Oxidative Stress in Human Toxicology

Hofer, Tim

doi:10.3390/antiox10081159

Cited by 7 publications

(6 citation statements)

References 14 publications

(15 reference statements)

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“…35 These small RNA molecules participate in various physiological processes, including development, immune response, and metabolism. 36 The expression of miRNAs can be influenced by cellular stress, including oxidative stress, 37 which is a significant mechanism in toxicology, 38 highlighting the relevance of miRNAs in toxicological processes. 39 Numerous studies have confirmed the involvement of miRNAs in regulating pesticide resistance in various pests.…”

Section: Discussionmentioning

confidence: 99%

miR-317-3p and miR-283-5p Play a Crucial Role in Regulating the Resistance to Indoxacarb in Spodoptera frugiperda by Targeting GSTs4

Wu,

Lv,

Guo

et al. 2024

J. Agric. Food Chem.

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Spodoptera frugiperda is primarily controlled through chemical insecticides. Our RNA-seq data highlight the overexpression of GSTs4 in indoxacarb-resistant S. frugiperda. However, the exact role of GSTs4 in indoxacarb resistance and its regulatory mechanisms remains elusive. Therefore, we investigated the functional role of GSTs4 in S. frugiperda and explored the underlying post-transcriptional regulatory mechanisms. GSTs4 was highly overexpressed (27.6-fold) in the indoxacarb-resistant strain, and GSTs4 silencing significantly increases the susceptibility of S. frugiperda to indoxacarb, increasing mortality by 27.3%. miR-317-3p and miR-283-5p can bind to the 3′UTR of GSTs4, and the targeting relationship was confirmed by dual-luciferase reporter assays. Injecting miR-317-3p and miR-283-5p agomirs reduces GSTs4 levels by 64.8 and 42.3%, respectively, resulting in an increased susceptibility of S. frugiperda to indoxacarb. Conversely, the administration of miR-317-3p and miR-283-5pantagomirs increases GSTs4 expression and reduces larval susceptibility to indoxacarb. These findings demonstrate that miR-317-3p and miR-283-5p contribute to indoxacarb resistance in S. frugiperda by regulating the overexpression of GSTs4.

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Section: Discussionmentioning

confidence: 99%

miR-317-3p and miR-283-5p Play a Crucial Role in Regulating the Resistance to Indoxacarb in Spodoptera frugiperda by Targeting GSTs4

Wu,

Lv,

Guo

et al. 2024

J. Agric. Food Chem.

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“…In support of this, clinical studies have observed markers of persistent endothelial dysfunction, such as impaired endothelial vasodilation, up to 24 h following a 1 h exposure to DEP [ 5 , 51 , 89 ]. Prolonged endothelial oxidative stress and dysfunction can have significant, adverse responses such as excessive pulmonary and systemic pro-inflammatory responses, thrombus formation, and the progression of atherosclerosis [ 14 , 36 , 38 ]. Therefore, inefficient endothelial intracellular stress resolution may be a key mechanism of how inhaled materials promote the development of respiratory and systemic diseases.…”

Section: Discussionmentioning

confidence: 99%

Epithelial MAPK signaling directs endothelial NRF2 signaling and IL-8 secretion in a tri-culture model of the alveolar-microvascular interface following diesel exhaust particulate (DEP) exposure

