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Impact of Physicochemical Properties and Surface Chemistry of Nanomaterials on Toxicity
Published in Vineet Kumar, Nandita Dasgupta, Shivendu Ranjan, Nanotoxicology, 2018
Akhela Umapathi, Anubhav Kaphle, Pundarikanakallahalli Nagaraju Navya, Sourabh Monnappa Kuppanda Jafri, Nikhath Firdose, Devendra Jain, Sangly Pranesh Srinivas, Harishkumar Madhyastha, Radha Madhyastha, Hemant Kumar Daima
The accumulation of nanomaterials in organs of the reticuloendothelial system along with an increase in phagocytic cells unbalances reactive oxygen species homeostasis and antioxidant defenses. This kind of scenario makes vital organs such as the liver and spleen the first targets of oxidative stress, leading to organ failure. Oxidative stress induced by nanomaterials can influence cell signaling in three stages. In the first stage, a lower level of oxidative stress boosts transcription of resistance genes by the transcription factor nrf2. In the second stage, elevated levels of oxidative stress stimulate inflammation signaling through NFκB. In the last stage, a very high level of oxidative stress is coupled with the initiation of apoptotic pathways and necrosis (Li et al. 2008; Rallo et al. 2011).
Terpenoids in Treatment of Liver Disease
Published in Dijendra Nath Roy, Terpenoids Against Human Diseases, 2019
Sujan Chatterjee, Debajyoti Patra, Pujita Ghosh, Akash Prasad, Kaustav Dutta Chowdhury
Terpenoids such as OA and UA may provide some hepatoprotection against liver damage induced by acetaminophen, a drug that is well known for its hepatotoxicity. Generally, Nrf2 binds to Keap1 in the cytoplasm, and the remaining Keap1 molecules are inactivated and easily degraded. Under oxidative stress, terpenoids activate Nrf2 by dissociating it from Keap1 via Keap1 modification or Nrf2 phosphorylation. Activated Nrf2 then translocates into the nucleus and interacts with anti-oxidant response element (ARE), promoting the expression of cytoprotective target genes including anti-oxidant enzymes and phase II detoxifying enzymes to protect the liver (Zhang et al. 2013b).
Pathological Manifestations and Mechanisms of Metal Toxicity
Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
Arsenic has also been shown to activate the Nrf2-Keap1 (nuclear factor erythroid 2-related factor 2-Kelch-like ECH-associated protein) pathway through a p62-dependent mechanism. Nrf2 is a transcription factor activated in response to oxidative stress that is responsible for detoxification and establishment of redox balance; however, in the case of As, it is still unclear if this alternative way to activate the pathway may be associated with a non-protective mechanism that can potentiate toxicity and/or carcinogenicity (Lau, Whitman, Jaramillo, & Zhang, 2013).
The expression of microRNAs and exposure to environmental contaminants related to human health: a review
Published in International Journal of Environmental Health Research, 2022
Maria Rosaria Tumolo, Alessandra Panico, Antonella De Donno, Pierpaolo Mincarone, Carlo Giacomo Leo, Roberto Guarino, Francesco Bagordo, Francesca Serio, Adele Idolo, Tiziana Grassi, Saverio Sabina
Adverse health effects associated with DEP exposure could be mediated in part by oxidative stress. Yamamoto and colleagues described an association between miR-144 and oxidative stress. The randomized crossover design of the study included 13 subjects with mild asthma exposed to DEP. miRNA profiling using Nanostring nCounter® assay showed increased levels of miR-21-5p, miR-30e, miR-215, and miR-144 in their peripheral blood. The validation phase by qRT-PCR confirmed a significant up-regulation of miR-144. To investigate the biological function of miR-144, the authors conducted a PCR analysis that showed a negative association of nuclear factor, erythroid-derived 2 (NRF2) and its downstream antioxidant genes with miR-144. The latter was also positively correlated with 8-OH-dG (Yamamoto et al. 2013). NRF2 is a transcription factor that regulates the expression of detoxifying enzymes, determining an adaptive response to oxidant pollutants exposure (Lodovici and Bigagli 2011).
Sub-acute exposure to Sudan IV-adulterated palm oil induces oxidative stress and represses the expression of Nrf2 and antioxidant genes in male albino rats
Published in Journal of Environmental Science and Health, Part C, 2021
Ofem E. Eteng, Ceaser A. Moses, Emmanuel I. Ugwor, Joe E. Enobong, Adio J. Akamo, Dorcas I. Akinloye, Irene O. Sadiku, Arikpo Iwara, Eyong Ubana
With the understanding that biochemical events observed at the cellular level are usually preceded by molecular changes, we further investigated the effects of S4D exposure on the expression of genes involved in the antioxidative response. Nrf2, a transcription factor encoded by the NFE2L2 gene, binds to antioxidant response elements in the promoter regions of genes involved in mitigating oxidative stress.33 We observed that exposure to S4D for 21 days inhibited the hepatic expression of Nrf2 relative to β-actin—no previous study has reported this. The effects of diminished Nrf2 expression may be far-reaching. For a better perspective, Nrf2-deficient mice have been shown to be markedly vulnerable to a wide array of oxidative-linked diseases and chemical toxicities.34–36 Gene products of Nrf2/ARE signaling cascade include, but are not limited to, CAT, GPx, and GSR,37 whose expressions were also observed to be repressed in S4D-exposed rats (alone and in PO). While underlying mechanisms remain unclear, repressed expression of Nrf2 and antioxidant genes may contribute to the oxidative stress and damage invoked by exposure to S4D.
Apigenin attenuates tetrabromobisphenol A-induced cytotoxicity in neuronal SK-N-MC cells
Published in Journal of Environmental Science and Health, Part A, 2023
Eun Mi Choi, So Young Park, Kwang Sik Suh, Suk Chon
Nrf2 is a crucial transcription factor that mediates protection against oxidants. The antioxidant properties of Nrf2 are mainly exerted by stimulating the transcription of antioxidant proteins, and the Nrf2 pathway regulates both mitochondrial and cytosolic ROS production through NADPH oxidase.[33] To explore the mechanism of apigenin-mediated protection against oxidative stress, we measured the levels of the transcription factor Nrf2. TBBPA (20 µM) significantly reduced the nuclear Nrf2 levels (Fig. 7). Nrf2 levels reduced by 20 µM TBBPA were significantly restored by apigenin (0.1 and 1 µM).