China
Africa
Explore chapters and articles related to this topic
Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
Associations were more pronounced among participants with one or two minor alleles of the NFE2L2 SNP rs 2364725. The NFE2L2 gene is believed to be involved in the defense against oxidative stress.714 Speculation that the defense is more activated in patients with common alleles, whereas patients with at least one minor allele are more susceptible to PM. In contrast, they observed inverse associations between QTc and PNC, a proxy for UFP, in accordance with two chamber studies706,715 that reported QTc shortening in healthy nonsmoking subjects who were exposed to UFP.
Cardiovascular Disease and Oxidative Stress
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
Marco Fernandes, Alisha Patel, Holger Husi
Counter-balance of the deleterious effects of oxidative-stress can also be attainable by promoting activation of up-stream factors responsible for the regulation of cell-mediated response to oxidative stress (Gazaryan and Thomas, 2016). This is in part orchestrated by binding of the nuclear factor erythroid 2-related factor 2 (NFE2L2) to cis-regulatory elements, commonly known as antioxidant response elements (ARE) in the promotor region of target genes (Huang et al., 2000). Without external oxidoreductive stimuli, the Kelch-like ECH-associated protein 1(KEAP) promotes continuous ubiquitination and consequent proteasome degradation of NFE2L2, leading to suppression of its transcriptional activity (Lo et al., 2006). Along this line, a number of drugs are currently being developed to attempt to explore how to disrupt the NFE2L2-KEAP1 interface, like the tecfidera (dimethyl fumarate), bardoxolone, and BTB domain and CNC homolog 1 (Bach1) and consequently activating the NFE2L2/ARE pathway. This would then lead to an increased expression of ROS detoxifying enzymes and/or synthesis of pro-antioxidant molecules (Gazaryan and Thomas, 2016; Gesslbauer and Bochkov, 2017). Another approach encompasses mechanisms to cope with damage induced by oxidative stress without changing either basal activity of detoxifying enzymes or levels of pro-antioxidant molecules (Gesslbauer and Bochkov, 2017), thereby lessen the effect of inflammation and aiming to correct disrupted intracellular events due to ROS-induction damage (Gesslbauer and Bochkov, 2017). Attenuation of inflammation by pharmacological intervention has been addressed by altering or interfering with key players in the inflammatory process, such as acting on secretory mediators like inhibiting IL-18, chemokines, and TNF-alpha, using compounds such as Anakinra (Brown, 1989; Toldo et al., 2012), Etanercept (Gao et al., 2015), Infliximab (Gerlach et al., 2014), and Evasin-3 (Montecucco et al., 2010).
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.