Vitucci,

Simmons,

Martin

et al. 2024

Part Fibre Toxicol

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Background Particulate matter 2.5 (PM2.5) deposition in the lung’s alveolar capillary region (ACR) is significantly associated with respiratory disease development, yet the molecular mechanisms are not completely understood. Adverse responses that promote respiratory disease development involve orchestrated, intercellular signaling between multiple cell types within the ACR. We investigated the molecular mechanisms elicited in response to PM2.5 deposition in the ACR, in an in vitro model that enables intercellular communication between multiple resident cell types of the ACR. Methods An in vitro, tri-culture model of the ACR, incorporating alveolar-like epithelial cells (NCI-H441), pulmonary fibroblasts (IMR90), and pulmonary microvascular endothelial cells (HULEC) was developed to investigate cell type-specific molecular responses to a PM2.5 exposure in an in-vivo-like model. This tri-culture in vitro model was termed the alveolar capillary region exposure (ACRE) model. Alveolar epithelial cells in the ACRE model were exposed to a suspension of diesel exhaust particulates (DEP) (20 µg/cm2) with an average diameter of 2.5 µm. Alveolar epithelial barrier formation, and transcriptional and protein expression alterations in the directly exposed alveolar epithelial and the underlying endothelial cells were investigated over a 24 h DEP exposure. Results Alveolar epithelial barrier formation was not perturbed by the 24 h DEP exposure. Despite no alteration in barrier formation, we demonstrate that alveolar epithelial DEP exposure induces transcriptional and protein changes in both the alveolar epithelial cells and the underlying microvascular endothelial cells. Specifically, we show that the underlying microvascular endothelial cells develop redox dysfunction and increase proinflammatory cytokine secretion. Furthermore, we demonstrate that alveolar epithelial MAPK signaling modulates the activation of NRF2 and IL-8 secretion in the underlying microvascular endothelial cells. Conclusions Endothelial redox dysfunction and increased proinflammatory cytokine secretion are two common events in respiratory disease development. These findings highlight new, cell-type specific roles of the alveolar epithelium and microvascular endothelium in the ACR in respiratory disease development following PM2.5 exposure. Ultimately, these data expand our current understanding of respiratory disease development following particle exposures and illustrate the utility of multicellular in vitro systems for investigating respiratory tract health.

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“…Moreover, practically all types of ROS, including free radical species and non-radical species, can induce the oxidative cleavage of proteins by glutamyl side chain oxidation or α-amidation pathways, leading to the generation of carbonyl groups on protein side chains. As we all know, the oxidation of lipids and proteins produces lipid peroxides and protein carbonyl groups, respectively, leading to the initiation of various tissue damages and aging related to oxidative stress, as well as involving the pathogenesis of many age-related degenerative diseases [ 24 , 26 ]. In the present study, we have found an increase on the serum levels of TBARS and protein carbonyl in aged mice.…”

Section: Discussionmentioning

confidence: 99%

“…They also suggested that the activities of SOD and GSH-Px in the kidneys were significantly diminished during aging [ 37 ]. Fortunately, the decline in antioxidant defenses against oxidative stress during aging can be enhanced or maintained by supplementing extracellular antioxidants [ 26 ]. In addition, the green tea tannins could also help the residual kidneys to scavenge free radicals in rats with nephrectomy [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

Senescence-Mediated Redox Imbalance in Liver and Kidney: Antioxidant Rejuvenating Potential of Green Tea Extract

Hsu

Chen

Tsai

2021

IJERPH

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This study investigates the catechin composition and protective effect of green tea extract on senescence-mediated redox imbalance in the livers and kidneys of aged mice. The results showed that the seven catechins in the green tea extract analyzed in this study could be completely separated within 30 min and the main components of catechins in green tea extract were EGCG, EGC and ECG. In terms of the anti-senescence effects of green tea extract, green tea extract supplementation at doses of 125, 625 and 1250 mg/kg for 4 weeks significantly alleviated the senescence-mediated redox imbalance, as exhibited from significantly (p < 0.05) reduced thiobarbituric acid-reactive substances (TBARS) and protein carbonyls levels in the serum, and increased glutathione (GSH) and total thiols contents in the plasma. Additionally, hepatic and renal protein carbonyls levels were significantly diminished (p < 0.05) and the activities of superoxide dismutase (SOD), catalase, glucose-6-phosphate dehydrogenase (G6PD), glutathione peroxidase (GSH-Px) and glutathione reductase (GSH-Rd) in the liver and kidney were remarkably elevated (p < 0.05). Overall, these results clearly show that green tea extract exhibits extremely potent protective effects against senescence-mediated redox imbalance in the livers and kidneys of mice by inhibiting oxidative damage of lipids and proteins and increasing the activities of antioxidant enzymes in organs.

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Oxidative Stress in Human Toxicology

Abstract: This Special Issue (same name as title) focuses on human exposure to foreign chemicals (xenobiotics) that cause oxidative stress [...]

Cited by 7 publications

References 14 publications

miR-317-3p and miR-283-5p Play a Crucial Role in Regulating the Resistance to Indoxacarb in Spodoptera frugiperda by Targeting GSTs4

miR-317-3p and miR-283-5p Play a Crucial Role in Regulating the Resistance to Indoxacarb in Spodoptera frugiperda by Targeting GSTs4

Epithelial MAPK signaling directs endothelial NRF2 signaling and IL-8 secretion in a tri-culture model of the alveolar-microvascular interface following diesel exhaust particulate (DEP) exposure

Senescence-Mediated Redox Imbalance in Liver and Kidney: Antioxidant Rejuvenating Potential of Green Tea Extract

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