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Plant-Derived Compounds as New Therapeutics for Substance Use Disorders
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Kevin S. Murnane, Mary Frances Vest
In the context of dopamine systems, stimulation of CB2 receptors reduces microglial activation following exposure to a dopamine neurotoxin (Price et al., 2009). CB2 receptor stimulation mitigates dopamine neurotoxin-associated oxidative stress, which occurs when ROS are formed during the endogenous metabolism of dopamine and its metabolites. It can occur with alterations in the expression of antioxidant proteins, including superoxide dismutase, catalase and glutamate-cysteine ligase, which are rate-limiting toward GSH synthesis (Weng et al., 2018). Such oxidative stress is believed to be a critical mediator of cell death and neurodegeneration of dopamine systems (Weng et al., 2018). Both of the plant-derived compounds, cannabidiol and BCP, reverse dopamine neurotoxin-induced degeneration and increase the expression and activity of antioxidant and neuroprotective enzymes (García-Arencibia et al., 2007; Ojha et al., 2016; Wang et al., 2018). These promising results strongly support the development of plant-derived medications for SUDs that target the ECS, particularly the CB2 receptor.
Orthomolecular Parenteral Nutrition Therapy
Published in Aruna Bakhru, Nutrition and Integrative Medicine, 2018
Arturo O'Byrne-Navia, Arturo O'Byrne-De Valdenebro
As reported by Xu and colleagues in a model of experimental cadmium exposure (Xu et al. 2015), ALA significantly protected cadmium-treated HepG2 cell cultures against cytotoxicity and lipid peroxidation, and it was able to reverse cellular GSH deficit (p < 0.05). The authors also reported an increase in the activity and the expressions of glutamate cysteine ligase (γ-GCL), a limiting critical first step enzyme in the glutathione metabolism.
Assessing the Toxic Load and Detoxification Strategies
Published in Len Wisneski, The Scientific Basis of Integrative Health, 2017
GSH is made available in three ways: (1) synthesis via a two-step process catalyzed by the enzymes glutamate cysteine ligase (GCL) and glutathione synthetase; (2) regeneration of oxidized glutathione (GSSG) to reduced GSH by glutathione reductase; and (3) recycling of cysteine from conjugated glutathione.69
Quercetin ameliorates the hepatic apoptosis of foetal rats induced by in utero exposure to fenitrothion via the transcriptional regulation of paraoxonase-1 and apoptosis-related genes
Published in Biomarkers, 2021
Khairy A. Ibrahim, Mohammed Eleyan, Soad A. Khwanes, Rania A. Mohamed, Heba Ali Abd El-Rahman
Furthermore, stimulation of the cellular defense system against oxidative stress is considered an indirect pathway of the antioxidant activity of quercetin. In this pathway, quercetin can maintain the cellular redox status by modulating the nuclear factor 2-antioxidant response element (Nrf2 –ARE) which restores the cellular activity of antioxidant proteins like GST, SOD, CAT, PON1, and glutamate-cysteine ligase (Gan and Johnson 2014). Glutamate-cysteine ligase plays a central regulatory role in cellular defense against oxidative stress by regulating the biosynthesis of T-SH. Thus, the co-treatment with quercetin may elevate the level of T-SH by increasing its synthesis via modulation of the glutamate-cysteine ligase activity (Myhrstad et al.2002). Moreover, quercetin may increase the activity of AChE by regulating choline acetyltransferase which normalises the levels of acetylcholine (Braun et al.2017).
Nanosized silver, but not titanium dioxide or zinc oxide, enhances oxidative stress and inflammatory response by inducing 5-HETE activation in THP-1 cells
Published in Nanotoxicology, 2020
Wing-Lam Poon, Jetty Chung-Yung Lee, Kin Sum Leung, Harri Alenius, Hani El-Nezami, Piia Karisola
The level of total glutathione (GSH, both oxidized and reduced forms) was quantified by the color-generating reaction between glutathione and DTNB (5,5′-Dithiobis(2-nitrobenzoic acid)) in the cells after the NM exposure. N-Ag yielded significant increase of total GSH at 24 h when compared to unexposed controls (Figure 1(A)). Other tested particles (ZnO and TiO2) did not cause any changes except b-ZnO, which significantly increased the level of total glutathione at 6 h, but the effect was resolved already at 24 h (Figure 1(A)). These results were supported by the increased expression of the GCLC gene in the microarray study (Figure 1(B)). GCLC encodes the catalytic subunit of glutamate-cysteine ligase (GCL), catalyzing the first rate-limiting step in glutathione synthesis.
Oxidative stress impairs cGMP-dependent protein kinase activation and vasodilator-stimulated phosphoprotein serine-phosphorylation
Published in Clinical and Experimental Hypertension, 2019
Anees A. Banday, Mustafa F. Lokhandwala
Male Sprague-Dawley rats (200 to 250 g) were obtained from Harlan (Indianapolis, Indiana) and divided into 4 experimental groups: V, animals maintained on tap water (vehicle); BSO, animals provided with 30 mM L-buthionine sulfoximine (Sigma, St. Louis MO); T, animals provided with 1 mM tempol (Sigma); BSO+T, animals receiving BSO plus tempol. BSO induces oxidative stress by inhibiting glutamate cysteine ligase, a key enzyme for glutathione synthesis. Both BSO and tempol (an antioxidant) were provided in drinking water for 3 weeks. Conscious BP of rats was measured by radio telemetry (DSI, Minneapolis, MN) as detailed before (18). Briefly, anesthesia was induced by 5% isoflurane and maintained at 2–2.5% isoflurane throughout the surgery. Abdominal aorta was exposed by making a midline abdominal incision and an implantable radio transmitter was inserted into the abdominal aorta and secured with tissue adhesive (Vetbond from 3M St Paul, MN). The body of the transmitter was sutured to the abdominal musculature and animals were allowed to recover for 7–10 days prior to the recording of blood pressure. Blood pressure was measured throughout the treatment and daily recordings of individual rats were averaged.