pathway for Antimicrobial Quaternary Ammonium Compounds
Published in Journal of Toxicology and Environmental Health, Part A, 2022
Description of Event. Accumulation of QAC in the mitochondria of epithelial cells results in decreased ATP production, which leads to apoptotic or necrotic cell death (Figure 1). QACs inhibit mitochondrial complex I (Datta et al. 2017; Inácio et al. 2013) that reduces NADH and translocates 4 protons from the mitochondrial matrix to the intermembrane space, which is a primary driver of the electrochemical gradient.