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Nanoparticles and Viruses as Mitophagy Inducers in Immune Cells
Published in Bertrand Henri Rihn, Biomedical Application of Nanoparticles, 2017
Housam Eidi, Zahra Doumandji, Lucija Tomljenovic, Bertrand Henri Rihn
Autophagy induction by nanomaterials can be explained by several mechanisms, as shown in Figure 6.2. Actually, NPs induce autophagy via the oxidative stress mechanism (Li et al. 2008) or mitochondrial damage (Figure 6.3; He and Klionsky 2009). The role of the oxidative stress mechanism can be explained by the accumulation of damaged proteins and subsequent endoplasmic reticulum stress. Autophagy can be induced by fullerene in HeLa cells and can be inhibited by different antioxidants such as reduced glutathione, N-acetyl-L-cysteine, and L-ascorbic acid (Li et al. 2008).
Overview of biological mechanisms of human carcinogens
Published in Journal of Toxicology and Environmental Health, Part B, 2019
Nicholas Birkett, Mustafa Al-Zoughool, Michael Bird, Robert A. Baan, Jan Zielinski, Daniel Krewski
HCV replicates exclusively within the cellular cytoplasm. Therefore, HCV does not directly interact with DNA, and potentially pro-carcinogenic events are restricted to the cytoplasm. HCV replication is directly linked to the endoplasmic reticulum and lipid metabolism. The proteins expressed by HCV interact with cellular components. Chronic inflammation and endoplasmic reticulum stress lead to oxidative stress and disruption of the intracellular redox state that gives rise to genomic damage. Several HCV proteins interact directly with cellular signaling cascades and affect cell metabolism and replication. The HCV core protein may interact with cyclin/CDK complexes and affect cell-cycle control. HCV produces steatosis by impairing lipid excretion and metabolism and by enhancing lipid genesis in the liver. The carcinogenic effect of HCV is enhanced through a positive feedback loop involving steatosis, insulin resistance and endoplasmic reticulum stress.
Neurotoxicity and physiological stress in brain of zebrafish chronically exposed to tributyltin
Published in Journal of Toxicology and Environmental Health, Part A, 2021
In summary, our study demonstrated that TBT altered physiological stress responses and neurotoxicity in brain tissues of zebrafish. These effects reflect increased oxidative stress and altered neurobiological parameters, as well as changes in CYP1 activity and Hsp70 content, as well as regulation of expression levels of genes related to endoplasmic reticulum stress (ERS), apoptosis and Nrf2 pathway. The present results provide new data for characterizing molecular mechanisms of TBT-mediated toxicity in zebrafish.