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Intracellular Redox Status and Disease Development: An Overview of the Dynamics of Metabolic Orchestra
Published in Jyoti Ranjan Rout, Rout George Kerry, Abinash Dutta, Biotechnological Advances for Microbiology, Molecular Biology, and Nanotechnology, 2022
Sharmi Mukherjee, Anindita Chakraborty
Oxidative stress has an association with the pathophysiology of inflammatory lung diseases like chronic obstructive pulmonary disease (COPD) and asthma. Elevated supply of blood, high oxygen levels, and exposure to environmental toxins make lungs highly susceptible to oxidative attack (McGuinness and Sapey, 2017). Exogenous ROS from environmental stressors like cigarette smoking or endogenous ROS fromthe inflammatoryprocess and mitochondrial dysfunction triggers oxidative stress and associated with the progression of disease complications (Salama et al., 2014). Oxidative stress increase bronchial inflammation, arachidonic acid release, vascular permeability with airway oedema, hypersecretion and hyperplasia of the mucous gland, corticosteroid resistance by inhibiting glucocorticoid receptor expression, senescence, and the release of neurokinins and tachykinins with an elevation of neurogenic inflammation, impaired bronchodilator responses, and small airway fibrosis (Babusikova et al., 2012; Domej et al., 2014; Kirkham and Barnes, 2013). Oxidative stress in the lungs involves activation of alveolar macrophages and lung resident epithelial cells, generating chemotactic molecules and cytokines that recruit neutrophils, monocytes, and lymphocytes (Van Eeden, 2013). These lead to persistent inflammation, chronic oxidative stress, leading to lung cell apoptosis, autophagy, and repair mechanism defects (Rahman and Adcock, 2006).
Biological Effects of Millimeter and Submillimeter Waves
Published in Ben Greenebaum, Frank Barnes, Biological and Medical Aspects of Electromagnetic Fields, 2018
Stanislav I. Alekseev, Marvin C. Ziskin
The histological and molecular changes in the skin of 8-week-old male C57BL/6 mice exposed to an fs-pulsed THz beam were studied by Jo et al. (2014). The skin on the back of mice was exposed to 3-THz radiation with a pulse width of <200 fs and a repetition rate of 1 kHz for 1 h. The THz pulse energy was about 0.26 nJ/pulse. Accumulated energy in the exposed area (1 cm2) for 1 h was ~1.15 J/cm2. Skin biopsy samples were taken at 1 and 24 h after exposure. No histological changes were found in either 1 or 24 h post-exposure samples. The authors did not find any inflammatory cells or damaged skin cells such as sunburn cells. The collagen fibers in the dermis were also normal. A microarray analysis revealed that some genes in the exposed skin samples were either biologically activated or suppressed. For instance, the gene transcription of substance P, which is involved in local inflammation, decreased while the transcription of calcitonin gene-related peptide, another neuropeptide that is associated with neurogenic inflammation in eczema, increased significantly. These results are at variance with the histological data. The authors did not provide any explanation for these effects. Any information about the temperature elevation in the exposed skin is also missing.
Treatment Options for Chemical Sensitivity
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
Vanilloid-sensitive nerves may be stimulated to release prestored pro-inflammatory neuropeptides by both exogenous and endogenous stimuli. Some of these agents, such as bradykinin, have their own receptors; others may act on VRs. Protons are unique in that they have their own receptors (called acid-sensitive ion channels or ASICs) but they act also on VRs (Figure 6.43). The competitive VR antagonist capsazepine ameliorates carrageenan-induced inflammation in vivo, implying a role for an endogenous vanilloid in initiating the inflammatory cascade. Generally speaking, the tachykinin Substance P (SP) released from vanilloid-sensitive nerves causes smooth muscle cells to contract (e.g., bronchospasm, small vessel spasm) and opens endothelial gaps (plasma extravasation) by interacting at NK-1Rs. Also, SP can stimulate mucus secretion and activate various inflammatory cells. The patient will have phlegm in the throat, having to clear it several times. Also the patient will have a blocking of vasodilation, accounting for the cold hands, feet, as well as the total body cold sensitivity. The predominant effect of calcitonin gene-related peptide (CGRP) is vasodilation. There are several important positive feedback mechanisms involved in neurogenic inflammation. For example, SP released from vanilloid-sensitive nerves activates mast cells. Mast cells liberate histamine, which, in turn, stimulates vanilloid-sensitive nerves to release more SP. It is easy to visualize how the defunctionalization of sensory nerves by vanilloids may prevent, or at least ameliorate, neurogenic inflammatory symptoms. Often incitant avoidance and/or injection neutralizing doses will turn off the incident dose reaction.
Genetic variants affecting chemical mediated skin immunotoxicity
Published in Journal of Toxicology and Environmental Health, Part B, 2022
Isisdoris Rodrigues de Souza, Patrícia Savio de Araujo-Souza, Daniela Morais Leme
TRPV1 activation also promotes release of substance P (SP). SP is a proinflammatory neuropeptide that increases both vasodilation and vascular permeability, upregulates the ICAM-1 expression in human dermal microvascular endothelial cells, stimulates T cell proliferation and enhances expression of proinflammatory cytokines (Kanda and Watanabe 2002; Quinlan et al. 1998; Scholzen and Luger 2004; Weger et al. 2007). SP mediates the chemotaxis of neutrophils, stimulates keratinocyte proliferation, and provokes histamine release from skin mast cells (Ayasse et al. 2020; Borici-Mazi, Kouridakis, and Kontou-Fili 1999). The activation of T cells, mast cells and macrophages by SP, contributes to the imbalance of the immune responses in the early stages of psoriasis (Ayasse et al. 2020). SP might also enhance expression of corticotropin-releasing hormone receptor 1 (CRHR-1) on human mast cell surfaces. Mast cell activation by CRH leads to IL-8, TNF-α, and VEGF secretion and is related to stress induced skin conditions as noted in psoriasis and AD (Asadi et al. 2012). Thus, TRPV1 is an important promoter of neurogenic inflammation, pain, itch and skin diseases (Roosterman et al. 2006); and the capsaicin test –
Health risk assessment and distribution of VOCs during excavation processes for the remediation of contaminated sites
Published in Human and Ecological Risk Assessment: An International Journal, 2019
Kai Zhang, Shuhao Liu, Sidi Wang, Mingyue Zhao, Jianli Jia
Many researchers have assessed the effects of VOCs on human health (Ma et al.2009; Ma et al.2008; Le Cloirec 2012; Liu et al.2008). The main effects of volatile organic pollutants on human health are usually related to the central nervous and hematopoietic systems. However, VOCs also have toxic effects on the immune system and on various internal organs (Qian and Dai 2006). For example, the potential impact of long-term exposure to xylene on human health is similar to that of benzene, which causes lymphatic leukemia (Sekizawa et al.2007). Furthermore, exposure to VOCs has been closely linked to many blood disorders (Lee et al.2002). In addition, VOCs can also cause damage to the outer layer of the skin (Huss-Marp et al. 2004), and exposure to VOCs can increase neurogenic inflammation accompanied by an enhanced histamine response (Kimata 2004).